Cancer News and Discussions

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A Cerenkov luminescence imaging device to help spot cancerous tumors
https://medicalxpress.com/news/2022-04- ... erous.html
by Bob Yirka , Medical Xpress
A team of researchers affiliated with several institutions in the U.S. and one in the U.K. has developed a new type of Cerenkov luminescence imaging device to help doctors spot cancerous tumors. In their paper published in the journal Nature Biomedical Engineering, the group describes the device, how it works and possible uses for it in clinical settings.

Cerenkov luminescence is a type of electromagnetic radiation where charged particles pass through a dielectric medium at a speed that is faster than regular light in the medium. It is commonly measured by astrophysicists looking at stars and other researchers working in nuclear reactors. Prior research has shown that Cerenkov luminescence can also be generated in the human body as light passes through tissue. It has been suggested that Cerenkov luminescence could be used to help differentiate tumor tissue from normal tissue, and some work has been done to create Cerenkov luminescence imaging (CLI) devices. But to date, such devices have suffered from a variety of issues that have prevented their use in clinical settings. In this new effort, the researchers have designed and built a complete CLI device that has already passed an initial clinical trial.
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Regulating the regulators of the immune system
https://medicalxpress.com/news/2022-04-immune.html
by Katherine Unger Baillie, University of Pennsylvania

Checkpoint inhibitors have become important tools in the cancer-fighting arsenal. By blocking proteins that normally restrain the immune response, these drugs can help the immune system destroy cancer cells.

But they don't work in all patients. And now a new study in Nature Immunology led by researchers from Penn's School of Veterinary Medicine suggests a possible reason why: Not only can these drugs encourage the activity of cancer killing T cells, but they can, in some cases, also activate a population of regulatory T cells that serve the opposing function—to rein in that attack.

In the study, immunologists led by Penn Vet professor Christopher Hunter and doctoral student Joseph Perry discovered that blocking the activity of the checkpoint protein PD-L1, which interacts with a T cell receptor PD-1, enhanced the activity of a subset of T cells known as effector regulatory T cells, or effector Tregs. This intervention unexpectedly reduced the ability of mice to control a parasite infection.

The findings reveal a complexity to how the body "regulates the regulators" of the immune system, says Hunter. "Once you have those Tregs to control your T cell response, you also need to control them," he says. "It's like with a car. You have the ignition, the accelerator, and you also need a brake. PD-1 is a brake not only on killer T cells but also on Tregs."

T cells may be best known for their roles in fighting infections and killing cancer cells. But the immune system also has several mechanisms in place to counterbalance those responses to prevent out-of-control inflammation that could damage healthy tissue. Tregs are one aspect of this balancing act.
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Researchers find genetic 'Achilles heel' in ovarian and uterine cancers
https://medicalxpress.com/news/2022-04- ... erine.html
by Allessandra Dicorato, Broad Institute of MIT and Harvard
Although the outlook for people with some types of cancers has improved in the past 20 years, outcomes for patients with uterine and ovarian cancers remain much the same. Patients often have advanced disease before they are diagnosed, and genes that drive tumor formation have proved difficult to target with new treatments.

Now, researchers from the Cancer Dependency Map (DepMap) project at the Broad Institute of MIT and Harvard have identified a hidden vulnerability in ovarian and uterine cancers—as well as a way to exploit it that could inspire new, much-needed drugs for these cancers.

A team led by institute director Todd Golub and DepMap director Francisca Vazquez studied 851 human cancer cell lines to look for genes that uterine and ovarian cancers heavily rely on to survive, known as dependencies. Scientists already knew that uterine and ovarian cancer cells have high levels of a protein called SLC34A2, which imports phosphate into cells. Golub's team disabled another protein in these cells, called XPR1, which exports phosphate out of cells, and found that this killed them. The results, published in Nature Cancer, suggest that the XPR1 gene is a genetic vulnerability in these cells and that phosphate buildup could be toxic to cells. The team adds that disrupting phosphate transport in cancer cells, such as with a protein they used to disable XPR1 in their experiments, could be an effective treatment strategy.

