Oncology: In-Depth Description

Image Credit: Scientific Frontline / AI generated

Oncology is the branch of medicine and biology dedicated to the study, diagnosis, treatment, and prevention of cancer. Derived from the Greek word onkos (meaning "mass" or "bulk"), this field focuses on understanding neoplasms (tumors) and the complex biological mechanisms that cause uncontrolled cell division. The primary goal of oncology is to improve patient survival and quality of life through the development of therapeutic interventions and the early detection of malignancies.

Dresden Research Group Uncovers New Key Mechanism in Cancer Cells

The research group led by Dr. Mohamed Elgendy (4th from left).
Photo Credit: © MSNZ

A study by the Mildred Scheel Early Career Center group led by Dr. Mohamed Elgendy at the TUD Faculty of Medicine provides fundamental insights into cancer biology. Published in the renowned journal Nature Communications, the study shows for the first time that the protein MCL1 not only inhibits programmed cell death but also plays a central role in tumor metabolism. 

The researchers have succeeded in tracing two classic hallmarks of cancer – the evasion of apoptosis (a form of programmed cell death) and the dysregulation of energy metabolism – back to a common molecular mechanism. 

Stanford Medicine study identifies immune switch critical to autoimmunity, cancer

Edgar Engleman, MD, professor of pathology
Photo Credit: Courtesy of Stanford School of Medicine

A single signaling pathway controls whether immune cells attack or befriend cells they encounter while patrolling our bodies, researchers at Stanford Medicine have found. Manipulating this pathway could allow researchers to toggle the immune response to treat many types of diseases, including cancers, autoimmune disorders and those that require organ transplants.

The research, which was conducted in mice, illuminates the mechanism of an important immune function that prevents inappropriate attacks on healthy tissue. Called peripheral immune tolerance, the key cellular players, known as regulatory T cells (or Tregs, pronounced “tee-regs”), were first described in the late 1990s in a series of discoveries that were recently recognized with the 2025 Nobel Prize in physiology or medicine.

A platform to test new cancer treatments

Differentiated hepatic cells growing in a flask re-gain the appearance of cells present in liver.
Image Credit: © FAMOL, UNIGE

Overcoming acquired treatment resistance is one of the major challenges in the fight against cancer. While combination therapies hold promise, their toxicity to healthy tissue remains a major hurdle. To anticipate these risks, researchers at the University of Geneva (UNIGE) have developed in vitro models of the kidneys, liver, and heart – three organs particularly sensitive to such therapies. This fast, animal-free approach paves the way for safer evaluation of new treatments. The findings are published in Biomedicine & Pharmacotherapy. 

Recent advances in immunotherapy, targeted therapies, and gene therapies have significantly improved survival rates for patients with cancer. However, over time, many tumors develop resistance to these treatments, undermining their effectiveness. This phenomenon, known as ‘acquired resistance’, has become one of the major challenges in oncology. 

UCLA team discovers how to target ‘undruggable’ protein that fuels aggressive leukemia

B-lymphoblastic leukemia, a type of blood cancer.
Image Credit: Courtesy of the Rao Laboratory.

Researchers at the UCLA Health Jonsson Comprehensive Cancer Center have identified a small molecule that can inhibit a cancer-driving protein long considered impossible to target with drugs — a discovery that could open the door to a new class of treatments for leukemia and other hard-to-treat cancers. 

The compound, called I3IN-002, disrupts the ability of a protein known as IGF2BP3 to bind and stabilize cancer-promoting RNAs, a mechanism that fuels aggressive forms of acute leukemia. The study published in the journal Haematologica, found the molecule not only slowed leukemic cell growth but also triggered cancer cell death and reduced the population of leukemia-initiating cells that sustain the disease.

“This project has been more than a decade in the making,” said Dr. Dinesh Rao, professor of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA and senior author of the study. “We discovered IGF2BP3 years ago as an important driver in acute leukemias, and for a long time there were no tools to target it. To finally show that we can inhibit this protein and disrupt its function in cancer cells is incredibly exciting.” 

