cancer research essay

Treatment Research

A new cellular immunotherapy approach shrank tumors in 3 of 7 patients with metastatic colon cancer, in a small NCI clinical trial. Normal white blood cells from each patient were genetically engineered to produce receptors that recognize and attack their specific cancer cells.

When it comes to cancer drugs, researchers are moving away from a paradigm called the maximum tolerated dose. Instead, they’re focusing more on identifying doses that produce fewer side effects but are still effective against a person’s cancer.

Reshaping the cancer clinical trials infrastructure to overcome key bottlenecks will involve embracing technology and collaboration, and inviting innovation, explain NCI Director Dr. W. Kimryn Rathmell and NCI Special Advisor Dr. Shaalan Beg.

In a new study in mice, researchers showed they could enhance radiation therapy by boosting levels of the BAMBI protein in MDSC immune cells in the tumor microenvironment. After radiation, T cells flooded into the tumor and killed tumors elsewhere in the body.

In a clinical trial, people being treated for cancer who participated in virtual mind–body fitness classes were less likely to be hospitalized, and had shorter stays when they were hospitalized, than people who did not take the classes.

NCI’s James H. Doroshow, M.D., reflects on the accomplishments of NCI-MATCH, a first-of-its-kind precision medicine cancer trial, and gives an overview of three new successor trials: ComboMATCH, MyeloMATCH, and iMATCH.

A new study, conducted largely in mice, may help explain why a currently used molecular marker—called mismatch repair deficiency—doesn’t always work to predict which patients will respond to immunotherapies called immune checkpoint inhibitors.

New approach may increase the effectiveness of T-cell-based immunotherapy treatments against solid tumors.

A cancer-infecting virus engineered to tamp down a tumor’s ability to suppress the immune system shrank tumors in mice, a new study shows. The modified oncolytic virus worked even better when used along with an immune checkpoint inhibitor.

Despite recommendations, a new analysis shows few people with cancer undergo germline testing to learn if their cancer may have been caused by gene changes inherited from a parent. Germline testing can help doctors determine the best treatments for a patient and help identify people whose family members may be at higher risk of cancer.

ComboMATCH will consist of numerous phase 2 cancer treatment trials that aim to identify promising drug combinations that can advance to larger, more definitive clinical trials.

A new study has compared three formulations of an mRNA vaccine designed to treat cancers caused by human papillomavirus (HPV) infections. All three vaccines showed promise in mice.

Researchers have identified a mechanism by which cancer cells develop specific genetic changes needed to become resistant to targeted therapies. They also showed that this process, called non-homologous end-joining (NHEJ), can potentially be disrupted.

For some people with cancer, is 6 months of immunotherapy the only treatment they might ever need? Or 4 weeks of immunotherapy followed by minor surgery? Results from several small clinical trials suggest these scenarios may be bona fide possibilities.

Two research teams have developed ways of overcoming barriers that have limited the effectiveness of CAR T-cell therapies, including engineering ways to potentially make them effective against solid tumors like pancreatic cancer and melanoma.

In people with cancer treated with immune checkpoint inhibitors, a rare, but often fatal, side effect is inflammation in the heart, called myocarditis. Researchers have now identified a potential chief cause of this problem: T cells attacking a protein in heart cells called α-myosin.

Researchers have modified a chemo drug, once abandoned because it caused serious gut side effects, so that it is only triggered in tumors but not normal tissues. After promising results in mice, the drug, DRP-104, is now being tested in a clinical trial.

Two research teams have developed a treatment approach that could potentially enable KRAS-targeted drugs—and perhaps other targeted cancer drugs—flag cancer cells for the immune system. In lab studies, the teams paired these targeted drugs with experimental antibody drugs that helped the immune system mount an attack.

Inflammation is considered a hallmark of cancer. Researchers hope to learn more about whether people with cancer might benefit from treatments that target inflammation around tumors. Some early studies have yielded promising results and more are on the horizon.

NCI researchers are developing an immunotherapy that involves injecting protein bits from cytomegalovirus (CMV) into tumors. The proteins coat the tumor, causing immune cells to attack. In mice, the treatment shrank tumors and kept them from returning.

FDA has approved the combination of the targeted drugs dabrafenib (Tafinlar) and trametinib (Mekinist) for nearly any type of advanced solid tumor with a specific mutation in the BRAF gene. Data from the NCI-MATCH trial informed the approval.

People with cancer who take immunotherapy drugs often develop skin side effects, including itching and painful rashes. New research in mice suggests these side effects may be caused by the immune system attacking new bacterial colonies on the skin.

Researchers have developed tiny “drug factories” that produce an immune-boosting molecule and can be implanted near tumors. The pinhead-sized beads eliminated tumors in mice with ovarian and colorectal cancer and will soon be tested in human studies.

Women are more likely than men to experience severe side effects from cancer treatments such as chemotherapy, targeted therapy, and immunotherapy, a new study finds. Researchers hope the findings will increase awareness of the problem and help guide patient care.

Research to improve CAR T-cell therapy is progressing rapidly. Researchers are working to expand its use to treat more types of cancer and better understand and manage its side effects. Learn how CAR T-cell therapy works, which cancers it’s used to treat, and current research efforts.

Experts say studies are needed on how to best transition telehealth from a temporary solution during the pandemic to a permanent part of cancer care that’s accessible to all who need it.

Removing immune cells called naive T cells from donated stem cells before they are transplanted may prevent chronic graft-versus-host disease (GVHD) in people with leukemia, a new study reports. The procedure did not appear to increase the likelihood of patients’ cancer returning.

A specific form of the HLA gene, HLA-A*03, may make immune checkpoint inhibitors less effective for some people with cancer, according to an NCI-led study. If additional studies confirm the finding, it could help guide the use of these commonly used drugs.

The success of mRNA vaccines for COVID-19 could help accelerate research on using mRNA vaccine technology to treat cancer, including the development of personalized cancer vaccines.

Aneuploidy—when cells have too many or too few chromosomes—is common in cancer cells, but scientists didn’t know why. Two new studies suggest that aneuploidy helps the cells survive treatments like chemotherapy and targeted therapies.

New research suggests that fungi in the gut may affect how tumors respond to cancer treatments. In mice, when bacteria were eliminated with antibiotics, fungi filled the void and impaired the immune response after radiation therapy, the study found.

FDA has approved belumosudil (Rezurock) for the treatment of chronic graft-versus-host disease (GVHD). The approval covers the use of belumosudil for people 12 years and older who have already tried at least two other therapies.

In lab studies, the antibiotic novobiocin showed promise as a treatment for cancers that have become resistant to PARP inhibitors. The drug, which inhibits a protein called DNA polymerase theta, will be tested in NCI-supported clinical trials.

A drug called avasopasem manganese, which has been found to protect normal tissues from radiation therapy, can also make cancer cells more vulnerable to radiation treatment, a new study in mice suggests.

While doctors are familiar with the short-term side effects of immune checkpoint inhibitors, less is known about potential long-term side effects. A new study details the chronic side effects of these drugs in people who received them as part of treatment for melanoma.

Cholesterol-lowering drugs known as PCSK9 inhibitors may improve the effectiveness of cancer immune checkpoint inhibitors, according to studies in mice. The drugs appear to improve the immunotherapy drugs’ ability to find tumors and slow their growth.

Researchers have developed a nanoparticle that trains immune cells to attack cancer. According to the NCI-funded study, the nanoparticle slowed the growth of melanoma in mice and was more effective when combined with an immune checkpoint inhibitor.

A comprehensive analysis of patients with cancer who had exceptional responses to therapy has revealed molecular changes in the patients’ tumors that may explain some of the exceptional responses.

Researchers are developing a new class of cancer drugs called radiopharmaceuticals, which deliver radiation therapy directly and specifically to cancer cells. This Cancer Currents story explores the research on these emerging therapies.

FDA has recently approved two blood tests, known as liquid biopsies, that gather genetic information to help inform treatment decisions for people with cancer. This Cancer Currents story explores how the tests are used and who can get the tests.

Cancer cells with a genetic feature called microsatellite instability-high (MSI-high) depend on the enzyme WRN to survive. A new NCI study explains why and reinforces the idea of targeting WRN as a treatment approach for MSI-high cancer.

Efforts to contain the opioid epidemic may be preventing people with cancer from receiving appropriate prescriptions for opioids to manage their cancer pain, according to a new study of oncologists’ opioid prescribing patterns.

The gene-editing tool CRISPR is changing the way scientists study cancer, and may change how cancer is treated. This in-depth blog post describes how this revolutionary technology is being used to better understand cancer and create new treatments.

FDA’s approval of pembrolizumab (Keytruda) to treat people whose cancer is tumor mutational burden-high highlights the importance of genomic testing to guide treatment, including for children with cancer, according to NCI Director Dr. Ned Sharpless.

Patients with acute graft-versus-host disease (GVHD) that does not respond to steroid therapy are more likely to respond to the drug ruxolitinib (Jakafi) than other available treatments, results from a large clinical trial show.

NCI is developing the capability to produce cellular therapies, like CAR T cells, to be tested in cancer clinical trials at multiple hospital sites. Few laboratories and centers have the capability to make CAR T cells, which has limited the ability to test them more broadly.

An experimental drug may help prevent the chemotherapy drug doxorubicin from harming the heart and does so without interfering with doxorubicin’s ability to kill cancer cells, according to a study in mice.

In people with blood cancers, the health of their gut microbiome appears to affect the risk of dying after receiving an allogeneic hematopoietic stem cell transplant, according to an NCI-funded study conducted at four hospitals across the globe.

A novel approach to analyzing tumors may bring precision cancer medicine to more patients. A study showed the approach, which analyzes gene expression using tumor RNA, could accurately predict whether patients had responded to treatment with targeted therapy or immunotherapy.

Bone loss associated with chemotherapy appears to be induced by cells that stop dividing but do not die, a recent study in mice suggests. The researchers tested drugs that could block signals from these senescent cells and reverse bone loss in mice.

Some experts believe that proton therapy is safer than traditional radiation, but research has been limited. A new observational study compared the safety and effectiveness of proton therapy and traditional radiation in adults with advanced cancer.

