Cancer News and Discussions

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Improving drug therapy for relapsed leukemia
https://medicalxpress.com/news/2022-09- ... kemia.html
by Haleigh Ehmsen, Northwestern University
A combination of two drugs showed promise in treating relapsed or refractory acute myeloid leukemia (AML) with mutations in the FMS-like tyrosine kinase 3 (FLT3) gene, according to a Northwestern Medicine study published in the Journal of Clinical Oncology .

The combination of venetoclax, an inhibitor of BCL2, and gilteritinib, an FLT3 inhibitor, has the potential to improve outcomes and allow patients to utilize oral medications instead of treatments that must be delivered in the hospital, according to senior author Jessica Altman, MD, professor of Medicine in the Division of Hematology and Oncology.

According to a previous study published in the New England Journal of Medicine, survival of patients with refractory or relapsed AML is improved when using gilteritinib, compared to chemotherapy. Gilteritinib targets the FLT3 mutation. Typically, relapsed or refractory AML has a median overall survival of four to seven months with standard chemotherapy approaches.

In the current phase II trial, investigators studied the efficacy of adding venetoclax to gilteritinib. Investigators treated patients with relapsed or refractory AML with venetoclax and gilteritinib daily. Of the 61 patients enrolled, 56 of them had disease with the FLT3 mutation and 64% of those with the mutation had received prior FLT3 inhibitor therapy.

The study found a molecular response, defined as FLT3-ITD VAF less than or equal to 10 in 60% of participants with FLT3 -ITD who attained a modified complete remission, which was higher than with gilteritinib alone.
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Photodynamic therapy offers promise for cancer treatment
https://medicalxpress.com/news/2022-09- ... tment.html
by Marcia Kaye, University of Toronto Mississauga
While chemotherapy drugs can be lifesaving, they don't work for all patients or for all cancers. But a team of UTM researchers is looking at new ways to use special types of light to target cancer cells resistant to current drug therapy—in an approach that might be easier on some patients than traditional chemotherapy.

Photodynamic therapy—the use of precisely targeted light, usually from a laser, that activates or "turns on" a drug to kill cells—has been used mostly to treat skin cancers, since it's easier to deliver light to the outside of the body. But light doesn't travel very far through body tissues. So how to safely get the light to cancers that are deeper inside, such as in the pancreas or breast? And how to recognize which cancers will respond to the cell-killing drugs and which will be resistant? The challenge is to get the light as close as possible to red light. Of all the colors in the visible light spectrum, red has the longest wavelength, which enables it to penetrate tissue, but also the lowest energy, which minimizes harm to healthy cells.

Karishma Kailass, a Ph.D. candidate in the department of chemical and physical sciences, found that using an approach called two-photon light, where two tiny particles of light hit at exactly the same time, achieved this result. It doubled the wavelength, halved the energy and, together with a special cancer-killing molecule that's activated only by light, successfully destroyed cancer cells that would otherwise have been resistant to conventional chemotherapy.
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T cells use force to destroy cancer cells
https://phys.org/news/2022-09-cells-cancer.html
by University of New South Wales
As a part of our immune defenses, cytotoxic T cells—or killer T cells—seek out and destroy cells that are infected or cancerous. This process is essential for the body's defense against diseases.

These specialized immune cells are armed with lytic granules containing two key components for immune attack: perforin (proteins that punch holes in the target cells) and granzymes (which gain access via these holes and ultimately kill disease-causing cells).

T cells snuggle up to targeted diseased cells and form an intimate junction between the two, called the "cytotoxic immunological synapse."

A research team at UNSW Sydney's EMBL Australia Node in Single Molecule Science in the School of Biomedical Sciences has found that mechanical forces generated by T cells influence how effectively perforin can punch through tumor cell membranes. In a paper published today in Developmental Cell, they describe the cell interactions and the integration of forces at both the front and rear of the cell.
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Breast cancer findings 'suggest a new set of criteria for avoiding radiation'
https://medicalxpress.com/news/2022-09- ... teria.html
by Maureen Salamon, Harvard Medical School
Women diagnosed with early-stage breast cancer often can choose to have a lumpectomy, which removes only cancerous tissue and a thin margin of surrounding healthy cells instead of the entire breast. Current cancer guidelines for most women under 65 recommend following lumpectomy with radiation therapy, which targets stray cancer cells that might otherwise cause breast cancer to recur or spread to other parts of the body.

A new study presented at the 2022 annual meeting of the American Society of Clinical Oncology could eventually expand an option for skipping radiation to some women as young as 55. However, limitations in necessary testing could hinder the approach from becoming widespread, according to a Harvard expert.

A lower risk for breast cancer recurrence

Landmark 2004 research, augmented by later studies, helped cancer experts develop guidelines defining which women with early-stage breast cancer could safely omit radiation after lumpectomy.