Prognostic tool could help clinicians identify high-risk cancer patients

In a new study, MIT researchers and their collaborators identified a practical, powerful predictor that could help clinicians spot high-risk lymphoma patients early and tailor treatments to improve survival.
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Aggressive T-cell lymphoma is a rare and devastating form of blood cancer with a very low five-year survival rate. Patients often relapse after receiving initial therapy, making it especially challenging for clinicians to keep this destructive disease in check.

In a new study, researchers from MIT, in collaboration with researchers involved in the PETAL consortium at Massachusetts General Hospital, identified a practical and powerful prognostic marker that could help clinicians identify high-risk patients early, and potentially tailor treatment strategies to improve survival.

The team found that, when patients relapse within 12 months of initial therapy, their chances of survival decline dramatically. For these patients, targeted therapies might improve their chances for survival, compared to traditional chemotherapy, the researchers say.

UCLA study uncovers how a key protein helps breast cancer cells survive in hostile conditions

NBCn1 (purple) sits in the cell membrane and brings two sodium ions (2Na⁺) and one carbonate ion (CO₃²⁻) into the cell, raising its internal pH. This helps breast cancer cells stay alkaline and survive in low-oxygen, acidic tumor environments.
Illustration Credit: Courtesy of UCLA/Health

UCLA scientists have characterized the structure and function of a key survival protein in breast cancer cells that helps explain how these tumors resist environmental stress and thrive in acidic, low-oxygen environments that would normally be toxic to healthy cells.

Breast cancer cells rely on a transporter protein called NBCn1 to bring alkali ions into the cell and maintain a favorable internal pH. Using advanced cryo-electron microscopy combined with computational modeling, the researchers showed that NBCn1 moves two sodium ions and one carbonate ion through an efficient “elevator-like” motion that minimizes energy use. This allows NBCn1 to achieve a high transport rate of approximately 15,000 ions per second, helping tumor cells maintain an internal pH that promotes survival, division and resistance to acidic stress. 

The shape of the cell nucleus influences the success of cancer treatment

Photo Credit: Thor Balkhed

Cancer cells with a cell nucleus that is easily deformed are more sensitive to drugs that damage DNA. These are the findings of a new study by researchers at Linköping University. The results may also explain why combining certain cancer drugs can produce the opposite of the intended effect. The study has been published in the journal Nature Communications. 

A few years ago, a new type of drug was introduced that exploits deficiencies in cancer cells’ ability to repair damage to their DNA. These drugs, called PARP1 inhibitors, are used against cancers that have mutations in genes involved in DNA repair, such as the breast cancer gene 1 (BRCA1). This gene has such a central role in the cell’s ability to repair serious DNA damage that mutations in it greatly increase the risk of developing cancer, often at a young age. The risk is so high that some women with a mutated BRCA1 gene choose to have their breasts and ovaries surgically removed to prevent cancer. 

Immune cells turn damage into repair

Intestines one week after abdominal irradiation, showing proliferating epithelial cells (in brown).
Image Credit: Julius Fischer / TUM 

Patients receiving intensive cancer treatments often suffer from severe damage to the intestinal lining. Researchers from the Technical University of Munich (TUM) and the Leibniz Institute for Immunotherapy (LIT) have discovered that certain immune cells can trigger healing processes. They use inflammatory signals to do so - which is surprising, as inflammation in the intestine was previously thought to be primarily harmful. This finding could open new possibilities for therapies. 

Regulatory T cells (Tregs), a specialized type of immune cells, are usually seen as “peacekeepers” that prevent excessive immune attacks. In a study  published in Signal Transduction and Targeted Therapy, researchers from the Department of Radiation Oncology at the TUM University Hospital and the LIT Cooperation Group “Innate Immune Sensing in Cancer and Transplantation” uncovered how the body's own immune system can be harnessed to repair the intestinal lining and improve survival.  