In people with cancer, the abscopal effect occurs when radiation—or another type of localized therapy—shrinks a targeted tumor but also causes untreated tumors in the body to shrink. Researchers are trying to better understand this phenomenon and take advantage of it to improve cancer therapy.

An experimental drug, AMG 510, that targets mutated forms of the KRAS protein completely shrank tumors in cancer mouse models and data from a small clinical trial show that it appears to be active against different cancer types with a KRAS mutation.

Researchers have engineered an oncolytic virus to kill cancer cells and boost the immune response against tumors. In a new study, the virus provided T cells around tumors with a hormone they need for their own cell-killing functions.

FDA has approved entrectinib (Rozlytrek) for the treatment of children and adults with tumors bearing an NTRK gene fusion. The approval also covers adults with non-small cell lung cancer harboring a ROS1 gene fusion.

A new NCI-supported study showed that altering cancer cell metabolism by feeding mice a diet very low in the nutrient methionine improved the ability of chemotherapy and radiation therapy to shrink tumors.

An NCI-funded clinical trial is testing the immunotherapy drug nivolumab (Opdivo) in people who have advanced cancer and an autoimmune disease, such as rheumatoid arthritis, lupus, or multiple sclerosis, who are often excluded from such trials.

Researchers have identified a protein called CD24 that may be a new target for cancer immunotherapy. The protein is a ‘don’t eat me’ signal that prevents immune cells called macrophages from engulfing and eating cells.

Injecting cells undergoing necroptosis, a form of cell death, into tumors in mice kickstarted an immune response against the tumors, researchers have found. When combined with immunotherapy, the treatment was effective at eliminating tumors in mice.

Researchers have identified proteins that may play a central role in transforming T cells from powerful destroyers to depleted bystanders that can no longer harm cancer cells. The findings could lead to strategies for boosting cancer immunotherapies.

Did you know that NCI supports clinical trials of new treatments for pet dogs with cancer? Learn more about NCI’s comparative oncology studies and how they may also help people with cancer.

Researchers have discovered a potential way to turn on one of the most commonly silenced tumor-suppressor proteins in cancer, called PTEN. They also found a natural compound, I3C, that in lab studies could flip the on switch.

New findings from a clinical trial suggest that a single dose of radiation therapy may control painful bone metastases as effectively as multiple lower doses of radiation therapy.

The expanding use of cancer immunotherapy has revealed a variety of side effects associated with this treatment approach. Researchers are now trying to better understand how and why these side effects occur and develop strategies for better managing them.

The investigational immunotherapy drug bintrafusp alfa (also called M7824), a bifunctional fusion protein, shrank the tumors of some patients with advanced HPV-related cancers, according to results from a phase 1 clinical trial.

A new study provides insight into how cancer immunotherapy works and suggests ways to enhance the treatment’s effectiveness. The NCI-led study, published in Science, examined the effect of high potassium levels on T cells.

Pain is a common and much-feared symptom among people with cancer and long-term survivors. As more people survive cancer for longer periods, there is a renewed interest in developing new, nonaddictive approaches for managing their chronic pain.

Home — Essay Samples — Nursing & Health — Cancer — Cancer Outline And The Importance Of Cancer Research

Cancer Outline and The Importance of Cancer Research

• Categories: Cancer

About this sample

Words: 1492 |

Published: Jul 30, 2019

Words: 1492 | Pages: 3 | 8 min read

• Sustaining proliferative signaling where cancer cells produce internal autocrine signals using mutated oncogenes (that promotes excessive cell growth) and tumor suppressor genes (does not stop cell proliferation.) despite receiving cell signals from neighboring cells to stop growing.
• Evading growth suppressors: Cancerous cells alter tumor suppressor genes such that despite having damaged DNA, it continues to proliferate and lack contact inhibition.
• Activating invasion and metastasis: Cancer cells moves away from its original location to move into distant body regions and organs using blood vessels and invade surrounding tissues and vessels to form new colonies and secondary tumors.'
• Enabling replicative immortality: Cancerous cells evade senescence by lengthening their telomeric DNA using manipulated telomerase at the end of chromosomes that enables to divide indefinitely (unlike normal cells with shortening telomeres after every cell division until seizure - senescence) and avoid apoptosis
• Inducing angiogenesis: Cancer cells form new blood vessels by manipulating and sending molecular signals to normal cells surrounding tumor that are capable of new vasculature production. This helps them to receive sufficient nutrients and oxygen and remove waste products.
• Resisting cell death: Cancerous cells either inactivate TP53 tumor suppressor which detect abnormalities in cells and cause apoptosis or carry defects in proteins involved in programmed cell death thereby avoiding it which causes accumulation of damaged cells.
• Age: Individuals aged 55 years and above are more susceptible in being diagnosed with cancer
• Patient’s Lifestyle: Cigarette Smokers have increased risk for cancer
• Environment: Acquiring specific chronic infections/bacteria such as Hepatitis B and hepatitis C that heightens susceptibility for liver cancer, Exposure to either ultraviolet radiation from the sun or ionizing radiation from medical imaging devices like x-rays, medication which are immunosuppressive that reduce both nonspecific and specific immune functions raising cancer development risk, carcinogen exposure or consumption that cause mutations in genetic activity like benzene and mercury
• Hereditary: Individuals inheriting oncogenes which are cancer proliferation genes or having at risk genes which requires environmental stimulation to alter modify it into cancer such as basal cell carcinoma.
• Blood tests: To detect any abnormally high amounts of tumour markers (chemical produced by cancer cells) in bloodstream
• Diagnostic imaging: X-rays - to check for potentially malignant tumors from still picture taken from inside the body, computed tomography (CT scan) - for 3D cross-sectional image of internal body organs that displays any tumors with dye injected into patient to increase contrast in image, ultrasonography - Using high frequency sound waves to reflect off bodily tissues for producing sonograms, Magnetic resonance imaging (MRI) to produce detailed cross sections of body by compelling tissues to emit radio waves
• Biopsy: surgically removed sample of patient's tissue is examined microscopically to check if it’s benign or malignant.
• Chemotherapy: Using drugs to target and kill cells dividing quickly such as blood or bone marrow cells.
• Surgery: Using incisions to remove both tumor, surrounding tissues and optionally lymph nodes to prevent cancer relapse
• Radiation therapy: Using high-energy rays either externally (from large machine in cancer treatment areas) or internally (placing low radiation doses inside specific tissues of patient’s body) to cause damage to both cancerous and surrounding normal cellular DNA, thereby interrupting cell division and growth.
• Hormone Therapy: Providing hormone therapy medication to patients for suppressing hormone synthesis and blocking hormonal action for cancers that require hormones to grow.
• Non-specific Immunotherapy: Using monoclonal antibodies to either attached to cancer cells and stimulate immune system to recognize and destroy cancer cells or using other types of monoclonal antibodies for carrying drugs/radioactive isotopes directly to cancer cells.
• Refraining from tobacco consumption
• Participation in physical activity to maintain healthier weights
• Consuming healthier diet consisting of fruits, vegetables and limiting polyunsaturated fats and processed meats
• Limiting alcohol consumption
• Applying sunscreen for protection against harmful UV rays
• Getting immunizations against hepatitis B and the human papillomavirus
• Individuals going for health screenings to increase detection of cancers especially in early stages to improve chances of treating them.

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Essay on Cancer for Students and Children

500+ words essay on cancer.

Cancer might just be one of the most feared and dreaded diseases. Globally, cancer is responsible for the death of nearly 9.5 million people in 2018. It is the second leading cause of death as per the world health organization. As per studies, in India, we see 1300 deaths due to cancer every day. These statistics are truly astonishing and scary. In the recent few decades, the number of cancer has been increasingly on the rise. So let us take a look at the meaning, causes, and types of cancer in this essay on cancer.

Cancer comes in many forms and types. Cancer is the collective name given to the disease where certain cells of the person’s body start dividing continuously, refusing to stop. These extra cells form when none are needed and they spread into the surrounding tissues and can even form malignant tumors. Cells may break away from such tumors and go and form tumors in other places of the patient’s body.

Types of Cancers

As we know, cancer can actually affect any part or organ of the human body. We all have come across various types of cancer – lung, blood, pancreas, stomach, skin, and so many others. Biologically, however, cancer can be divided into five types specifically – carcinoma, sarcoma, melanoma, lymphoma, leukemia.

Among these, carcinomas are the most diagnosed type. These cancers originate in organs or glands such as lungs, stomach, pancreas, breast, etc. Leukemia is the cancer of the blood, and this does not form any tumors. Sarcomas start in the muscles, bones, tissues or other connective tissues of the body. Lymphomas are the cancer of the white blood cells, i.e. the lymphocytes. And finally, melanoma is when cancer arises in the pigment of the skin.

Get the huge list of more than 500 Essay Topics and Ideas

Causes of Cancer

In most cases, we can never attribute the cause of any cancer to one single factor. The main thing that causes cancer is a substance we know as carcinogens. But how these develop or enters a person’s body will depend on many factors. We can divide the main factors into the following types – biological factors, physical factors, and lifestyle-related factors.

Biological factors involve internal factors such as age, gender, genes, hereditary factors, blood type, skin type, etc. Physical factors refer to environmental exposure of any king to say X-rays, gamma rays, etc. Ad finally lifestyle-related factors refer to substances that introduced carcinogens into our body. These include tobacco, UV radiation, alcohol. smoke, etc. Next, in this essay on cancer lets learn about how we can treat cancer.

Treatment of Cancer

Early diagnosis and immediate medical care in cancer are of utmost importance. When diagnosed in the early stages, then the treatment becomes easier and has more chances of success. The three most common treatment plans are either surgery, radiation therapy or chemotherapy.

If there is a benign tumor, then surgery is performed to remove the mass from the body, hence removing cancer from the body. In radiation therapy, we use radiation (rays) to specially target and kill the cancer cells. Chemotherapy is similar, where we inject the patient with drugs that target and kill the cancer cells. All treatment plans, however, have various side-effects. And aftercare is one of the most important aspects of cancer treatment.

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Home > Cancer Research Catalyst > Cancer Survivors: In Their Words

Cancer Survivors: In Their Words

This year alone, an estimated 1.8 million people will hear their doctor say they have cancer. The individual impact of each person can be clouded in the vast statistics. In honor of National Cancer Survivor Month,  Cancer Today would like to highlight several personal essays we’ve published from cancer survivors at different stages of their treatment. 