"Patients with ovarian cancer are in desperate need of better therapies, and this XPR1 finding is both surprising and exciting as a starting point for drug discovery," said Golub, who co-led the project. "The challenge now will be to convert this discovery into a therapeutic strategy."
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Improving interferon therapy for blood cancers

by Melissa Rohman, Northwestern University
https://medicalxpress.com/news/2022-04- ... ncers.html
[Northwestern Medicine investigators have discovered a novel signaling pathway activated by interferons, a group of immune system proteins, that suppresses the anti-tumor response of interferons in patients with a particular type of blood cancer, according to findings published in Nature Communications.

Targeting this pathway in combination with interferon therapy may provide a novel approach to improving therapy response and overall patient outcomes.

"Things are not simple with the way the immune system operates. There are different breaks and balances that control the immune response. Here, we defined a unique signaling circuit and identified cellular events that happen when interferon binds to its receptor and starts modifying cellular responses," said Leonidas Platanias, MD, Ph.D., the Jesse, Sara, Andrew, Abigail, Benjamin and Elizabeth Lurie Professor of Oncology, director of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University and senior author of the study.

Interferons are a group of immune system signaling proteins and are part of the body's first line of defense against disease. When released by host cells, interferons trigger immune cells to fight off viruses and cancer by inhibiting tumor growth, survival, migration and other pro-tumorigenic properties.
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Nanocapsule carrying a CRISPR-Cas9 editing tool used for noninvasive brain delivery and tumor cell targeting
https://phys.org/news/2022-04-nanocapsu ... brain.html
by Bob Yirka , Phys.org
An international team of researchers has developed a nanocapsule that is capable of crossing the blood brain barrier (BBB) to carry the CRISPR-Cas9 editing tool to treat a brain tumor. In their paper published in the journal Science Advances, the group describes how they created their capsule and how well it worked when tested in mice with a glioblastoma.

Glioblastomas are notoriously difficult to treat. The tumors appear in the brain and their growth damages tissue. Treatment options include surgical removal, direct injections of therapies meant to kill the cancer cells or inserting CRISPR viruses into the bloodstream. Each of these options has a downside, from damaged brain tissue to ineffectiveness due to difficulties with therapies crossing the BBB. In this new effort, the researchers have tried a new approach, using a nanocapsule to carry the CRISPR-Cas9 editing tool to the brain tumor where it targets a gene that is responsible for the development of new cells—a capsule that is capable of safely crossing the BBB.
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Cancer cells found to repair their own membranes after attack by T cells
https://medicalxpress.com/news/2022-04- ... ranes.html
by Bob Yirka , Medical Xpress
A team of researchers from Genetch, Inc., the Howard Hughes Medical Institute and the Peter MacCallum Cancer Center, has found that cancerous tumor cells are able to survive attacks by repairing holes in their membranes caused by a protein released from T cells. In their paper published in the journal Science, the group describes how they used high resolution imaging to learn more about what happens when T cells, known as cytotoxic T lymphocytes (CTLs), attack cancerous tumor cells. Norma Andrews, with University of Maryland, College Park, has published a Perspectives piece in the same journal issue outlining the work done by the team.

Prior research has shown that the way CTLs kill cells infected by a virus or bacteria, and sometimes those that are cancerous, is by glomming onto the cell and then releasing two protein toxins: perforin and granzyme. The first, perforin, eats holes through the cell's membrane. The second then enters the cell through the holes and sets off apoptosis, which is normal programmed cell death. In this new effort, the researchers have learned how cancer cells respond to such an attack.
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Reprogrammed macrophages promote spread of breast cancer
https://medicalxpress.com/news/2022-04- ... ancer.html
by German Cancer Research Center
Metastatic breast cancer cells abuse macrophages, a type of immune cell, to promote the settlement of cancer metastases in the lungs. The reprogrammed macrophages stimulate blood vessel cells to secrete a cocktail of metastasis-promoting proteins that are part of the so-called metastatic niche. This was demonstrated by scientists from the German Cancer Research Center and the Stem Cell Institute HI-STEM in mice that had been transplanted with human breast cancer cells. The work enabled the scientists to identify new targets and develop initial concepts to better restrain the metastatic spread of breast cancer.