Nasal drops fight brain tumors noninvasively

Researchers at WashU Medicine have developed a noninvasive medicine delivered through the nose that successfully eliminated deadly brain tumors in mice. The medicine is based on a spherical nucleic acid, a nanomaterial (labeled red) that travels along a nerve (green) from the nose to the brain, where it triggers an immune response to eliminate the tumor.
Image Credit: Courtesy of Alexander Stegh

Researchers at Washington University School of Medicine in St. Louis, along with collaborators at Northwestern University, have developed a noninvasive approach to treat one of the most aggressive and deadly brain cancers. Their technology uses precisely engineered structures assembled from nano-size materials to deliver potent tumor-fighting medicine to the brain through nasal drops. The novel delivery method is less invasive than similar treatments in development and was shown in mice to effectively treat glioblastoma by boosting the brain’s immune response.

Glioblastoma tumors form from brain cells called astrocytes and are the most common kind of brain cancer, affecting roughly three in 100,000 people in the U.S. Glioblastoma generally progresses very quickly and is almost always fatal. There are no curative treatments for the disease, in part because delivering medicines to the brain remains extremely challenging.

Focused Ultrasound Passes First Test in Treatment of Brain Cancer in Children

Pediatric oncologist Stergios Zacharoulis and biomedical engineer Elisa Konofagou are pioneering the use of focused ultrasound to treat brain cancer in children and dozens of other brain diseases
Photo Credit: Rudy Diaz / Columbia University Vagelos College of Physicians and Surgeons.

Columbia University researchers are the first to show that focused ultrasound—a non-invasive technique that uses sound waves to enhance the delivery of drugs into the brain—can be safely used in children being treated for brain cancer.

The focused ultrasound technique, developed by Columbia engineers, was tested in combination with chemotherapy in three children with diffuse midline glioma, a rare and aggressive brain cancer that is universally fatal.

The study found that focused ultrasound successfully opened the blood-brain barrier in all three patients, allowing the chemotherapy drug to reach the tumors and leading to some improvement in patient mobility, though all three patients eventually died from their disease or complications of COVID.

Customised cells to fight brain cancer

Visualisation of cell death induced by CAR-T cells. A real-time imaging experiment (images taken at 0, 5 and 10 minutes) shows a CAR-T cell in contact with a glioblastoma cell (artificially marked in green). This contact causes the CAR-T cell to concentrate granules (lytic granules, shown in pink) containing the proteins necessary for the death of the target cell. These proteins penetrate the cancer cell and induce its death. After 10 minutes, the cancer cell begins to die, as indicated by the loss of its structure (evidenced by the appearance of "bubbles").
Image Credit: © Denis Migliorini

With a five-year survival rate of less than 5%, glioblastoma is one of the most aggressive types of brain cancer. Until now, all available treatments, including immunotherapy — which involves strengthening the immune system to fight cancer— have proved disappointing. CAR-T cells are genetically modified immune cells manufactured in the laboratory and designed to identify and destroy cancer cells. By targeting a protein present in the tumor environment, a team from the University of Geneva (UNIGE) and the Geneva University Hospital (HUG) has developed CAR-T cells capable of destroying glioblastoma cells. Their efficacy in an animal model of the disease paves the way for clinical trials in humans. These results are published in the Journal for ImmunoTherapy of Cancer. 

A cellular protein, FGD3, boosts breast cancer chemotherapy, immunotherapy

The research team included, front row, from left: graduate student Junyao Zhu, biochemistry professor David Shapiro, and senior researcher Chengiian Mao; back row, from left: graduate students Abigail Spaulding, Xinyi Dai and Qianjin Jiang.
Photo Credit: Fred Zwicky

A naturally occurring protein that tends to be expressed at higher levels in breast cancer cells boosts the effectiveness of some anticancer agents, including doxorubicin, one of the most widely used chemotherapies, and a preclinical drug known as ErSO, researchers report. The protein, FGD3, contributes to the rupture of cancer cells disrupted by these drugs, boosting their effectiveness and enhancing anticancer immunotherapies.