In  this essay , psychiatrist Adam P. Stern’s cerebral processing of his metastatic kidney cancer diagnosis gives rise to piercing questions. When he drops off his 3-year-old son to daycare, he ponders a simple exchange: his son’s request for a routine morning hug before he turns to leave. “Will he remember me, only a little, just enough to mythologize me as a giant who used to carry him up the stairs? As my health declines, will he have to learn to adjust to a dad who used to be like all the other dads but then wasn’t?” he questions. 

In  another essay from a parent with a young child, Amanda Rose Ferraro describes the abrupt change from healthy to not healthy after being diagnosed with acute myeloid leukemia in May 2017. After a 33-day hospital stay, followed by weeklong chemotherapy treatments, Ferraro’s cancer went into remission, but a recurrence required more chemotherapy and a stem cell transplant. Ferraro describes harrowing guilt over being separated from her 3-year-old son, who at one point wanted nothing to do with her. “Giving up control is hard, but not living up to what I thought a mother should be was harder. I had to put myself first, and it was the hardest thing I had ever done,” she writes.

In January 1995, 37-year-old Melvin Mann was diagnosed with chronic myelogenous leukemia, which would eventually mean he would  need to take a chance on a phase I clinical trial that tested an experimental drug called imatinib—a treatment that would go on to receive U.S. Food and Drug Administration approval under the brand name Gleevec. It would also mean trusting a system with a documented history of negligence and abuse of Black people like him: “Many patients, especially some African Americans, are afraid they will be taken advantage of because of past unethical experiments like the infamous Tuskegee syphilis study​,” Mann writes, before describing changes that make current trials safer. Mann’s been on imatinib ever since and has enjoyed watching his daughter become a physician and celebrating 35 years of marriage.

In  another essay , Carly Flumer addresses the absurdity of hearing doctors reassure her that she had a good cancer after she was diagnosed with stage I papillary thyroid cancer in 2017. “What I did hear repeatedly from various physicians was that I had the ‘good cancer,’ and that ‘if you were to have a cancer, thyroid would be the one to get,’” she writes.

In another piece for Cancer Today , Flumer shares  how being diagnosed with cancer just four months after starting a graduate program shaped her education and future career path.

For Liza Bernstein, her breast cancer diagnosis created a paradox as she both acknowledged and denied the disease the opportunity to define who she was. “In the privacy of my own mind, I refused to accept that cancer was part of my identity, even though it was affecting it as surely as erosion transforms the landscape,” she writes . “Out in the world, I’d blurt out, ‘I have cancer,’ because I took questions from acquaintances like ‘How are you, what’s new?’ literally. Answering casual questions with the unvarnished truth wasn’t claiming cancer as my identity. It was an attempt to dismiss the magnitude of it, like saying ‘I have a cold.’” By her third primary breast cancer diagnosis, Bernstein reassesses and moves closer to acceptance as she discovers her role as advocate.

As part of the staff of  Cancer Today , a magazine and online resource for cancer patients, survivors and caregivers, we often refer to a succinct tagline to sum up our mission: “Practical knowledge. Real hope.” Part of providing information is also listening closely to cancer survivors’ experiences. As we celebrate National Cancer Survivor Month, we elevate these voices, and all patients and survivors in their journeys.

Cancer Today is a magazine and online resource for cancer patients, survivors, and caregivers published by the American Association for Cancer Research.  Subscriptions to the magazine are free ​ to cancer patients, survivors and caregivers who live in the U.S. 

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Since the beginning of 2017, Chinese Journal of Cancer has published a series of important questions in cancer research and clinical oncology, which spark diverse thoughts, interesting communications, and potential collaborations among researchers all over the world. In this article, 8 more questions are presented as follows. Question 86. In which circumstances is good supportive care associated with a survival advantage in patients with cancer? Question 87. Can we develop animal models to mimic immunotherapy response of cancer patients? Question 88. What are the mechanisms underlying hepatitis B virus-associated non-hepatocellular cancers? Question 89. Can we more precisely target tumor metabolism by identifying individual patients who would benefit from the treatment? Question 90. What type of cranial irradiation-based prophylactic therapy combination can dramatically improve the survival of patients with extensive small-cell lung cancer? Question 91. How can postoperative radiotherapy prolong overall survival of the patients with resected pIIIA-N2 non-small cell lung cancer? Question 92. What are the key molecular events that drive oral leukoplakia or erythroplakia into oral cancer? Question 93. How could we track the chemotherapeutics-driven evolution of tumor genome in non-small cell lung cancer for more effective treatment?

To accelerate our endeavors to overcome cancer, Chinese Journal of Cancer has launched a program of publishing 150 most important questions in cancer research and clinical oncology [ 1 ]. Since the beginning of 2017, Chinese Journal of Cancer has published a series of important questions in cancer research and clinical oncology [ 2 – 12 ], which spark diverse thoughts, interesting communications, and potential collaborations among researchers all over the world. In this article, Questions 86–93 are selected and presented. This program of collecting and publishing the key questions is still ongoing. Please send your thoughtful questions to Ms. Ji Ruan via email: [email protected].

Question 86: In which circumstances is good supportive care associated with a survival advantage in patients with cancer?

Background and implications.

It is well documented that good supportive care throughout the treatment and survival phases of cancer as well as palliative care towards the end of life improve the quality of life of the patients [ 13 ]. In some circumstances, good supportive care may also prolong survival. Quintin et al. [ 14 ] performed a global analysis of data from multiple trials and showed that quality of life and presenting symptoms were prognostic factors for survival of patients with cancer in addition to other clinical characteristics. For example, febrile neutropenia following chemotherapy is a life-threatening adverse effect and can be mitigated by giving the chemotherapy with granulocyte colony stimulating factor (G-CSF). It is well documented that mortality from infection is reduced by G-CSF [ 15 ]; however, it is not clear that this may be translated into an overall survival advantage. Prophylactic use of antiemetics increases the tolerance of chemotherapy, allowing full dose to be given and courses of chemotherapy to be completed, which has been shown to prolong survival [ 16 ]. Good symptom control with chemotherapy may also prolong survival. In a randomized study, second-line chemotherapy was given with or without early palliative care to patients with non-small cell lung cancer, and the results showed that those receiving the palliative care in addition to their chemotherapy had significantly longer survival than those receiving chemotherapy only (11.6 vs. 8.9 months, P  = 0.02) [ 17 ]. Further, it is intriguing that psychosocial support may prolong survival. A weekly psychosocial support group and self-hypnosis for pain was added to anticancer therapy for breast cancer patients in a randomized trial and resulted in prolonged survival as compared with those who only received anticancer therapy [ 18 ]. The relationship between social networks and social support has been equivocal although a large breast cancer study showed an increase in both all-cause mortality and breast cancer mortality in women who are socially isolated [ 19 , 20 ]. Certainly, the narratives of exceptional survivors of incurable cancer ascribed some of their outcomes to family support [ 21 ].

Clearly, in some circumstances, the addition of good supportive care which addresses cancer-associated symptoms and adverse effects of treatment can be added to anticancer treatment to prolong survival. More researches are needed to better define when this occurs.

Affiliation and email

Sansom Institute for Health Research, University of South Australia, Adelaide, South Australia 5001, Australia.

[email protected].

Question 87: Can we develop animal models to mimic immunotherapy response of cancer patients?

Efforts on immuno-oncology (I/O) research to fight cancer are in exponential phase of growth due to recent breakthrough in the development of immune checkpoint inhibitors and unprecedented rate of regulatory approval to shorten the otherwise lengthy bench to bedside process. The prevalent models include syngeneic, genetically engineered, and partially humanized mouse models each with its advantages and limitations. The lack of precise animal models that would be capable of mimicking human immune microenvironment is one of the major challenges for proper preclinical evaluation of I/O therapies and identifying patients most likely to be benefited from specific I/O strategies.

The ideal animal models should also possess effective biomarkers for monitoring the immune functions of the host as well as therapeutic effects of I/O. In current clinical practice, the remarkable progress in the development of immune checkpoint inhibitors went solo without parallel advancement of definitive patient selection tool. The cost, toxicities, and the time delay for the 40%–60% of patients not benefiting from immunotherapy makes it imperative to identify valid prognostic biomarkers [e.g., programmed death-ligand 1 (PD-L1) expression, mismatch repair (MMR) deficiency, cluster of differentiation 8 (CD8) T cell infiltrates, tumor mutation burden] that could predict patient response and facilitate differentiation of durable response versus transient response. Given the dynamic nature of the immune response and the complexity of immune/tumor interaction, development of biomarkers for immunotherapies is highly challenging. Presence of tumor-specific antigens, expression of immunosuppressive molecules [PD-L1, indoleamine 2,3-dioxygenase (IDO), and so on] by tumor cells, and mutation load and landscape all contribute to the response of tumor cells to I/O therapies. While most of the biomarker-searching efforts had focused on tumor characteristics, the role of host immune system is equally important. The effectiveness of a given immunotherapeutic approach depends on a pre-existing immune state of a patient.

In summary, development of clinically relevant animal models possessing discerning prognostic markers is critical to fulfill the promise of immunotherapy as a paradigm-shifting strategy to fight the most aggressive and intractable cancers.

Qian Shi and Meng Qiao.

Affiliation and emails

Crown Biosciences Inc., Taicang, Jiangsu Province, 215400, P. R. China.

[email protected]; [email protected].

Question 88: What are the mechanisms underlying hepatitis B virus-associated non-hepatocellular cancers?

