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  • #61
    Study reveals effective strategy to extend the benefit of immunotherapy for prostate cancer

    It's a scientific riddle tangled up in a complex web. How do you turn an immune cold cancer into one that responds to immunotherapy?

    Researchers led by the University of Michigan Rogel Cancer Center started with a simple thread: an inhibitor that showed promise against metastatic castration-resistant prostate cancer cells. This is the most challenging type of prostate cancer – advanced disease that has become resistant to hormone-based treatment.

    From there, they continued to untangle the web to discover multiple levels of cellular processes that were preventing the immune system from mounting a response. Break past them with this inhibitor and suddenly what's considered an immune cold tumor turns red hot.

    Chinnaiyan is senior author of the paper published in Nature Cancer.

    Researchers started by screening a library of 167 inhibitors against prostate cancer cells. They found one, ESK981, had the most impact.

    ESK981 is a class of drugs called multi-tyrosine kinase inhibitors, which are designed to hit multiple targets. This means it functions like a combination therapy, able to block cancer on more than one front. It was originally developed to check blood vessel growth and has already been tested in phase 1 clinical trials, which found it to be safe and well-tolerated.

    In cell lines and mice with metastatic castration-resistant prostate cancer, researchers found ESK981 inhibited tumor growth.

    "The response was intriguing, but we wanted to understand the mechanism at play with ESK981 in prostate cancer cells," Chinnaiyan says.

    They discovered several cellular processes were occurring. First was the role of a type of cell death called autophagy. The authors surprisingly found that ESK981 was a potent inhibitor of autophagy in tumor cells. This caused the cancer cells to produce a protein called CXCL10, which led to recruitment of immune T cells to the tumor.

    But there was one more layer to go. Ultimately, they traced it back to PIKfyve, a type of protein called a lipid kinase. The authors discovered that ESK981 directly targets PIKfyve, affecting these multiple processes involved in metabolism and cell death.

    The researchers confirmed this by knocking down PIKfyve in cell lines and mice. They saw the same processes occur: tumors stopped growing, autophagy was controlled and more T cells were recruited to the tumor. When they added an immune checkpoint inhibitor to the PIKfyve knockdown, the impact was even greater, significantly reducing tumors.

    "Overcoming resistance to immunotherapy is an urgent need in prostate cancer. PIKfyve is a promising target, especially combined with an immune checkpoint inhibitor. This combination has potential to extend the benefit of immunotherapy to patients whose tumors have previously not responded," Chinnaiyan says.

    Based on these findings, researchers have begun phase 2 clinical trials using ESK981 alone or in combination with the immunotherapy nivolumab for metastatic castration-resistant prostate cancer.:

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    • #62
      The new blood test promising to detect a variety of cancers

      Any fight against cancer is a race against time. The earlier the disease is detected, the greater the chances of survival.

      For some time now, researchers have been working on new kinds of blood tests that promise rapid early detection. One of these tests is now said to be able to detect more than 50 different types of cancer with the help of a single sample - and with a level of accuracy that would allow it to be launched on the market.

      Some experts, however, say they are still waiting for some questions to be answered.

      Scientists have been working on finding indications of tumours in the blood for a long time. Such procedures are also called liquid biopsies.

      With these, blood samples can be analysed for what's known as free DNA (cfDNA) circulating in the blood. If cancer cells split, proteins that identify tumours and fragments of genetic material often get into the blood stream.

      With a liquid biopsy, genome sequencing is used to detect cancer-typical methylation signatures - i.e. the telltale characteristics of this DNA.

      The Galleri test recently presented in the Annals of Oncology journal is also based on this method. According to an independent assessment by Sonja Loges, Director of the Department of Personalised Oncology at the University Hospital Mannheim in Germany, the US scientists carried out their research extremely systematically.

      "They first compared three different sequencing methods and then identified the one that was significantly more sensitive than the others."

      In the second step, all genes were sequenced and those that had a high association with cancer were compiled. "From this, the authors then developed a so-called panel in the third step, which they tested with a larger group of patients as well as a comparison group," explains Loges, who is also head of the Department of Personalised Medical Oncology at the German Cancer Research Centre.