The new findings were the happy result of experiments involving ErSO, an experimental drug that killed 95-100% of estrogen-receptor-positive breast cancer cells in a mouse model of the disease. ErSO upregulates a cellular pathway that normally protects cancer cells from stress, said University of Illinois Urbana-Champaign biochemistry professor David Shapiro, who led the new work with Illinois graduate student Junyao Zhu. But when that protective pathway is ramped up, the system goes awry.

Scientists move closer to better pancreatic cancer treatments

Tumor and peritoneal metastases are shown in yellow.
Image Credit: UCR/Pellecchia lab

Last year, researchers at the University of California, Riverside, developed a novel “molecular crowbar” strategy to degrade the oncogenic enzyme Pin1, a protein that is overexpressed in many tumors including pancreatic cancer. They designed compounds that bind to Pin1 and destabilize its structure, causing its cellular degradation. 

This approach not only targets cancer cells directly but also addresses tumor-supporting cells like cancer-associated fibroblasts and macrophages where Pin1 is active, potentially overcoming the treatment resistance posed by the fibrous tumor microenvironment in pancreatic cancer.  

The UCR team led by Maurizio Pellecchia, a distinguished professor of biomedical sciences in the School of Medicine, has now collaborated with a team of scientists led by Dr. Mustafa Raoof at City of Hope in Duarte, California, to further test these degraders in pancreatic and gastrointestinal cancers with the goal of developing a new class of therapeutics that can “remove” harmful proteins rather than just block them.

Thyroid gland new possible target for prostate cancer treatment

Lukas Kenner, visiting professor at the Department of Molecular Biology.
Photo Credit: Medizinische Universität Wien

A hormone produced in the thyroid gland can play a key role in the development of prostate cancer. This is shown in a new study by an international research group led by Umeå University, Sweden, and the Medical University of Vienna, Austria. By blocking a receptor for the hormone, the growth of tumor cells in the prostate was inhibited. In the long term, the discovery may open up a new way of attacking certain types of aggressive prostate cancer.

"The results indicate that the receptor in question is a driving force in the growth of cancer. Substances that block it could thus be a target for future drugs against prostate cancer," says Lukas Kenner, visiting professor at Umeå University and the one who has led the study that is published in Molecular Cancer.

The receptor in question is called thyroid hormone receptor Beta, TRβ. It binds the thyroid hormone triiodothyronine, T3. In laboratory experiments, the activation of T3 has led to a sharp increase in the number of prostate cancer cells. However, when the receptor TRβ was inhibited with the help of an active substance, NH-3, significantly reduced the growth of cancer cells. NH-3 is a substance that is only used in research to block TRβ.

OHSU researchers develop promising drug for aggressive breast cancer

New research reveals a drug developed by scientists at Oregon Health & Science University may develop into a new treatment for an especially aggressive form of breast cancer.
Photo Credit: Oregon Health & Science University

A new molecule developed by researchers at Oregon Health & Science University offers a promising avenue to treat intractable cases of triple-negative breast cancer — a form of cancer that is notoriously aggressive and lacks effective treatments.

In a study published today in the journal Cell Reports Medicine, researchers describe the effect of a molecule known as SU212 to inhibit an enzyme that is critical to cancer progression. The research was conducted in a humanized mouse model.

“It’s an important step forward to treat triple-negative breast cancer,” said senior author Sanjay V. Malhotra, Ph.D., co-director of the Center for Experimental Therapeutics in the OHSU Knight Cancer Institute. “Triple-negative breast cancer is an aggressive form of cancer and there are no effective drugs available right now.”

Combination of immunotherapy and targeted therapy improves survival for patients with advanced colorectal cancer

Human colorectal cancer cells
Image Credit: National Cancer Institute

A new study led by UCLA investigators found that combining zanzalintinib, a targeted therapy drug, and atezolizumab, an immune checkpoint inhibitor, helped patients with metastatic colorectal cancer, the second most common cause of cancer death in the U.S., live longer and control their disease better than with the standard treatment drug regorafenib. 