Hepatitis B virus (HBV) infection is a strong risk factor for the development of hepatocellular carcinoma. Epidemiological studies have also shown that HBV infection may increase the incidence of several types of non-hepatocellular cancers, including gastric adenocarcinoma, pancreatic ductal carcinoma, and non-Hodgkin lymphoma (NHL). Clinical studies further suggested that some of these HBV-associated non-hepatocellular cancers, for instance a subtype of NHL, diffuse large B cell lymphoma, exhibit a more aggressive disease course with poor prognosis, independent of its pathological subtype. However, what are the mechanisms underlying these associations and whether the viral infection is indeed disease-causing or rather a contributing co-factor remain unclear. Two major hypotheses, direct viral infection of the corresponding cell types and chronic viral antigen stimulations, have been proposed. In both scenarios, infection may result in dysregulation of host cellular processes and increased genome instability, and in the case of direct infection, like in hepatocellular carcinoma, integration of viral DNA into the host genome may lead to activation of selective oncogenes. More detailed morphological and molecular studies, including characterization of the genome of these HBV-associated non-hepatocellular cancers and the repertories of infiltrating immune cells, may provide further clues to this question. It will also be of interest to determine if there is an association between genotype (strain of HBV) and phenotype (type of cancer). Finally, in areas/countries with a high prevalence of infection and initiated the mandatory HBV vaccine program decades ago, theoretically, the incidence of these non-hepatocellular cancers should decrease with time. Of note, this may be complicated by the increased contribution of other risk factors, especially life style-related factors. Chronic HBV infection is endemic in some parts of Asia, Africa, and South America and remains to be a public health burden in these areas. Further understanding the molecular mechanisms underlying the HBV-associated cancers will help us to develop novel or more precise therapies for the affected patients.

Yao Liu and Qiang Pan-Hammarström.

Division of Clinical Immunology, Department of Laboratory Medicine, Karolinska University Hospital, Huddinge, Stockholm SE 141 86, Sweden.

[email protected]; [email protected].

Question 89: Can we more precisely target tumor metabolism by identifying individual patients who would benefit from the treatment?

Background and implication.

During the process of tumorigenesis, tumor cells must face two challenges: first, obtaining the nutrients needed for the rapid growth; and second, evading the surveillance and attack from the host immune system. Tumor cell’s unique metabolic program can be used to meet these challenges. Glycolysis is the major metabolic process used by malignant tumors, even when oxygen supply is adequate, which is termed as “the Warburg effect”. Glycolysis decreases the pH value of the tumor microenvironment (TME); therefore, tumor cells can inhibit the activities of antigen-presenting cells (APCs) and cytotoxic T lymphocytes (CTLs) by controlling the acidity of TME, eventually leading to tumor cell immune escape. A second group of metabolism-related modification directly targets the major histocompatibility complex-I (MHC-I) and related molecules and hence sensitizes cancer cells to the cytolytic actions of the anti-tumor adaptive immune response.

Recent findings from in vitro and in vivo studies have shown that targeting tumor and immune cell metabolism hold the promising possibilities toward clinical therapeutics for treating cancer [ 22 , 23 ]. However, clinical benefit has only been observed in a small number of patients [ 24 – 28 ]. Most patients still do not respond to these new therapies, and nearly all patients with certain types of cancer (i.e., pancreatic and colorectal cancers) do not respond. The reason is probably because tumor metabolism may vary over the course of tumor development, or some hidden tumor metabolic products modulate signaling pathways important for immune cell activation. A new hypothesis has been proposed that tumor cells can change their metabolism by waves of gene regulation to adjust to their different needs [ 29 ]. Some of these waves are originated by deregulated expression of oncogenes, which have already been linked to metabolic remodeling. On the other hand, different parts of solid tumor sometimes possess different epigenetic characteristics and may be derived from distinct cancer stem cell populations. Therefore, the most serious challenge in reshaping the tumor-specific metabolism and immune profiles in TME is to understand the metabolic heterogeneity which is extremely complicated depending not only on tumor and immune cell types but also on tumor stages and subset of patient population.

Nevertheless, the success associated with these new approaches has opened new investigations addressing several questions: How much metabolism pathways represent true vulnerabilities for tumor development and immunosuppression in different types and stages of cancer? Are there other factors that may be blocking, even temporarily, which is critical for tumor control? How different subsets of tumor cell populations respond to metabolic intervention? Can we identify ahead of time the patients who would benefit from metabolic targeted therapy?

Notably, tumor and immune cells share similar metabolic needs and reprogramming during proliferation to support their increased biosynthetic and energy demands [ 30 , 31 ] and often compete for the same nutrients. Therefore, deprivation of nutrients in TME must be cautiously explored to eliminate potential negative impacts on the anti-tumor immunity. Understanding the underlying mechanisms of metabolic interplay between tumor and immune cells will provide new precise directions to manipulate the tumor metabolism for better treatment outcome.

Jianyang Wang and Zhouguang Hui.

Department of Radiation Oncology (JW and ZH), Department of VIP Medical Services (ZH), National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100021, China.

[email protected]; [email protected].

Question 90: What type of cranial irradiation-based prophylactic therapy combination can dramatically improve the survival of patients with extensive small-cell lung cancer?

Brain metastasis is a common reason of treatment failure in small-cell lung cancer (SCLC), particularly in extensive disease which represents approximately two-thirds of newly diagnosed SCLCs. Recent studies have found that thoracic radiotherapy (TRT) can increase the 2-year overall survival (OS) rate of patients with extensive SCLC after chemotherapy [ 32 – 34 ]. However, it remains controversial that whether prophylactic cranial irradiation (PCI) can prolong OS [ 35 – 38 ]. The combination of TRT and PCI may boost the chances of survival, but there will be not much predictable OS benefit even if more prospective studies with large sample sizes are conducted. After first-line chemotherapy, the comprehensive treatment based on TRT and PCI, such as combining with new anti-metastatic drugs, will make great strides toward OS improvement. The application of more accurately targeted therapy is now available and promising. Maintenance treatment with sunitinib can prolong progression-free survival (PFS) in extensive SCLC [ 39 ]. Recent studies on new drugs targeting the signaling pathways (e.g., Notch signaling) related to neuroendocrine differentiation, DNA reparation, and immune checkpoint are ongoing. The Notch signaling pathway influences multiple processes in normal cell morphogenesis, including the differentiation of multipotent progenitor cells (neuron differentiation), cell apoptosis, and cell proliferation. Rovalpituzumab tesirine (Rova-T) targeting the Notch signaling pathway showed promising results in a phase I trial [ 40 ]. Poly ADP-ribose polymerase (PARP) is DNA repairase and is critical in DNA damage repair. By inhibiting PARP, proliferation of malignant cells can be suppressed. Veliparib, a PARP inhibitor, has yielded antitumor activity in SCLC [ 41 ]. Researches on immunotherapy primarily focus on cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) and programmed cell death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) inhibitors. Nivolumab alone and in combination with ipilimumab resulted in encouraging response rates (RR) in a phase I/II trial in the relapsed tumor setting [ 42 ]. The development of anti-metastasis agents is clearly critical for further improving the survival benefits of the patients with extensive SCLC. In addition, advanced irradiation technique is expected to be adopted in future clinical trails to decrease irradiation-induced injury in hippocampus for protecting cognitive function [ 43 ].

Lei Deng and Zhouguang Hui.

Department of Radiation Oncology (LD and ZH), Department of VIP Medical Services (ZH), National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100021, China.

[email protected]; [email protected].

Question 91: How can postoperative radiotherapy prolong overall survival of the patients with resected pIIIA-N2 non-small cell lung cancer?

For patients with resected pIIIA-N2 non-small cell lung cancer (NSCLC), the main reason of treatment failure is locoregional and/or distant relapse. Adjuvant chemotherapy can prolong overall survival to some extent. However, the role of postoperative radiotherapy is not well defined.

A meta-analysis study on postoperative radiotherapy published in 1998 concluded that postoperative radiotherapy did not prolong the survival, even in patients with stage III and pN2 NSCLC, which may due to the toxicities with suboptimal, outdated irradiation equipment and techniques [ 44 ]. Improvements in conformal radiotherapy techniques have led to a resurgence of interest in studying the effect of postoperative radiotherapy on pIIIA-N2 NSCLC. Several retrospective, large-size, case–control studies have shown that postoperative radiotherapy using three dimensional conformal radiotherapy (3D-CRT) or intensity modulated radiation therapy (IMRT) techniques can prolong overall survival [ 45 ]. However, the benefit still needs to be confirmed by randomized clinical trials (RCTs). Up to now, there are three such phase III RCTs. CALGB 9734, the earliest one, failed because of slow accrual [ 46 ]. LUNGART, the ongoing one, began in 2007 and aims to enroll 700 patients by its conclusion in 2022. The other ongoing phase III multi-center RCT ( {"type":"clinical-trial","attrs":{"text":"NCT00880971","term_id":"NCT00880971"}} NCT00880971 ), conducted by our institute, has accrued 400 patients over planned 500 patients. However, due to the heterogeneity of pIIIA-N2 NSCLC, only certain subgroups of patients may benefit from postoperative radiotherapy. Selecting suitable candidates or the populations at high risk who may benefit from postoperative radiotherapy is the next and profound task.

It is expected that by combining with targeted therapy and/or immunotherapy, the therapeutic effects of postoperative radiotherapy can be enhanced. For patients with completely resected NSCLC with epidermal growth factor receptor (EGFR) activating mutation, two recently reported RCTs have showed that adjuvant EGFR tyrosine kinase inhibitors (TKIs) significantly prolonged disease-free survival as compared with adjuvant chemotherapy [ 47 , 48 ]. Therefore, for pIIIA-N2 NSCLC patients with EGFR-activating mutation receiving EGFR TKIs, the value of postoperative radiotherapy should be further evaluated. Theoretically, any new agent that can inhibit metastasis could enhance the efficacy of postoperative radiotherapy, and more efforts are warranted in this direction.

Yu Men and Zhouguang Hui.

Department of VIP Medical Services, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100021, China.

[email protected]; [email protected].

Question 92: What are the key molecular events that drive oral leukoplakia or erythroplakia into oral cancer?

The natural history of cancer is poorly understood. The main reason is that in the vast majority of the cases, malignant tumors are diagnosed after becoming clinically perceptible. The paradox is that, for patients dying from cancer, the time from diagnosis to death is often much shorter than the long period preceding diagnosis. Most of our knowledge is based on the analysis of established malignant tumors in comparison with histologically normal tissue, and the use of naturally occurring or genetically engineered animal models that may not recapitulate the natural history of human cancer. Initiation is thought to be the first step of the multistep model of cancer development, followed by promotion and progression. However, the stepwise and sequential progression model is being challenged by some clinical observations. One of the best examples is the natural history of oral leukoplakia or erythroplakia, the most frequent, potentially malignant lesions of the oral cavity. They can remain for many years without changing, can regress spontaneously or after cessation of tobacco smoking, alcohol drinking, or smokeless tobacco, and can transform to invasive squamous cell carcinoma (SCC) at the same site or at distance from the potentially malignant lesion. The reported rate of malignant transformation has been low in community-based studies in developing countries (0.06% per year) and higher in observational studies in western countries involving patients followed in hospital-based academic centers (1%–5% per year) [ 49 ].