Cancer spreads within the body as individual cells detach from the primary tumor and travel to distant body regions via the bloodstream or lymphatic system. Before they can grow into a metastasis at a secondary site, they must communicate with their new environment through a variety of molecular interactions. "In order to settle in this new, hostile milieu, the cancer cells corrupt the microenvironment to support their growth," says Thordur Oskarsson of the German Cancer Research Center (DKFZ) and the stem cell institute HI-STEM. Researchers refer to this as the tumor cells creating a "metastatic niche."
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Discovery of MCLA-158, the first clinical candidate screened in organoids targeting cancer stem cells of solid tumors
https://medicalxpress.com/news/2022-04- ... eened.html
by Institute for Research in Biomedicine (IRB Barcelona)
Scientists from an international consortium led by Dr. Eduard Batlle, head of the Colorectal Cancer laboratory at IRB Barcelona, ICREA researcher and group leader of CIBER de Cáncer (CIBERONC), together with the Dutch company Merus N.V., reveal the preclinical data that has led to the discovery of MCLA-158 and its mechanism of action on cancer stem cells. Named Petosemtamab, the antibody MCLA-158 prevents the onset of metastasis (that is, the spread of cancer to other vital organs) and slows the growth of primary tumors in experimental models of cancer.

Published today in Nature Cancer, the study also lays the groundwork for the use of organoids in the drug discovery process undertaken by pharmaceutical companies. Organoids are patient-derived samples that can be grown in the laboratory, and they reproduce certain aspects of the tumor compartment. Until now, their usefulness was being explored in personalized cancer medicine—meaning their value in helping physicians make decisions about the best treatment for each patient. However, for the selection of MCLA-158, a biobank of organoids from cancer patients was used for the first time to discriminate which new antibody, among hundreds, was most effective and believed to be most suitable for the majority of patients.
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Self-cleaning optical fiber can help in monitoring environment and diagnosing cancer
https://phys.org/news/2022-04-self-clea ... ancer.html
by Tampere University
Researchers at Tampere University have successfully developed a novel optical fiber design allowing the generation of rainbow laser light in the molecular fingerprint electromagnetic region. This new optical fiber with a self-cleaned beam can help in developing applications for, for example, pollutant tagging, cancer diagnostics, environmental monitoring, and food control. The finding was published in the journal Nature Communications.

When a high-powered ultrashort pulse of light interacts with a material such as a glass optical fiber, a range of highly nonlinear interactions take place that cause complex changes in both the temporal and spectral properties of the injected light. When taken to the extreme, such interactions can lead to the generation of a rainbow laser of light commonly referred to as a supercontinuum light source. Since its first demonstration in a special type of optical fiber in 2000, supercontinuum laser light has revolutionized many areas of science, ranging from metrology and imaging at unprecedented resolution to ultrabroadband remote sensing and even the detection of exoplanets.

The current bottleneck with current supercontinuum sources, however, is that they are based on optical fibers that support a single transverse intensity profile or mode, which inherently limits their optical power. What's more, conventional optical fibers are made of silica glass with transmission limited to the visible and near-infrared region of the spectrum. Extension of supercontinuum light to other wavelength regimes such as the mid-infrared requires optical fibers made of so-called soft glasses, but these possess a lower damage threshold than silica, limiting even more the power of the supercontinuum beam.
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Cancer origin identified through cell 'surgery'
https://phys.org/news/2022-05-cancer-cell-surgery.html
by University of Warwick
Research from the University of Warwick sheds new light on a key cause of cancer formation during cell division (or mitosis), and points towards potential solutions for preventing it from occurring.

When a cell divides normally, it makes a copy of every chromosome and then shares them equally between the two new cells. This function is carried out by a complex machine in the cell called the mitotic spindle. If something goes wrong at this stage, the two new cells will be aneuploid, meaning that they will not have the correct number of chromosomes and will make mistakes when sharing genetic information.

Cancer cells are aneuploid, so understanding how and why this happens is hugely significant in finding out how the disease originates. Professor Stephen Royle's research team at Warwick Medical School has identified exactly this.
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