      In total, the study included 2,823 people who had already been diagnosed with cancer and a control group of 1,254 people without cancer from more than 140 medical centres in the US.

      The Galleri test was able to detect signs of more than 50 different types of cancer and also assign them to the corresponding tissue in almost 90 per cent of the cases.:

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      • #63
        Aspirin trialled as potential treatment for aggressive breast cancer

        Aspirin is being trialled as part of a potential treatment for an aggressive form of breast cancer.

        Researchers hope the cheap and widely available drug could work well when combined with immunotherapy for patients with triple-negative breast cancer.

        The trial, funded by the Breast Cancer Now Catalyst Programme, which aims to speed up progress in research through innovation and collaboration, is the first clinical study to test if aspirin can make tumours more sensitive to immunotherapy in these patients.

        The research, led by Dr Anne Armstrong from the Christie NHS foundation trust in Manchester, will trial the drug avelumab both with and without aspirin before patients receive surgery and chemotherapy treatment.

        Breast Cancer Now said successful results could lead to further clinical trials of aspirin and avelumab for incurable secondary triple-negative breast cancer, which happens when cancer cells that started in the breast spread to other parts of the body.

        There are about 8,000 women diagnosed with triple-negative breast cancer in the UK each year, the charity said.

        It is a less common but often more aggressive type of breast cancer that disproportionately affects younger women and black women, the organisation added.

        Armstrong, a consultant medical oncologist and honorary senior lecturer, said: “Our earlier research has suggested that aspirin can make certain types of immunotherapy more effective by preventing the cancer from making substances that weaken the immune response.

        “Anti-inflammatory drugs like aspirin could hold the key to increasing the effectiveness of immunotherapy when used at the same time. Trialling the use of a drug like aspirin is exciting because it is so widely available and inexpensive to produce.

        “We hope our trial will show that, when combined with immunotherapy, aspirin can enhance its effects and may ultimately provide a safe new way to treat breast cancer.”

        Dr Simon Vincent, the director of research, support and influencing at Breast Cancer Now, said: “The 8,000 women diagnosed with triple-negative breast cancer in the UK each year face the frightening reality of limited treatment options – we urgently need to address this.

        “Research has already suggested aspirin could improve outcomes for many cancer patients and we hope that Dr Armstrong’s trial will show the same to be true for patients with triple negative breast cancer, so that we can prevent more lives being lost to this devastating disease.”

        Breast Cancer Now said the pharmaceutical firm Pfizer had provided the charity with funding through an independent medical research grant and given its researchers access to several Pfizer medicines.:

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        • #64
          Tampa's Morphogenesis wants to cure cancer with an affordable shot

          A group of scientists in Tampa is working to make treating cancer as easy as getting a shot.

          Why it matters: While most of today's cancer treatments tend to be toxic and expensive, Morphogenesis is working to develop immunotherapies that are safe and affordable.
          • "Affordability is key," co-founder Patricia Lawman told Axios. "If people can’t pay for it, what good is it?"

          How it works: The company’s ImmuneFx vaccine uses plasmid DNA to activate new white blood cells in the body that attach to tumors, making them impossible for the immune system to ignore.
          • At the company's Tampa lab between Busch Gardens and the Yuengling brewery, plasmid DNA is grown inside a bacteria before it is then purified, tested and put into vials.

          Who’s getting it: People have been receiving Morphogenesis' vaccine as part of trials at Moffitt Cancer Center in Tampa, the University of Southern California, the University of Utah and Harvard’s Dana Farber Cancer Institute.
          • Fox 13 talked to a Moffitt patient last month whose skin cancer is now in remission, thanks to the vaccine.
          • "We’ve been able to basically rescue them," Lawman said of the patients.

          What’s new: The company recently got a grant from the National Cancer Institute to develop a version of the vaccine to treat cervical cancer.
          • Its scientists are working on a vaccine that could be shipped and stored at room temperature and self- administered. That would benefit people in low-income countries who don’t have access to preventative treatments like Gardasil.
          • Lawman says the development toward room-temperature storage is going well. "It’s never been done in my knowledge before," she added.