We believe that the longitudinal and spatial dynamics of early-stage tumorigenesis in the oral cavity through comprehensive evaluation of cellular and molecular changes in the epithelial and stromal cells represent a unique setting to get more insight into the natural history of carcinomas. The disease is prevalent in different parts of the world and associated with various environmental agents: in western countries, it frequently affects patients with smoking and alcohol drinking history in the form of oral leukoplakia, whereas in Southeast Asia it frequently affects patients consuming areca nut, betel leaf, and quid who preferentially develop erythroplakia. Of note, oral potentially malignant lesions and SCC negative for human papillomavirus affecting patients with no smoking or alcohol drinking history, although representing a minority of all patients, have an increasing incidence over the past decades for unknown reasons. The oral cavity is easily accessible, and it is considered to be a molecular mirror of molecular alterations induced by smoking in the upper and lower aerodigestive tract. Prospectively validated in situ biomarkers of risk (e.g., loss of heterozygocity at prespecified chromosomal sites) can be used to define cohorts of patients with potentially malignant lesions at high risk of developing oral cancer. These elements represent a strong rationale for intensive exploration in this unique setting. It has the potential to foster international collaborations toward the better understanding of the biology of early-stage tumorigenesis, and provide an opportunity to develop personalized prevention strategies that will benefit patients far beyond the decreased incidence of oral cancer.

Pierre Saintigny.

Univ Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de recherche en cancérologie de Lyon; Department of Translational Research and Innovation, and Department of Medical Oncology, Centre Léon Bérard, Lyon, 69008, France.

[email protected].

Question 93: How could we track the chemotherapeutics-driven evolution of tumor genome in non-small cell lung cancer for more effective treatment?

Currently, effective drug treatments for the patients with non-small cell lung cancer (NSCLC) comprise mainly of standard platinum-based cytotoxic treatment, targeted therapies including inhibitors for epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), and immunotherapy. However, treatment resistance will inevitably occur in most patients after a certain period of time. This is believed to be partially caused by the heterogeneity in tumor genome. Cancer is a genomic disease, and cancer genome constantly undergoes changes under selective pressure from anticancer drug treatment. This alteration is also named tumor evolution, which partially explains acquired drug resistance. For example, some acquired secondary mutations, e.g., EGFR C797S, have been detected in the patient who initially harbors EGFR T790M mutation when resistance against first-line EGFR inhibitor occurs. Therefore, there is a need to dynamically monitor tumor clonal evolution in NSCLC patients. Methods for monitoring tumor evolution include multiregional sequencing and liquid biopsies. In multiregional sequencing, tumor masses from several regions are sequenced in parallel through next-generation sequencing. In liquid biopsies, a serial of circulating molecules or cells in the blood including circulating tumor DNAs (ctDNAs) and circulating tumor cells (CTCs) could reflect the information of tumor genome. These methods could represent the whole tumor genomic landscape and reflect tumor heterogeneity. In addition to this, longitudinal or serial monitoring tumor genome through liquid biopsies or multiregional sequencing could keep track of the tumor genome in both time and space. Of course, it remains a technical challenge in collecting biopsy samples from multiple time points in the same patient. Advances in imaging-guided transthoracic biopsy of lung lesions are the hope for delivering personalized treatments in response to the evolving tumor genome for dramatically improving treatment outcomes in NSCLC patients.

Yi Xiong and Zhi-Xing Lu.

Xiangya school of medicine, Central South University, Changsha, Hunan 410008, P. R. China.

[email protected]; [email protected].

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Research Recap: Younger Adults at a Higher Risk of 17 Cancers

dusanpetkovic / Getty Images

A study published this week from researchers at the American Cancer Society in The Lancet Public Health adds to growing evidence that young adults are more likely to develop several types of cancer than older generations.

We’ve covered this phenomenon before . Research published last year in JAMA Network Open showed that people in their 30s, and young women in particular, saw disproportionately high rates of cancer between 2010 and 2019. Breast, thyroid, and colon or rectal cancers were diagnosed the most in people under 50. Cancers of the appendix and the intrahepatic bile duct grew the fastest among this group.

How do the latest findings add to the conversation about rising cancer rates in young adults? 

Different from other studies of early-onset cancer rates, this new paper tracked both case rates and mortality rates. It also encompasses more cancer types than many of the major studies published recently. 

Here’s what you need to know.

At Least 17 Cancers Are Increasing in Younger Generations

17 of the 34 cancers included in the study became more common in younger adults compared to older generations:

• Colorectal cancer
• Endometrial cancer
• Gallbladder and other biliary cancers
• Kidney cancer
• Pancreatic cancer
• Non-cardia gastric cancer
• Gastric cardia cancer
• Testicular cancer
• Small intestine cancers
• Estrogen receptor-positive breast cancer
• Ovarian cancer
• Liver cancer (females) 
• Non-HPV-associated oral and pharyngeal cancers
• Anal cancer (males)
• Kaposi sarcoma (males)

Many of these cancers are considered rare, meaning there are fewer than 200,000 cases per year.

8 Cancers Have Been Increasing By Age Group Since 1920

To understand how cancer diagnoses and death rates have changed over the years, researchers divided patients into “birth cohorts,” which were separated by five-year intervals from 1920 to 1990.

In addition to the cancers identified in previous research, the authors found that each cohort had a higher risk of developing eight cancer types than the groups before them:

• Liver cancers (females) 
• Non-HPV-related oral cavity and pharyngeal cancers (female)

Rates for the other nine cancer types declined for the first few decades of the study, but have picked up in younger generations.

The risk of developing cancer is two to three times greater for millennials compared to baby boomers for small intestine cancer, kidney cancer, pancreatic cancer, and liver and intrahepatic bile duct cancer in females.

An Increase in Diagnoses Doesn’t Mean an Increase in Death Rates

While cancer rates have climbed over time, death rates don’t always follow suit. However, mortality risk increased alongside incidence rates for liver cancer in females, endometrial cancer, gallbladder cancer, testicular cancer, and colorectal cancer.

Why This Matters

It’s important to understand cancer trends in young people because they can provide insight about exposure to carcinogenic factors in early life and young adulthood, the authors write. Elevated cancer risk in young people “foreshadow future disease burden as these young cohorts carry their increased risk into older age, when cancers most frequently occur.”

There are lots of reasons why cancer rates may be rising in young adults, and they likely differ by cancer type:

• 10 of the 17 cancers that are more prevalent in young adults are obesity-related. Obesity and the other chronic health conditions that often accompany obesity, like diabetes and heart disease, have been shown to exacerbate cancer growth.
• Certain lifestyle factors may play a role, too. Scientists suspect that young adults today are more likely to eat more ultra-processed foods, live a more sedentary lifestyle, and be exposed to more environmental chemicals than people who were young adults decades ago. 
• Changes in hormonal contraceptive use could affect reproductive cancer rates in females, and trends in smoking and alcohol consumption may play a role in liver and oral cancers.

Methodology

The researchers analyzed health records data for more than 23 million patients ages 25 to 84 years old who were diagnosed with cancer between 2000 and 2019. They analyzed incidence rates for 34 cancer types and death rates for 25 cancer types.

Sung H, Jiang C, Bandi P, et al.  Differences in cancer rates among adults born between 1920 and 1990 in the USA: an analysis of population-based cancer registry data .  Lancet Public Health . 2024;9(8):e583-e593. doi:10.1016/S2468-2667(24)00156-7

Koh B, Tan DJH, Ng CH, et al.  Patterns in cancer incidence among people younger than 50 years in the US, 2010 to 2019 .  JAMA Netw Open. 2023;6(8):e2328171. doi:10.1001/jamanetworkopen.2023.28171

National Cancer Institute. Cancer stat facts: common cancer sites .

Sung H, Siegel R, Rosenberg PS, et al.  Emerging cancer trends among young adults in the USA: analysis of a population-based cancer registry .  Lancet Public Health . 2019;4(3):e137-e147. doi:10.1016/S2468-2667(18)30267-6

Bell CF, Lei X, Haas A, et al. Risk of cancer after diagnosis of cardiovascular disease . JACC CardioOncol . 2023;5(4):431-440. doi:10.1016/j.jaccao.2023.01.010

By Claire Bugos Bugos is a senior news reporter at Verywell Health. She holds a bachelor's degree in journalism from Northwestern University.

• DOI: 10.1007/s11684-024-1085-3
• Corpus ID: 271765875

Artificial intelligence methods available for cancer research.

• Ankita Murmu , Balázs Győrffy
• Published in Frontiers in Medicine 8 August 2024
• Medicine, Computer Science

163 References

A systematic review of artificial intelligence techniques in cancer prediction and diagnosis, stacking-based ensemble learning of decision trees for interpretable prostate cancer detection, diagnostic classification of cancers using extreme gradient boosting algorithm and multi-omics data, predicting breast cancer survivability: a comparison of three data mining methods, predicting synergism of cancer drug combinations using nci-almanac data, multiclass magnetic resonance imaging brain tumor classification using artificial intelligence paradigm, breast cancer diagnosis using genetically optimized neural network model, deepsynergy: predicting anti-cancer drug synergy with deep learning, artificial intelligence in healthcare operations to enhance treatment outcomes: a framework to predict lung cancer prognosis, random forest-based modelling to detect biomarkers for prostate cancer progression, related papers.

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Cancer diagnosis can be devastating, but for some it gives permission to live more radically

Professor of Sociology, Te Herenga Waka — Victoria University of Wellington

Professor of Sociology & Director, Sydney Centre for Healthy Societies, University of Sydney

Professor of Maori & Public Health, Te Kunenga ki Pūrehuroa – Massey University

Associate Professor in Surgery, University of Otago

Professor of Social and Health Psychology, Te Kunenga ki Pūrehuroa – Massey University

Associate Professor in Health Promotion, University of Otago

Disclosure statement

Kevin Dew receives funding from The Marsden Fund..