The findings simultaneously published in The Lancet and presented at the European Society for Medical Oncology Congress; mark the first time an immunotherapy-based regimen has demonstrated a survival benefit in the vast majority of patients with metastatic colorectal cancer.

“This study represents an important step forward for a group of patients who have historically had very few treatment options,” said Dr. J. Randolph Hecht, professor of clinical medicine at the David Geffen School of Medicine at UCLA and first author of the study. “We may finally be finding ways to make immunotherapy work for more patients with colorectal cancer.”

ADC Improves Outcomes for Patients with Advanced Triple-Negative Breast Cancer Who are Ineligible for Immune Checkpoint Inhibitors

Dr. Sara Tolaney, chief of the Division of Breast Oncology at Dana-Farber, is the senior author on the ASCENT-03 study.
Photo Credit: Courtesy of Dana-Farber Cancer Institute

Patients with an aggressive form of breast cancer who are not candidates for immune checkpoint inhibitor therapy showed significantly improved progression-free survival when treated with the antibody drug conjugate sacituzumab govitecan compared to standard chemotherapy. These findings, which stem from the ASCENT-03 trial in triple-negative breast cancer co-led by investigators at Dana-Farber Cancer Institute, are presented today at the European Society for Medical Oncology (ESMO) Congress 2025 in Berlin, Germany. They are also published simultaneously in the New England Journal of Medicine.

Triple-negative breast cancer (TNBC) accounts for about 15% of all breast cancer cases and is often difficult to treat. The 5-year survival rate for patients with metastatic disease is about 15%. Moreover, around 60% of patients with metastatic TNBC have tumors that lack the molecular marker PD-L1. This absence indicates the tumors will not respond to immune checkpoint inhibitors. For most patients with previously untreated TNBC, chemotherapy is the primary treatment option.

Broad-Bayer collaboration leads to drug candidate for a hard-to-treat type of lung cancer

Broad Communications Scientists in the Broad-Bayer oncology alliance have developed a drug candidate, sevabertinib, that could be a new lung cancer treatment.
Illustration Credit: Agnieszka Grosso

An alliance of scientists at the Broad Institute and Bayer Pharmaceuticals have developed a drug candidate, sevabertinib, that could be a new treatment for a group of lung cancer patients who have few options today.

In a new study published in Cancer Discovery, the team described their efforts to develop sevabertinib. They tested the compound in various lung cancer models and showed its potential to treat non-small cell lung cancers that harbor certain mutations in the ERBB2 gene, which encodes the HER2 protein. These mutations occur in 2 to 4 percent of patients with non-small cell lung cancer, or roughly 40,000 to 50,000 people diagnosed globally each year. These patients tend to be women, including those who are younger, have never smoked, and have a poor prognosis. 

The study also reported data from two participants in Bayer’s phase 1/2 clinical trial of the compound. Based on these findings and other data from this ongoing clinical trial, the drug candidate is currently under Priority Review at the FDA, an expedited review of therapies that treat serious conditions. If approved, it would be the first FDA-approved cancer drug based on Broad discoveries, and the first new medicine from the Broad-Bayer oncology research alliance. 

When healing turns harmful: adrenal support cells tied to cancer origin

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A new study from Karolinska Institutet, shows that support cells in the adrenal gland can regenerate hormone-producing tissue after birth. The same cells may also act as a starting point for adrenal tumors, offering new insights into cancer development and potential treatment strategies.

“We found that these glial-like cells not only help maintain healthy tissue but, in some paragangliomas, also carry the same tumor-initiating genetic event,” explains Susanne Schlisio, group leader at the Department of Oncology-Pathology and last author of the study. 

“In tumors with germline VHL mutations, subsets of these support cells showed loss of chromosome 3p, the ‘second hit’ leading to VHL inactivation. This suggests they may be the origin of certain tumors,” says Dr. Michael Mints, docent at the same department and co-corresponding author of the study.