          Fun fact: While trying to raise the funds to get Morphogenesis off the ground, Lawman and her husband and co-founder, Michael, lived on a Key Largo alligator farm, transporting the animals and serving gator bites in the snack shack.
          • In some ways, she says, wrangling alligators was harder than curing cancer. "They’re different stressors," she says.
          • And while alligators may seem more appealing on some days than trying to handle investors, she’s since raised more than $35 million — a huge feat considering only 2.3% of female founders and CEOs raised a comparable amount last year.

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          • #65
            Team Identifies Molecular Mechanisms and Biomarkers in Ovarian Cancer

            UT Southwestern faculty have discovered what appears to be an Achilles’ heel in ovarian cancers, as well as new biomarkers that could point to which patients are the best candidates for possible new treatments.

            The finding, published in the journal Cell, was made in part using a research tool invented in a UT Southwestern lab in the Cecil H. and Ida Green Center for Reproductive Biology Sciences.

            The research was led by W. Lee Kraus, Ph.D., Professor of Obstetrics and Gynecology and Pharmacology and a member of the Harold C. Simmons Comprehensive Cancer Center.

            “Many researchers are trying to find dependencies in cancers by asking why a cancer cell amplifies a gene, increases the levels of a protein, or upregulates a critical cellular pathway. These changes give that cancer a selective advantage, but at the same time they can become an Achilles’ heel – something that, if the alteration was blocked, would kill the cancer or stop its growth,” he said.

            Dr. Kraus and his team, including lead author Sridevi Challa, Ph.D., a postdoctoral researcher in the lab, found that ovarian cancers massively amplify an enzyme, NMNAT-2, that makes NAD+. NAD+ is the substrate for a family of enzymes called PARPs, which chemically modify proteins with ADP-ribose from NAD+. In this study, the team found that one PARP family member, PARP-16, uses NAD+ to modify ribosomes, the protein synthesizing machines of the cell.

            A challenge for this work was that a single ADP-ribose group attached to a protein is difficult to detect. Dr. Kraus and his team overcame this problem by developing a synthetic mono(ADP-ribose) detection reagent made up of natural protein domains fused together, which can be used to detect ADP-ribosylated proteins in cells and patient samples.

            In collaboration with UT Southwestern clinicians, led by Jayanthi Lea, M.D., Professor of Obstetrics and Gynecology and member of the Simmons Cancer Center, Dr. Kraus and his team screened human ovarian cancer patient samples using the mono(ADP-ribose) detection reagent to identify those with low or high levels of mono(ADP-ribose).

            “We were able to show that when ribosomes are mono(ADP-ribosyl)ated in ovarian cancer cells, the modification changes the way they translate mRNAs into proteins,” Dr. Kraus said. “The ovarian cancers amplify NMNAT-2 to increase the levels of NAD+ available for PARP-16 to mono(ADP-ribosyl)ate ribosomes, giving them a selective advantage by allowing them to fine-tune the levels of translation and prevent toxic protein aggregation. But that selective advantage also becomes their Achilles’ heel. They’re addicted to NMNAT-2, so inhibition or reduction of NMNAT-2 inhibits the growth of the cancer cells.”

            This study identified mono(ADP-ribose) and NMNAT-2 as potential biomarkers for ovarian cancers, which may allow clinicians to determine which ovarian cancer patients may respond well and which will not. Even more ovarian cancer patients might do well if an inhibitor is developed for PARP-16, which blocks ribosome mono(ADP-ribosyl)nation.

            Dr. Kraus, an expert in PARPs, said medical science has had great success in developing FDA-approved PARP-1 inhibitors, and an inhibitor for PARP-16 is likely.

            “No PARP-16 inhibitors are currently in clinical trials, but labs in academia and the pharmaceutical industry are developing specific and potent inhibitors of PARP-16. Such a drug could be an effective therapeutic for treating ovarian cancers,” he said.

            Dr. Kraus is a founder and consultant for Ribon Therapeutics Inc., and ARase Therapeutics Inc. He is also co-holder of U.S. patent 9,599,606 covering the mono(ADP-ribose) detection reagent, which has been licensed to and is sold by EMD Millipore.