Alex Broom receives funding from the Australian Research Council.

Kerry Chamberlain receives funding from the Marsden Fund.

Chris Cunningham, Elizabeth Dennett, and Richard Egan do not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.

Te Herenga Waka — Victoria University of Wellington , Te Kunenga ki Pūrehuroa – Massey University , and University of Otago provide funding as members of The Conversation NZ.

University of Sydney , Te Herenga Waka—Victoria University of Wellington , University of Otago , and Te Kunenga ki Pūrehuroa – Massey University provide funding as members of The Conversation AU.

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A diagnosis of life-limiting cancer can be overwhelming and cause feelings of panic and anxiety. But for some people, it provides a license to live life differently, including quitting toxic jobs and becoming more adventurous.

In our recently published research , we sought to understand the impact of a cancer diagnosis and subsequent experiences for cancer survivors.

We talked with 81 New Zealanders (23 Māori and 58 non-Māori) who had lived longer than expected with a life-limiting or terminal diagnosis of cancer (four to 32 years since first diagnosis), and 25 people who were identified as their supporters.

We found there are vastly different ways in which people experience and respond to a cancer diagnosis, but for some it’s a prompt to make significant changes. Of the 81 participants, 26 expressed the view, unsolicited, that cancer had some positive impact on their lives – without downplaying the negative impacts it could have as well.

A licence to change

Being told you only have limited time left to live can undoubtedly be a shock. But it can lead to profound change.

It’s not uncommon for people who receive a serious diagnosis to draw up a “ bucket list ”. Some people in our study took the opportunity to travel or move to a new home.

For others, the diagnosis provided a chance to rethink their lives and make more significant changes to the way they lived. They decided to be culturally more adventurous and to take up new skills.

Many of these people quit their jobs or changed to jobs that suited them better. Many changed their relationships with the people around them. One talked about showing more affection for his children, another was kinder and stopped fretting over small things.

Some decided to be more selective and no longer be around people who were negative. Others took up new hobbies or crafts which they felt were healing. For one person, the cancer diagnosis provided the impetus to look at things and people differently, which they thought would not have happened otherwise.

Individuals could also undergo a transformation to become what they felt they were meant to be in life. One person, given two months to live, embraced rongoā (Māori traditional healing), including its spiritual side. They now love their “journey” and feel this was what they were “supposed to do”.

For many, a diagnosis of cancer gave them license to be different people and to resist conforming to social norms, including having a job, being thrifty or not taking risks.

Disrupting diagnoses

One person, given only months to live, moved out of her flat, gave away her possessions, quit her job that she described was toxic, and returned home to say goodbye to her family.

Most importantly for her, she worked on experiencing “joy” – after receiving the diagnosis, she realised she had lost it. But she continues to live many years later. After a while, she had to find a new flat, get a new job and the recovery of her joy was challenged:

I had to start working again. And, of course, with working again, joy goes down, time goes down, rest goes down, spirituality goes down.

But not everyone has the opportunity to change. Some peoples’ lives were limited because of the physical effects of the cancer, its treatment, or because of their personal, social or financial resources.

Some go to great lengths to ensure their lives change as little as possible after diagnosis to maintain a sense of normality.

Why we need to know

Given the fear a cancer diagnosis can elicit, it is important to see there are different ways of responding.

It is also worth knowing there are people who live longer than expected. Many people in our study were given just months to live, but one woman was still alive 12 years after being told she had a year left.

Beyond that, this research documents how the disruption produced by a cancer diagnosis can prompt people to breach social norms. Where people have the capacity and resources to change, those around them and their health professionals can support them in taking opportunities to live life differently.

We heard people say they think of their cancer as a friend or an amazing opportunity. Some even felt thankful.

The possibility of cancer providing opportunities for some in no way diminishes the grief or a sense of loss, fear and anxiety that can accompany such diagnoses.

Our research supports a reframing of cancer narratives, to consider ways of tempering the negative impacts of a diagnosis – while remaining cognisant of the struggle that can follow such news, and the variability in people’s capacity to engage with that struggle.

• New Zealand
• Cancer diagnosis
• Cancer survival

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Research News

Hackensack Meridian CDI Lab Publishes Papers Pointing the Way Toward an Exhaled-Breath Test for Lung Cancer

July 18, 2024

Hackensack Meridian Health

CDI scientists publish groundbreaking papers on lung cancer breath test and immune system’s role in fighting diseases. These discoveries could revolutionize cancer detection and treatment, potentially improving patient outcomes.

Scientists at the Center for Discovery and Innovation (CDI) have made exciting progress in cancer research. They’ve published two important papers that could change how we detect and treat cancer.

The first paper talks about a new way to test for lung cancer using a person’s breath. This test could be a game-changer because it’s quick, easy, and doesn’t hurt. The researchers found that certain chemicals in a person’s breath might show if they have lung cancer. This could help doctors find cancer earlier, which is really important for successful treatment.

The second paper is about how our bodies fight off infections and cancer. The scientists discovered that a part of our immune system, called neutrophils, can change to help fight diseases better. This finding could lead to new ways to boost our body’s natural defenses against cancer and infections.

Dr. David Perlin, who leads the CDI, says these discoveries are a big deal. They show how the CDI is working hard to find new ways to help patients. The research team used advanced technology and worked together with other experts to make these breakthroughs.

The breath test for lung cancer is especially exciting because it could be a simple way to check for cancer without invasive procedures. It might even help find other types of cancer in the future.

The study on neutrophils is also important because it gives us new ideas about how to make our immune systems stronger. This could lead to better treatments for both cancer and infections.

Overall, this research is a big step forward in understanding and fighting diseases. It shows how scientists are always working to find new ways to keep us healthy.

Home » All News » Cited Papers: Project 1- Role of DYNLL1 in the 53BP1 Axis of HDR Regulation

Cited Papers: Project 1- Role of DYNLL1 in the 53BP1 Axis of HDR Regulation

Published On: August 14, 2024 Shared by Brian Phillips

1. Bunting SF, Callen E, Wong N, Chen HT, Polato F, Gunn A, Bothmer A, Feldhahn N, Fernandez- Capetillo O, Cao L, Xu X, Deng CX, Finkel T, Nussenzweig M, Stark JM, Nussenzweig A. 53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks. Cell. 2010;141(2):243-54. PubMed PMID: 20362325.

2. Bouwman P, Aly A, Escandell JM, Pieterse M, Bartkova J, van der Gulden H, Hiddingh S, Thanasoula M, Kulkarni A, Yang Q, Haffty BG, Tommiska J, Blomqvist C, Drapkin R, Adams DJ, Nevanlinna H, Bartek J, Tarsounas M, Ganesan S, Jonkers J. 53BP1 loss rescues BRCA1 deficiency and is associated with triplenegative and BRCA-mutated breast cancers. Nat Struct Mol Biol. 2010;17(6):688-95. Epub 2010/05/11. doi: 10.1038/nsmb.1831. PubMed PMID: 20453858; PMCID: PMC2912507.

3. Noordermeer SM, Adam S, Setiaputra D, Barazas M, Pettitt SJ, Ling AK, Olivieri M, Alvarez-Quilon A, Moatti N, Zimmermann M, Annunziato S, Krastev DB, Song F, Brandsma I, Frankum J, Brough R, Sherker A, Landry S, Szilard RK, Munro MM, McEwan A, Goullet de Rugy T, Lin ZY, Hart T, Moffat J, Gingras AC, Martin A, van Attikum H, Jonkers J, Lord CJ, Rottenberg S, Durocher D. The shieldin complex mediates 53BP1- dependent DNA repair. Nature. 2018;560(7716):117-21. Epub 20180718. doi: 10.1038/s41586-018-0340-7. PubMed PMID: 30022168; PMCID: PMC6141009.

4. Dev H, Chiang TW, Lescale C, de Krijger I, Martin AG, Pilger D, Coates J, Sczaniecka-Clift M, Wei W, Ostermaier M, Herzog M, Lam J, Shea A, Demir M, Wu Q, Yang F, Fu B, Lai Z, Balmus G, Belotserkovskaya R, Serra V, O’Connor MJ, Bruna A, Beli P, Pellegrini L, Caldas C, Deriano L, Jacobs JJL, Galanty Y, Jackson SP. Shieldin complex promotes DNA end-joining and counters homologous recombination in BRCA1-null cells. Nat Cell Biol. 2018;20(8):954-65. Epub 20180718. doi: 10.1038/s41556-018-0140-1. PubMed PMID: 30022119; PMCID: PMC6145444.

5. Gupta R, Somyajit K, Narita T, Maskey E, Stanlie A, Kremer M, Typas D, Lammers M, Mailand N, Nussenzweig A, Lukas J, Choudhary C. DNA Repair Network Analysis Reveals Shieldin as a Key Regulator of NHEJ and PARP Inhibitor Sensitivity. Cell. 2018;173(4):972-88 e23. Epub 20180412. doi: 10.1016/j.cell.2018.03.050. PubMed PMID: 29656893; PMCID: PMC8108093.

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7. He YJ, Meghani K, Caron MC, Yang C, Ronato DA, Bian J, Sharma A, Moore J, Niraj J, Detappe A, Doench JG, Legube G, Root DE, D’Andrea AD, Drane P, De S, Konstantinopoulos PA, Masson JY, Chowdhury D. DYNLL1 binds to MRE11 to limit DNA end resection in BRCA1-deficient cells. Nature. 2018;563(7732):522-6. Epub 20181031. doi: 10.1038/s41586-018-0670-5. PubMed PMID: 30464262; PMCID: PMC7155769.

8. Barazas M, Annunziato S, Pettitt SJ, de Krijger I, Ghezraoui H, Roobol SJ, Lutz C, Frankum J, Song FF, Brough R, Evers B, Gogola E, Bhin J, van de Ven M, van Gent DC, Jacobs JJL, Chapman R, Lord CJ, Jonkers J, Rottenberg S. The CST Complex Mediates End Protection at Double-Strand Breaks and Promotes PARP Inhibitor Sensitivity in BRCA1-Deficient Cells. Cell Rep. 2018;23(7):2107-18. doi: 10.1016/j.celrep.2018.04.046. PubMed PMID: 29768208; PMCID: PMC5972230.