Generally, this option is offered to women 65 or older who have small tumors with nonaggressive cells that haven't spread to the lymph nodes. Medically, this is described as a T1N0, grade 1-2 tumor. The tumors must be estrogen receptor-positive, meaning that the hormone estrogen helps fuel their growth. They also must have an adequate margin of normal tissue surrounding the tumor cut away to ensure all the cancer has been removed. Women who decide to omit radiation instead receive medication known as endocrine therapy for five years. This stops cancer cells from using hormones like estrogen to grow and spread.
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New wearable device measures the changing size of tumors below the skin
https://medicalxpress.com/news/2022-09- ... -skin.html
by Andrew Myers, Georgia Institute of Technology
Engineers at the Georgia Institute of Technology and Stanford University have created a small, autonomous device with a stretchable/flexible sensor that can be adhered to the skin to measure the changing size of tumors below. The non-invasive, battery-operated device is sensitive to one-hundredth of a millimeter (10 micrometers) and can beam results to a smartphone app wirelessly in real-time with the press of a button.

In practical terms, the researchers say, their device—dubbed FAST for "Flexible Autonomous Sensor measuring Tumors"—represents a wholly new, fast, inexpensive, hands-free, and accurate way to test the efficacy of cancer drugs. On a grander scale, it could lead to promising new directions in cancer treatment.

Each year researchers test thousands of potential cancer drugs on mice with subcutaneous tumors. Few make it to human patients, and the process for finding new therapies is slow because technologies for measuring tumor regression from drug treatment take weeks to read out a response. The inherent biological variation of tumors, the shortcomings of existing measuring approaches, and the relatively small sample sizes make drug screenings difficult and labor-intensive.
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Drug resistance is a powerful menace in certain breast and ovarian cancers. Now scientists are figuring out why
https://medicalxpress.com/news/2022-09- ... reast.html
by Delthia Ricks , Medical Xpress
Just as bacteria, viruses and fungi develop strategies to outsmart antimicrobial medications, cancer cells can become resistant to chemotherapy. And among tumors, those associated with triple negative breast cancer and ovarian tumors can develop a powerful form of resistance.

In an intriguing line of research, a multi-center team of U.S. researchers has found that epigenetic signatures in breast and ovarian cancers may ultimately guide physicians' treatment decisions for a subset of patients whose cancers are notoriously capable of thwarting chemo.

By pinpointing which molecular signatures correlate with optimum treatment response, oncologists can be better informed when designing treatment regimens for cancers with reputations for aggressive drug resistance.

Reporting in Science Translational Medicine, cancer biologists at Jackson Laboratory for Genomic Medicine in Farmington, Connecticut, spell out why triple negative breast cancer—TNBC—and ovarian carcinoma are especially difficult to treat. For one thing, loss of BRCA1 or BRCA2 gene activity is common in TNBC and ovarian cancer the scientists underscored, and has a potent bearing on prognosis. However, the type of alteration involving the genes can result in different responses to treatment, the researchers said.
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Promising new treatment for deadly pediatric tumors
https://medicalxpress.com/news/2022-09- ... umors.html
by Konstanze Adam, Wilhelm Sander-Stiftung
Alveolar rhabdomyosarcoma is a type of rare pediatric tumor. For more than 40 years there have not been any new developments regarding treatment. Research led by Prof. Dr. Anton Henssen at Charité University Berlin has now identified a new therapeutic option, using a drug that is currently under investigation for other types of cancer. The group observed that alveolar rhabdomyosarcoma cancer cells have high levels of DNA damage and are more dependent on the repair processes than non-cancer cells. This drug blocks the repair of DNA and forces cells to die, thus offering a new option for treating these patients.

Rhabdomyosarcomas are tumors that grow in the muscle tissue, predominantly in children and adolescents. Even though they are rare, they represent the second most common solid tumor in childhood. Alveolar rhabdomyosarcoma is a type of rhabdomyosarcoma characterized by a chromosome translocation that creates a new protein fusion called PAX3-FOXO1. Alveolar rhabdomyosarcomas are the more aggressive version, with an overall survival rate of 30% after five years. In Europe, it is estimated that around 500 new rhabdomyosarcoma cases are diagnosed every year, of which 100 are alveolar rhabdomyosarcoma. Despite many advances in cancer therapeutics, rhabdomyosarcoma treatment has not changed in the last four decades, therefore new and more effective treatments are needed.