            “Dr. Kraus’ research is not just a great advance in basic science. It has real promise for clinician investigators and cancer care practitioners because it shows a biomarker and a pathway a future drug could target. The fact that technology developed in his laboratory helped make these findings shows how our faculty builds on their findings to break new ground,” said Carlos L. Arteaga, M.D., Director of the Simmons Cancer Center.

            Other researchers who contributed to this study include Beman R. Khulpateea, Tulip Nandu, Cristel V. Camacho, Keun W. Ryu, Hao Chen, and Yan Peng.

            The research work was supported by a grant from the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK069710) as well as funds from the Cecil H. and Ida Green Center for Reproductive Biology Sciences Endowment to Kraus, and a postdoctoral fellowship from the Ovarian Cancer Research Alliance (GAA202103-0003) to Challa.

            Dr. Arteaga holds the The Lisa K. Simmons Distinguished Chair in Comprehensive Oncology. Kraus holds the Cecil H. and Ida Green Distinguished Chair in Reproductive Biology Sciences. Dr. Lea holds the Patricia Duniven Fletcher Distinguished Professorship in Gynecological Oncology.:

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            • #66
              New study examines ‘Achilles heel’ of cancer tumours, paving the way for new treatment strategies

              Researchers at UBC’s faculty of medicine and BC Cancer Research Institute have uncovered a weakness in a key enzyme that solid tumour cancer cells rely on to adapt and survive when oxygen levels are low.

              The findings, published today in Science Advances, will help researchers develop new treatment strategies to limit the progression of solid cancer tumours, which represent the majority of tumour types that arise in the body.

              Solid tumours rely on blood supply to deliver oxygen and nutrients to help them grow. As the tumours advance, these blood vessels are unable to provide oxygen and nutrients to every part of the tumour, which results in areas of low oxygen. Over time, this low-oxygen environment leads to a buildup of acid inside the tumour cells.

              To overcome this stress, the cells adapt by unleashing enzymes that neutralize the acidic conditions of their environment, allowing the cells to not only survive, but ultimately become a more aggressive form of tumour capable of spreading to other organs. One of these enzymes is called Carbonic Anhydrase IX (CAIX).

              “Cancer cells depend on the CAIX enzyme to survive, which ultimately makes it their ‘Achilles heel.’ By inhibiting its activity, we can effectively stop the cells from growing,” explains the study’s senior author Dr. Shoukat Dedhar, professor in UBC faculty of medicine’s department of biochemistry and molecular biology and distinguished scientist at BC Cancer.

              Dr. Dedhar and colleagues previously identified a unique compound, known as SLC-0111—currently being evaluated in Phase 1 clinical trials—as a powerful inhibitor of the CAIX enzyme. While pre-clinical models of breast, pancreatic and brain cancers have demonstrated the effectiveness of this compound in suppressing tumour growth and spread, other cellular properties diminish its effectiveness.

              In this study, the research team, which included Dr. Shawn Chafe, a research associate in Dr. Dedhar’s lab, together with Dr. Franco Vizeacoumar and colleagues from the University of Saskatchewan, set out to examine these cellular properties and identify other weaknesses of the CAIX enzyme using a powerful tool known as a genome-wide synthetic lethal screen. This tool looks at the genetics of a cancer cell and systematically deletes one gene at a time to determine if a cancer cell can be killed by eliminating the CAIX enzyme together with another specific gene.

              According to Dr. Dedhar, the results of their examination were surprising and point to an unexpected role of proteins and processes that control a form of cell death called ferroptosis. This form of cell death happens when iron builds up and weakens the tumour’s metabolism and cell membranes.

              “We now know that the CAIX enzyme blocks cancer cells from dying as a result of ferroptosis,” says Dr. Dedhar. “Combining inhibitors of CAIX, including SLC-0111, with compounds known to bring about ferroptosis results in catastrophic cell death and debilitates tumor growth.”

              There is currently a large international effort underway to identify drugs that can induce ferroptosis. This study is a major step forward in this quest.:

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              • #67
                These apps say they can detect cancer. But are they only for white people?