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11. Cong K, Peng M, Kousholt AN, Lee WTC, Lee S, Nayak S, Krais J, VanderVere-Carozza PS, Pawelczak KS, Calvo J, Panzarino NJ, Turchi JJ, Johnson N, Jonkers J, Rothenberg E, Cantor SB. Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency. Mol Cell. 2021;81(15):3128-44 e7. Epub 20210702. doi: 10.1016/j.molcel.2021.06.011. PubMed PMID: 34216544; PMCID: PMC9089372.

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14. Mirman Z, Lottersberger F, Takai H, Kibe T, Gong Y, Takai K, Bianchi A, Zimmermann M, Durocher D, de Lange T. 53BP1-RIF1-shieldin counteracts DSB resection through CST- and Polalpha-dependent fill-in. Nature. 2018;560(7716):112-6. Epub 20180718. doi: 10.1038/s41586-018-0324-7. PubMed PMID: 30022158; PMCID: PMC6072559.

15. Paniagua I, Tayeh Z, Falcone M, Hernandez Perez S, Cerutti A, Jacobs JJL. MAD2L2 promotes replication fork protection and recovery in a shieldin-independent and REV3L-dependent manner. Nat Commun. 2022;13(1):5167. Epub 20220908. doi: 10.1038/s41467-022-32861-5. PubMed PMID: 36075897; PMCID: PMC9458726.

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29. Douglas P, Sapkota GP, Morrice N, Yu Y, Goodarzi AA, Merkle D, Meek K, Alessi DR, Lees-Miller SP. Identification of in vitro and in vivo phosphorylation sites in the catalytic subunit of the DNA-dependent protein kinase. Biochem J. 2002;368(Pt 1):243-51. doi: 10.1042/BJ20020973. PubMed PMID: 12186630; PMCID: PMC1222982.

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Study Puts a $43 Billion Yearly Price Tag on Cancer Screening

The estimate focused on five cancers for which there is medically recommended screening — breast, cervical, colorectal, lung and prostate — and found that colonoscopies accounted for most of the costs.

By Gina Kolata

The United States spent $43 billion annually on screening to prevent five cancers, according to one of the most comprehensive estimates of medically recommended cancer testing ever produced.

The analysis, published on Monday in The Annals of Internal Medicine and based on data for the year 2021, shows that cancer screening makes up a substantial proportion of what is spent every year on cancer in the United States, which most likely exceeds $250 billion. The researchers focused their estimate on breast, cervical, colorectal, lung and prostate cancers, and found that more than 88 percent of screening was paid for by private insurance and the rest mostly by government programs.

Dr. Michael Halpern, the lead author of the estimate and a medical officer in the federally funded National Cancer Institute’s health care delivery research program, said his team was surprised by the high cost, and noted that it was likely to be an underestimate because of the limits of the analysis.

For Karen E. Knudsen, the chief executive of the American Cancer Society, the value of screening for the cancers is clear. “We are talking about people’s lives,” she said. “Early detection allows a better chance of survival. Full stop. It’s the right thing to do for individuals.”

“We screen for cancer because it works,” Dr. Knudsen added. “The cost is small compared to the cost of being diagnosed with late-stage disease.”

Other researchers say the finding supports their contentions that screening is overused, adding that there is a weak link between early detection and cancer survival and that the money invested in cancer testing is not being well spent.

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Collection  06 March 2024

Cancer Top 100 of 2023

This collection highlights the most downloaded* cancer research papers published by Scientific Reports in 2023. Featuring authors from around the world, these papers highlight valuable research from an international community.

You can also view the journal's overall Top 100 or the Top 100 within various subject areas . *Data obtained from SN Insights, which is based on Digital Science’s Dimensions.

Severe SARS-CoV-2 infection as a marker of undiagnosed cancer: a population-based study

• Adeline Dugerdil
• Laura Semenzato
• Antoine Flahault

Diabetes medications and cancer risk associations: a systematic review and meta-analysis of evidence over the past 10 years

• Yixian Chen
• Fidela Mushashi
• Rachel A. Murphy

Classification and diagnostic prediction of breast cancer metastasis on clinical data using machine learning algorithms

• Mahendran Botlagunta
• Madhavi Devi Botlagunta
• Mohd Asif Shah

Non-invasive screening of breast cancer from fingertip smears—a proof of concept study

• S. Francese

Combining machine learning with Cox models to identify predictors for incident post-menopausal breast cancer in the UK Biobank

• Xiaonan Liu
• Davide Morelli
• Lei Clifton

Mutational landscape of cancer-driver genes across human cancers

• Musalula Sinkala

Comprehensive liquid biopsy analysis as a tool for the early detection of minimal residual disease in breast cancer

• Dimitra Stergiopoulou
• Athina Markou
• Evi Lianidou

Diagnostic and prognostic potential of the microbiome in ovarian cancer treatment response

• Abigail E. Asangba
• Marina R. S. Walther-Antonio

Tumor organoid biobank-new platform for medical research

The effect of acute exercise on circulating immune cells in newly diagnosed breast cancer patients

• Tiia Koivula
• Salla Lempiäinen
• Ilkka Heinonen

Cancer incidence amongst UK firefighters

• Taylor A. M. Wolffe
• Andrew Robinson
• Anna A. Stec

The optimization of postoperative radiotherapy in de novo stage IV breast cancer: evidence from real-world data to personalize treatment decisions

• Minoru Miyashita
• Onyinye B. Balogun
• Dezheng Huo

Cancer-associated fibroblasts are the main contributors to epithelial-to-mesenchymal signatures in the tumor microenvironment

• Peter M. Szabo
• Saurabh Saha

A model to predict the prognosis of diffuse large B-cell lymphoma based on ultrasound images

• Wenqin Chen

Clustering by antigen-presenting genes reveals immune landscapes and predicts response to checkpoint immunotherapy

• Xutong Gong
• Rachel Karchin

Predicting EGFR mutational status from pathology images using a real-world dataset

• James J. Pao
• Mikayla Biggs
• Lee A. Albacker

Shared hotspot mutations in oncogenes position dogs as an unparalleled comparative model for precision therapeutics

• Lucas Rodrigues
• Joshua Watson
• Shaying Zhao

Polypropylene microplastics promote metastatic features in human breast cancer

• Jun Hyung Park
• Seungwoo Hong
• Hyun Jung Lee

Absolute dosimetry for FLASH proton pencil beam scanning radiotherapy

• Ana Lourenço
• Anna Subiel
• Russell Thomas

Cellular senescence affects energy metabolism, immune infiltration and immunotherapeutic response in hepatocellular carcinoma

Racial disparities in breast cancer treatment patterns and treatment related adverse events

• Nickolas Stabellini
• Jennifer Cullen
• Alberto J. Montero

Fc-competent multispecific PDL-1/TIGIT/LAG-3 antibodies potentiate superior anti-tumor T cell response

Anti-inflammatory effect of combining fish oil and evening primrose oil supplementation on breast cancer patients undergoing chemotherapy: a randomized placebo-controlled trial

• Aleksandra Arsic
• Predrag Krstic
• Vesna Vucic

Incidence and risk of pancreatic cancer in patients with chronic pancreatitis: defining the optimal subgroup for surveillance

• Hyo Suk Kim
• Tae-Geun Gweon
• Jae Hyuck Chang

A 3-month survival model after Gamma Knife surgery in patients with brain metastasis from lung cancer with Karnofsky performance status ≤ 70

• Hangeul Park
• Hyun-Tai Chung
• Eun Jung Lee

A novel facile synthesis of metal nitride@metal oxide (BN/Gd 2 O 3 ) nanocomposite and their antibacterial and anticancer activities

• Mayyadah H. Mohsin
• Khawla S. Khashan
• Ashok Aspatwar

Tubule-U-Net: a novel dataset and deep learning-based tubule segmentation framework in whole slide images of breast cancer

• Çisem Yazıcı

LINE-1 ORF1p as a candidate biomarker in high grade serous ovarian carcinoma

• Michael Gillette
• Ronny Drapkin

CAR-tropic extracellular vesicles carry tumor-associated antigens and modulate CAR T cell functionality

• V. M. Ukrainskaya
• O. E. Musatova
• A. G. Gabibov

Controlled tumor heterogeneity in a co-culture system by 3D bio-printed tumor-on-chip model

• Nafiseh Moghimi
• Seied Ali Hosseini
• Mohammad Kohandel

Incidence trends and spatial distributions of lung adenocarcinoma and squamous cell carcinoma in Taiwan

• Chun-Ju Chiang
• Wen-Chung Lee

Simultaneous activation of CXC chemokine receptor 4 and histamine receptor H1 enhances calcium signaling and cancer cell migration

• Jin-Woo Lee

Machine learning based combination of multi-omics data for subgroup identification in non-small cell lung cancer

• Seema Khadirnaikar
• Sudhanshu Shukla
• S. R. M. Prasanna

Risk factors for the development of triple-negative breast cancer versus non-triple-negative breast cancer: a case–control study

• Rajesh Dikshit
• Sudeep Gupta

Deep learning for multi-class semantic segmentation enables colorectal cancer detection and classification in digital pathology images

• John-Melle Bokhorst
• Iris D. Nagtegaal
• Francesco Ciompi

Identification of germline cancer predisposition variants in pediatric sarcoma patients from somatic tumor testing

• Piedad Alba-Pavón
• Olatz Villate

E-liquid exposure induces bladder cancer cells to release extracellular vesicles that promote non-malignant urothelial cell transformation

• Ryan D. Molony
• Chia-Hao Wu

Advances in methylation analysis of liquid biopsy in early cancer detection of colorectal and lung cancer

• Hyuk-Jung Kwon
• Sun Hye Shin
• Min Seob Lee

Systematic review of NTRK 1/2/3 fusion prevalence pan-cancer and across solid tumours

• Sophie O’Haire
• Fanny Franchini
• Maarten IJzerman

Pneumonitis associated with pembrolizumab plus chemotherapy for non-squamous non-small cell lung cancer

• Daichi Fujimoto
• Satoru Miura
• Nobuyuki Yamamoto

Efficient breast cancer mammograms diagnosis using three deep neural networks and term variance