One of the challenges in treating alveolar rhabdomyosarcoma is the lack of druggable factors present in the tumor. Besides the PAX3-FOXO1 fusion, alveolar rhabdomyosarcomas do not present many recurrent genetic mutations, thus limiting our ability to use drugs specific for this tumor. Simultaneously, cancer cells frequently present higher DNA damage, which allows the acquisition of new mutations. The damaged DNA needs to be repaired before the cells can divide to ensure that the integrity of the genome is maintained. In recent years, many drugs have been developed to block the repair of the DNA, with promising results in multiple cancer types.
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Potential melanoma target bypasses therapeutic resistance to immune checkpoint blockers
https://medicalxpress.com/news/2022-09- ... tance.html
by Jeff Hansen, University of Alabama at Birmingham
Over the last decade, immune checkpoint blockers, or ICBs, have revolutionized treatment for various advanced cancers, including melanoma, the most aggressive skin cancer that was considered largely incurable not long ago. However, three-fourths of advanced-melanoma patients are resistant to ICBs.

Now, in a report published in Nature Communications, researchers reveal a potential target—using the clinically approved drug ruxolitinib—to suppress ICB-resistant melanomas.

"Since ruxolitinib is clinically approved and being tested in patients with advanced solid tumors, non-small-cell lung cancer and triple-negative breast cancer, our study justifies further testing of ruxolitinib in patients with advanced melanoma that are resistant to ICBs," said Lewis Zhichang Shi, M.D., Ph.D., an associate professor in the University of Alabama at Birmingham Department of Radiation Oncology.

Shi notes that ruxolitinib will likely need to be combined with other therapeutic modalities to achieve a long-term cure.

For half a dozen years, it was known that tumor loss of interferon-gamma signaling was a major mechanism of resistance against two ICB drugs, anti-CTLA-4 and anti-PD-1. However, ways to overcome this resistance remained elusive.

This loss of interferon-gamma signaling in human melanomas is caused by dysregulation of genes in the interferon-gamma signaling pathway. However, in mouse models the knockdown mutations failed to show how a loss of interferon-gamma signaling in tumor cells modulated the activity of tumor-infiltrating T cells, or TILs, because those models still contain some interferon-gamma signaling. TIL immune cells are vital for cancer control because they are able to detect and destroy tumors. However, in a countermove, cancers learn to evade this destruction by upping immune checkpoint proteins on the surface of their cells, and these surface proteins send an "off" signal to TILs.
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Radical new treatment system lights up cancer therapy
https://phys.org/news/2022-09-radical-t ... erapy.html
by University of Tokyo

One approach to treating cancer is photodynamic therapy using photo-uncaging systems, in which light is used to activate a cancer-fighting agent in situ at the tumor. However, suitable agents must be stable under visible light, have an anti-tumor effect in low-oxygen environments, and have the ability to be activated by low-energy tissue-penetrative red light—a combination of properties that is difficult to achieve. Now, a team from The Institute of Industrial Science at The University of Tokyo has developed a new platform that uses, for the first time, organorhodium(III) phthalocyanine complexes to achieve this combination of traits.

Conventional photodynamic techniques depend on the formation of reactive oxygen species to destroy tumor cells, but many tumors contain environments that lack oxygen. Photo-uncaging systems, where the agent is administered in an inactive form and then activated, or "uncaged", in the location of the tumor, address this issue. They uncage alkyl radicals, which are known to be capable of inducing cell death both with and without the presence of oxygen. Alkyl radicals are converted into terminal aldehydes in the presence of oxygen, and these terminal aldehydes can also induce cell death. The team used molecules called "organorhodium(III) phthalocyanine (Pc) complexes" to develop, for the first time, a novel platform for photo-uncaging therapy.

"The organorhodium(III) phthalocyanine (Pc) complexes we developed are highly stable under ambient light during the processes of synthesis, purification, and measurement, but can be activated by a laser that gives out nanosecond pulses of red light," explains lead author Kei Murata. These nanosecond-pulsing lasers (pulsing for a billionth of a second) are relatively easy for medical staff to handle.
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Deliberately damaging DNA could boost the effectiveness of immunotherapy in kidney cancer
https://medicalxpress.com/news/2022-09- ... erapy.html
by Institute of Cancer Research
DNA damage is one of the foundational causes of cancer. But researchers have now found that deliberately causing DNA damage—by delivering additional treatments like radiotherapy—could improve the effectiveness of immunotherapy for some people with kidney cancer.

Immunotherapy can work by stimulating people's own immune systems to fight cancer more effectively. In people with kidney cancer who also have a mutation in the PBRM1 gene, damaging DNA before immunotherapy could further activate the immune system.

The study, led by scientists at The Institute of Cancer Research, London, and published in Genes and Development, sheds light on the role of PBRM1, and suggests that kidney cancer patients with mutations in the gene could benefit from a combined treatment of radiotherapy and immunotherapy.

Findings suggest that the PBRM1 gene is crucial in preventing cells from dividing when they contain damaged DNA. Researchers found that mutations in PBRM1 disrupt this process and allow the cells with damaged DNA to multiply, triggering inflammatory signals that are thought to enhance the patient's immune response against cancer.
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