                In a video, 30-year-old Stacey Everson tells the story of how she picked up her phone, snapped a selfie, and saved her own life. She might have easily overlooked the small, irregular mole on her upper left arm. But prompted by friends and family, she took a picture of the growth with an app named SkinVision, and followed up on the app’s recommendation that she see a doctor, urgently. The doctor removed and tested the growth. “A week later, it came back positive for early-stage melanoma,” she says. “Something like that, I wouldn’t have thought it would be cancer.”

                Her testimonial is one of several on the product’s website, and SkinVision is only one of several such artificial intelligence (AI)-based apps that aim to help anyone with a smartphone catch a slew of skin diseases – including lethal cancers – earlier than ever. The latest entrant is Google’s Derm Assist, a tool that aims to help users detect more than 288 common skin conditions. Almost 10bn internet users search for terms related to skin conditions each year, says Peggy Bui, a product manager at Google.

                Juanita Erickson, 93, and her 2nd generation robot companion, ElliQ in her studio apartment in Carlton Senior Living. ElliQ is an AI “companion” developed by the Israeli start-up Intuition Robotics. Erickson had two daughters with her first husband before he died in a small plane crash. As a teacher she was attending a teaching conference when she meet her second husband. They were married for 40 years. She has always been active: as a member of a writing group who wrote and performed, as a member a

                But few of those searchers receive expert care. The US faces a dearth of dermatologists, and many tend to cluster in urban areas, so large swaths of the population find themselves driving several hours to seek care, or waiting weeks or months for appointments.

                AI-based algorithms such as SkinVision, Derm Assist and others could ease these difficulties. None of them offer a diagnosis – at best, they flag growths as harmless or “high risk” and recommend whether a patient should seek care. But many moles turn out to be harmless, so the apps could help patients or primary care physicians – who might not feel confident identifying a skin cancer – figure out which patients really need specialist care.

                “There are many different ways that artificial intelligence can help with triage and decision making to provide support to the physician rather than trying to do their job,” says dermatologist Roxana Daneshjou of Stanford University. “There are opportunities for these algorithms to improve patient care.”

                Much more:

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                • #68
                  Britain begins world's largest trial of blood test for 50 types of cancer

                  Britain's state-run National Health Service will on Monday begin the world's biggest trial of Grail Inc's (GRAL.O) flagship Galleri blood test that can be used to detect more than 50 types of cancer before symptoms appear.

                  The Galleri test looks at the DNA in a patient's blood to determine if any come from cancer cells. Earlier diagnosis of cancers leads to dramatically increased survival rates.

                  The NHS said it wanted to recruit 140,000 volunteers in England to see how well the test worked as part of a randomised control trial. Half of the participants will have their blood sample screened with the Galleri test right away.

                  "We need to study the Galleri test carefully to find out whether it can significantly reduce the number of cancers diagnosed at a late stage," said Peter Sasieni, professor of cancer prevention at King's College London.

                  "The test could be a game changer for early cancer detection and we are excited to be leading this important research."

                  Lung cancer is by far the most common cause of cancer death in the United Kingdom, accounting for around a fifth of all cancer deaths. Lung, bowel, prostate and breast cancers account for 45% of the United Kingdom's cancer deaths, the NHS said.

                  U.S. life sciences company Illumina Inc (ILMN.O) said last month it had completed its $7.1 billion acquisition of Grail. Illumina said it will operate Grail separately from its existing business.:

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                  • #69
                    Why COVID Takes A Harsher Toll On Children With Cancer

                    Early in the pandemic, one bit of encouraging news was that children weren't as vulnerable to COVID-19 as adults.

                    But doctors who treat children with cancer had special concerns.

                    These kids have impaired white blood cells — the ones that fight infection. That can be a result of the cancer itself or of cancer treatments like chemotherapy. So when it comes to common respiratory infections like the flu, children with cancer tend to show more severe symptoms.

                    Would COVID also be more severe in this population?

                    To answer that question, doctors at St. Jude Children's Research Hospital collected reports of COVID cases among 1,500 cancer patients up to age 18, drawing from institutions in 45 countries. The data has been entered into a Global Registry of COVID-19 in Childhood Cancer created along with the International Society of Paediatric Oncology.