• Ahmed S. Elkorany
• Zeinab F. Elsharkawy

Nanosecond pulsed electric field suppresses growth and reduces multi-drug resistance effect in pancreatic cancer

• Wojciech Szlasa
• Olga Michel
• Julita Kulbacka

Termination of trastuzumab in HER2-positive metastatic breast cancer patients who received trastuzumab beyond progression

• Izzet Dogan
• Adnan Aydiner

Survival outcomes of patients with metastatic non-small cell lung cancer receiving chemotherapy or immunotherapy as first-line in a real-life setting

• Yaniss Belaroussi
• Fanny Bouteiller
• Sophie Cousin

Activated T cell therapy targeting glioblastoma cancer stem cells

• Ken Miyaguchi
• Hongqiang Wang

Genomic and molecular landscape of homologous recombination deficiency across multiple cancer types

The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice

• Chenchen Li

Region of interest (ROI) selection using vision transformer for automatic analysis using whole slide images

• Md Shakhawat Hossain
• Galib Muhammad Shahriar
• Suresh Advani

Modeling of intracranial tumor treating fields for the treatment of complex high-grade gliomas

• David J. Segar
• Joshua D. Bernstock
• Sumientra M. Rampersad

Appropriate screening mammography method for patients with breast implants

• Eun Young Ko
• Haejung Kim

Dual blockage of both PD-L1 and CD47 enhances the therapeutic effect of oxaliplatin and FOLFOX in CT-26 mice tumor model

• Reza Alimohammadi
• Ghanbar Mahmoodi Chalbatani
• Seyed Amir Jalali

Targeting BAP1 with small compound inhibitor for colon cancer treatment

• Minhwa Kang
• Seul Gi Park
• Jongbum Kwon

Machine learning-based approaches for cancer prediction using microbiome data

• Pedro Freitas
• Francisco Silva
• Hélder P. Oliveira

Identification of a hypoxia-related gene prognostic signature in colorectal cancer based on bulk and single-cell RNA-seq

• Yihuan Qiao
• Xunliang Jiang

Evaluation of automated techniques for extraction of circulating cell-free DNA for implementation in standardized high-throughput workflows

• Sarah Lehle
• Julius Emons
• Hanna Huebner

Epigenetic modification of gene expression in cancer cells by terahertz demethylation

• Hwayeong Cheon
• Junho K. Hur
• Joo-Hiuk Son

Breast cancer histopathology image-based gene expression prediction using spatial transcriptomics data and deep learning

• Md Mamunur Rahaman
• Ewan K. A. Millar
• Erik Meijering

The NK cell checkpoint NKG2A maintains expansion capacity of human NK cells

• Meike Kaulfuss
• Juliane Mietz
• Obinna Chijioke

TOR1B: a predictor of bone metastasis in breast cancer patients

• Minh Nam Nguyen
• Salima Akter
• Tae Gyu Choi

An integrative machine learning framework for classifying SEER breast cancer

• P. Manikandan
• C. Ponnuraja

Comparative dosimetric analysis of volumetric modulated arc therapy based craniospinal irradiation plans between Halcyon ring gantry and TrueBeam C-arm linear accelerator

• Biplab Sarkar
• Subhra Snigdha Biswal

Detection of oral squamous cell carcinoma in clinical photographs using a vision transformer

• Tabea Flügge
• Robert Gaudin
• Shankeeth Vinayahalingam

Histone H3-wild type diffuse midline gliomas with H3K27me3 loss are a distinct entity with exclusive EGFR or ACVR1 mutation and differential methylation of homeobox genes

• Pamela Ajuyah
• Chelsea Mayoh
• Dong-Anh Khuong-Quang

Discovery of rafoxanide as a novel agent for the treatment of non-small cell lung cancer

• Tingjun Liu

SLC11A2: a promising biomarker and therapeutic target in ovarian cancer

• Liming Tian
• Guofen Yang

HX009, a novel BsAb dual targeting PD1 x CD47, demonstrates potent anti-lymphoma activity in preclinical models

• Faming Zhang
• Qi-Xiang Li

Circulating cf-miRNA as a more appropriate surrogate liquid biopsy marker than cfDNA for ovarian cancer

• Aoife Ward Gahlawat
• Tania Witte
• Sarah Schott

Prediction of pathologic complete response to neoadjuvant systemic therapy in triple negative breast cancer using deep learning on multiparametric MRI

• Zijian Zhou
• Beatriz E. Adrada

Plasma proteome of growing tumors

• Shashi Gupta
• Matthew J. Westacott
• Nebojsa Janjic

High-throughput isolation of cancer cells in spiral microchannel by changing the direction, magnitude and location of the maximum velocity

• Vahid Omrani
• Mohammad Zabetian Targhi
• Reza Nosrati

Engineered E. coli Nissle 1917 for delivery of bioactive IL-2 for cancer immunotherapy

• Sarunas Tumas
• Trine Sundebo Meldgaard
• Morten O. A. Sommer

Identifying molecular targets of Aspiletrein-derived steroidal saponins in lung cancer using network pharmacology and molecular docking-based assessments

• Iksen Iksen
• Wasita Witayateeraporn
• Varisa Pongrakhananon

Antiproliferative effects of mitochondria-targeted N -acetylcysteine and analogs in cancer cells

• Micael Hardy
• Balaraman Kalyanaraman

Epigenetic alterations impede epithelial-mesenchymal transition by modulating centrosome amplification and Myc/RAS axis in triple negative breast cancer cells

• Laxmidhar Das

Targeting mTOR to overcome resistance to hormone and CDK4/6 inhibitors in ER-positive breast cancer models

• María Jimena Rodriguez
• María Cecilia Perrone
• Virginia Novaro

Four-year follow-up on fatigue and sleep quality of a three-armed partly randomized controlled study in breast cancer survivors with cancer-related fatigue

• the CRF study group

GPX4 overexpressed non-small cell lung cancer cells are sensitive to RSL3-induced ferroptosis

• Joo-Won Kim
• Dong Wha Min

Genetic determinants and absence of breast cancer in Xavante Indians in Sangradouro Reserve, Brazil

• Guilherme Bezerra de Castro

Pediatric T-cell acute lymphoblastic leukemia blast signature and MRD associated immune environment changes defined by single cell transcriptomics analysis

• Swati S. Bhasin
• Beena E. Thomas
• Deborah DeRyckere

Long-term use of denosumab and its association with skeletal-related events and osteonecrosis of the jaw

• Chin-Yao Shen
• Wei-Pang Chung

A novel 3D culture model for human primary mammary adipocytes to study their metabolic crosstalk with breast cancer in lean and obese conditions

• Marie Rebeaud
• Caroline Bouche
• Catherine Muller

Network pharmacology analysis reveals potential targets and mechanisms of proton pump inhibitors in breast cancer with diabetes

• Hanbin Wang
• Taolan Zhang

Prediction of breast cancer using blood microbiome and identification of foods for breast cancer prevention

• Jeongshin An
• Byung-In Moon

Improving the robustness and stability of a machine learning model for breast cancer prognosis through the use of multi-modal classifiers

• Nikhilanand Arya
• Sriparna Saha
• Snehanshu Saha

Biogenic copper oxide nanoparticles from Bacillus coagulans induced reactive oxygen species generation and apoptotic and anti-metastatic activities in breast cancer cells

• Masoumeh Dolati
• Farzaneh Tafvizi
• Parvaneh Jafari

Effects of the exercise-inducible myokine irisin on proliferation and malignant properties of ovarian cancer cells through the HIF-1 α signaling pathway

• Marziyeh Alizadeh Zarei
• Elahe Seyed Hosseini
• Hossein Nikzad

Potential of bacteriophage therapy in managing Staphylococcus aureus infections during chemotherapy for lung cancer patients

• Huangliang Zheng
• Sharon Shui Yee Leung

Diagnostic ability of deep learning in detection of pancreatic tumour

• M. G. Dinesh
• Nebojsa Bacanin
• Mohamed Abouhawwash

Artificial intelligence-based radiomics for the prediction of nodal metastasis in early-stage lung cancer

• Yoshihisa Shimada
• Norihiko Ikeda

CDCP1 expression is frequently increased in aggressive urothelial carcinoma and promotes urothelial tumor progression

• Miriam Saponaro
• Sina Flottmann
• Abdullah Alajati

Nrf2 inhibition increases sensitivity to chemotherapy of colorectal cancer by promoting ferroptosis and pyroptosis

• Yongzhou Huang
• Wenchang Yang
• Kaixiong Tao

Identification of TP53 mutations in circulating tumour DNA in high grade serous ovarian carcinoma using next generation sequencing technologies

• Leslie Calapre
• Tindaro Giardina
• Elin S. Gray

A comprehensive analysis of PANoptosome to prognosis and immunotherapy response in pan-cancer

• Lingling Zhuang

Meta-analysis of laparoscopic radical hysterectomy, excluding robotic assisted versus open radical hysterectomy for early stage cervical cancer

• Greg Marchand
• Ahmed Taher Masoud
• Malini Govindan

Prognostic impact of PD-L1 and TIGIT expression in non-small cell lung cancer following concurrent chemo-radiotherapy

• Masataka Mori
• Masatoshi Kanayama
• Fumihiro Tanaka

High dose of dexamethasone attenuates docetaxel-induced fluid retention in breast cancer treatment

• Yoshitaka Saito
• Ryota Kanno
• Mitsuru Sugawara

Cytotoxic and chemomodulatory effects of Phyllanthus niruri in MCF-7 and MCF-7 ADR breast cancer cells

• Ola E. Abdel-Sattar
• Rasha Mosa Allam
• Meselhy R. Meselhy

Automatic detection of circulating tumor cells and cancer associated fibroblasts using deep learning

• Siddarth Rawal
• Changhuei Yang

Transcriptional activity mediated by β-CATENIN and TCF/LEF family members is completely dispensable for survival and propagation of multiple human colorectal cancer cell lines

• Janna Fröhlich
• Andreas Hecht

Rewiring of the 3D genome during acquisition of carboplatin resistance in a triple-negative breast cancer patient-derived xenograft

• Mikhail G. Dozmorov
• Maggie A. Marshall
• J. Chuck Harrell

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