                    The study's findings are reported Thursday in The Lancet Oncology: "Global characteristics and outcomes of SARS-CoV-2 infection in children and adolescents with cancer."

                    Dr. Sheena Mukkada, an infectious disease specialist at St. Jude and one of the main authors of the study, spoke to NPR about how pediatric cancer patients have fared over the course of the pandemic. Her comments have been edited for length and clarity.

                    What did you think you would find when you began this study?

                    We were concerned because children with cancer do worse with respiratory viruses. So we always had fear that they were not going to do well.

                    Were your fears correct?

                    Of the kids with cancer, 20% had a severe critical infection with COVID. And death occurred in about 4% of all patients – considerably greater than the general pediatric population with COVID.

                    Little more:

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                    • #70
                      Study offers hope for an era of safer chemotherapy in breast cancer

                      Breast cancer is the deadliest and most common type of cancer in women. The treatment options often require administration of anti-cancer drugs in high doses, as the cells develop resistance towards chemotherapy, leading to painful side effects in patients. Recently researchers have identified that reducing the level of a protein called DSS1 can increase patients’ responsiveness to chemotherapy, therefore lowering the doses of the drug as well as the chances of side effects in patients.

                      Globally each year, more than 600,000 women succumb to deadly breast cancer—the most common cancer affecting women. While individual or combined effects of lifestyle and environmental factors contribute to the development of breast cancer in a large percentage of the female population, the formation of malignancy is usually associated with genetic factors. For example, BRCA1 and BRCA2 are two genes that impact a person's chances of developing breast cancer. Under normal conditions, the protein products of these genes help in repairing DNA damages, thereby reducing the chances of uncontrolled cell growth and tumor development. Any “mutation” or cellular level abnormalities that hinder the functioning of the BRCA genes, thus, predispose the person to a higher chance of developing breast cancer.

                      As such, for decades, researchers have been focusing on deciphering the role of BRCA genes and the cellular components associated with BRCA1 and BRCA2 proteins to understand the progression of breast cancer, and design appropriate targeted therapeutics to prevent and treat the disease. Now, a group of collaborating researchers from Japan and the USA has successfully identified a protein from the BRCA-associated cellular machinery that plays a critical role in the progression of breast cancer. The prominent researchers who were part of this research project were Kazuhiko Kuwahara (Fujita Health University School of Medicine, Japan), Naomi Gondo (Division of Immunology, Aichi Cancer Center Research Institute, Nagoya, Japan), Yasuhiro Sakai (Department of Joint Research laboratory of Clinical Medicine, Fujita Health University School of Medicine, Toyoake, Japan), Zhenhuan Zhang (Radiation Oncology Department, University of Florida, Gainesville, FL), and Andri Rezano (Department of Biomedical Sciences, Division of Cell Biology, Faculty of Medicine, Universitas Padjadjaran, West Java, Indonesia). The findings of the study, recently published in Laboratory Investigation, offer important leads for developing targeted therapy for the fatal disease, too.

                      In their study, the researchers started by looking closely at a protein complex called TRanscription–EXport-2 (TREX-2), which is involved in the transcription and export of mRNA from the nucleus. The complex is made up of several proteins, such as GANP, PCID2, DSS1, and centrin ¾, and as per earlier reports, aberrant expression of some of these proteins leads to DNA damage that results in tumor formation. Dr. Kuwahara, the corresponding author of the study, explains what made them look into TREX-2 complex proteins, “Earlier, we observed GANP-deficiency was closely associated with breast carcinogenesis. We were therefore interested to look into other protein components of the TREX-2 complex for their possible association with breast cancer.” Based on available published information, they focused on DSS1, a protein that is known to be associated with the stabilization of the BRCA2 protein in human cell lines.

                      To test their assumptions, the researchers conducted a series of studies that started with checking the expression levels of various TREX-2 complex proteins, including DSS1, in breast cancer tissues, followed by cellular level experiments. They found that the DSS1 protein expression was higher in human breast carcinoma tissues than in normal tissues. In contrast, the expression of PCID2 protein was normal in malignant tissues. They also found that low DSS1 expression is associated with longer survival time in patients. Interestingly, breast cancer cells with diminished DSS1 levels were more sensitive to standard anti-cancer drugs DXR and PTX, while a high level of DSS1 made the breast cancer cells resistant to these therapeutic agents.

                      The findings marked a breakthrough for breast cancer treatment research. Dr. Kuwahara summarizes, “Strong side effects of anti-cancer therapeutics add to the suffering of the patients and complicates the treatment modalities. Our research suggests depleting the DSS1 protein from breast cancer cells may make the cells chemosensitive, that is more responsive to lower doses of anti-cancer drugs, which means the chances of drug-induced adverse effects in patients with breast cancer will be reduced by this technique.”

                      The promising result of this study generates hope for an era of safer chemotherapy, in the near future, for patients suffering from breast cancer.:

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                      • #71
                        Coppertone issues sunscreen recall due to cancer risk

                        Coppertone announced Friday that it is recalling five of its aerosol sunscreens after finding benzene, a cancer-causing chemical, in some batches.

                        Why it matters: Exposure to benzene can result in an increased risk of cancer, depending on the level and extent of exposure, but the daily exposure levels detected in Coppertone aerosol sunscreens aren't expected to cause "adverse health consequences," according to the announcement.

                        The big picture: Coppertone said as of Sept. 30, it hadn't received any reports of "adverse events" regarding the products which were made between Jan. 10, 2021 and June 15, 2021.

                        "Out of an abundance of caution, we are recalling certain lots of these specific aerosol sunscreen spray products," the company said in a statement.:

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                        • #72
                          Cleveland Clinic testing breast cancer vaccine

                          Researchers at Cleveland Clinic have opened a study for a vaccine seeking to prevent triple-negative breast cancer, which is regarded as the strongest and most deadly form of the disease.

                          The first phase of the trial will determine how strong of a vaccine dose patients with early-stage triple-negative breast cancer can tolerate, according to a release from the clinic.

                          “We are hopeful that this research will lead to more advanced trials to determine the effectiveness of the vaccine against this highly aggressive type of breast cancer,” the Cleveland Clinic's G. Thomas Budd, who serves as the study's principal investigator, said in the statement.

                          Triple-negative breast cancer does not usually respond to hormonal or targeted therapies. It accounts for only about 12 to 15 percent of all breast cancers, but causes a disproportionately high percentage of breast cancer-related deaths, the clinic's release added.

                          “This vaccine approach represents a potential new way to control breast cancer,” Vincent Tuohy, the primary inventor of the vaccine, said in the statement.

                          The clinic's hope is that the vaccine, developed with Anixa Biosciences, would eventually be administered to healthy women to prevent the severe form of cancer from developing entirely, Budd said.

                          The study is funded by the Department of Defense and open to non-clinic patients. Its participants will include 18 to 24 patients who have finished treatment for early-stage triple-negative breast cancer in the last three years and are tumor-free but considered high-risk for recurrence, the clinic added.

                          The study is estimated to be completed in September of next year.:

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                          • #73
                            Chemotherapy made from 'caterpillar fungus' shows early promise in clinical trials

                            An experimental cancer drug made from a molecule found in a Himalayan fungus known as “caterpillar fungus” has shown early promise as a new treatment for patients with advanced tumours in a small clinical trial.

                            The new chemotherapy variety, known as NUC-7738 by researchers at the University of Oxford, is made from cordycepin, first found in a parasitic fungus species called Ophiocordyceps sinensis.

                            Commonly known as “caterpillar fungus,” thanks to its ability to kill and mummify moth larva in the wild, the active ingredient has been used as a herbal remedy in traditional Chinese medicine for centuries.

                            Now, researchers at the University of Oxford, in partnership with U.K.-based biopharmaceutical company NuCana, are testing the proposed anti-cancer, anti-oxidant, and anti-inflammatory effects of the compound in a small phase one trial involving 28 patients with advanced tumours that were resistant to conventional cancer treatment.

                            Cordycepin, referred as 3'-deoxyadenosine (or 3'-dA), is a naturally occurring nucleoside analogue. These analogues can be used in therapeutic drugs, including antiviral products used to prevent viral replication in infected cells.

                            Because the naturally occurring form of cordycepin breaks down quickly in the bloodstream, researchers altered the compound to make it resistant to this process, allowing it to enter cells independently.

                            The latest research shows that these changes make the proposed drug’s anti-cancer properties up to 40 times more potent than cordycepin alone.

                            According to trial findings published in early September, the patient cohort showed “encouraging signals of anti-tumour activity and prolonged disease stabilization" when given weekly escalating doses of NUC-7738.

                            "These findings provide proof of concept that NUC-7738 overcomes the cancer resistance mechanisms that limit the activity of 3'-dA and support the further clinical evaluation of NUC-7738 as a novel cancer treatment,” the researchers reported in their paper.

                            Once the safety of the drug has been demonstrated in Phase 1 of the trial, the researchers will begin planning for Phase 2.​:

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                            • #74
                              "Alarming" trend in colorectal cancer cases under 35

                              Young adults with colon cancer are just as likely to die from the disease as older people — in some cases, maybe even more likely — according to a study to be published today in the Journal of the National Cancer Institute.

                              Why it matters: Colorectal cancer is among the fastest-growing cancers among people younger than 50, and researchers aren't sure why.

                              What they're saying: "It struck us that these patients were younger, they had fewer comorbidities, they had better performance status and were more physically active and they less side effects from the treatment," said Kimmie Ng, director of the Dana-Farber's Young-Onset Colorectal Cancer Center.

                              "But their survival was exactly the same," she said.

                              Between the lines: While her study group had too few patients younger than 35 to have a statistically significant result, Ng said the team observed a "particularly concerning" trend of lower survival rates in that population.

                              The big picture: In May, the U.S. Preventive Services Task Force lowered the recommended age Americans should start getting screened for colon cancer, from age 50 to age 45.

                              The task force said the recommendation reflected the fact that colon cancer — the third-leading cause of cancer death for both men and women in the U.S. — is increasingly occurring among adults younger than 50.

                              What's next: It's still unknown whether cancers that happen in younger people are biologically different than cancers that happen in older people.

                              "We need to better understand what it is that is different about the very youngest patients," Ng said.:

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                              • #75
                                Cancer death rates fall 32 percent since 1991 peak

                                The U.S.'s cancer death rate has fallen by a third since a peak in 1991, sparked by a drop in lung cancer fatalities, according to a report from the American Cancer Society (ACS).

                                The “Cancer statistics, 2022” report published Wednesday documents a 32 percent decrease in cancer deaths from about 215 deaths per 100,000 people in 1991 to 146 fatalities per 100,000 in 2019 — the most recent year for data.

                                If the death rate had remained stable since 1991 instead of decreasing, researchers estimate that almost 3.5 million more cancer patients would have lost their lives in the 28-year period.

                                Researchers attribute the decline partly to a higher percentage of people with lung cancer living longer after diagnosis and to fewer people smoking cigarettes in recent years. The annual drop in lung cancer deaths outpaced the decline in overall cancer fatalities, falling nearly 5 percent per year between 2015 and 2019.

                                The national screening rate for lung cancer rose slightly from 3 percent in 2010 to 5 percent in 2018. But that converted to a higher percentage of earlier diagnoses and a higher survival rate at least three years after diagnosis.

                                Chemotherapy after surgery for breast and colon cancer and early detection efforts also contributed to the decrease in deaths, according to the report.

                                “Accelerating declines in the cancer death rate show the power of prevention, screening, early diagnosis, treatment, and our overall potential to move closer to a world without cancer,” the ACS said in a release.

                                Still, cancer remains the second leading cause of death in the country, with the report predicting 1.9 million new cases and more than 609,000 deaths will occur this year.

                                Lung cancer continues to cause the most cancer fatalities, with researchers estimating it will cause about 21 percent of cancer deaths this year.

                                The ACS noted that the report also does not account for the effects of the COVID-19 pandemic on diagnosis and treatment since the fatality data goes up to 2019.
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