This is the predicted protein structure of FNBP1. It is thought to drive cancer through alterations in splicing. An algorithm developed at the #CRG predicts there are 813 genes which aid cancer proliferation by altering cellular splicing. Study out now in Nature Communications. According to main author Miquel Anglada-Girotto, PhD candidate at the Serrano Lab, "these are not classic oncogenes but rather represent an entire new class of potential cancer drivers which can be targeted in isolation or in synergy with existing strategies. It’s an incredibly exciting new frontier to explore." The majority of the genes found have been overlooked historically because most cancer research focus on how mutations contribute to the disease. The research expands the list of possible therapeutic targets to monitor and tackle the disease. More info: https://lnkd.in/dx5Maa2S
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Here's a nice overview of our latest findings 🙂
This is the predicted protein structure of FNBP1. It is thought to drive cancer through alterations in splicing. An algorithm developed at the #CRG predicts there are 813 genes which aid cancer proliferation by altering cellular splicing. Study out now in Nature Communications. According to main author Miquel Anglada-Girotto, PhD candidate at the Serrano Lab, "these are not classic oncogenes but rather represent an entire new class of potential cancer drivers which can be targeted in isolation or in synergy with existing strategies. It’s an incredibly exciting new frontier to explore." The majority of the genes found have been overlooked historically because most cancer research focus on how mutations contribute to the disease. The research expands the list of possible therapeutic targets to monitor and tackle the disease. More info: https://lnkd.in/dx5Maa2S
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The significance of p53 mutant proteins Every other human cancer harbors a mutation in p53, with roughly 60–80% of these mutations linked to the acquisition of gain-of-function oncogenic properties (as per the gain-of-function theory). Before the loss of heterozygosity occurs, p53 mutant proteins can suppress the remaining wild-type p53 proteins through a dominant negative mechanism. This mechanism, as an alternative to the gain-of-function theory, could elucidate the advantageous nature of p53 missense mutations. While the gain-of-function theory has long accounted for the pattern of p53 mutations, conflicting observations have perpetuated its status as a postulation. Cancer transformation is underpinned by concerted interactions between oncogenic mutations and the cell state. Notably, p53 mutant proteins consistently exhibit ‘context-dependent functions. #sciencenewshighlights #ScienceMission https://lnkd.in/gtFzGNGu https://lnkd.in/gyZyWksP
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⭐Another #ICR10 scientific achievement of 2013: ICR researchers identified a possible new druggable target for a subtype of hard-to treat cancers. Professor Wojciech Niedzwiedz, who leads the Genome Instability and Cancer Team at the ICR, co-led the study, which uncovered one of the mechanisms behind the survival of cancer cells. The team showed that a protein called EXD2 nuclease has an important role in the ALT pathway, which supports survival in more than 10 per cent of cancers. ALT-reliant cancers use this pathway to avoid cell death, usually the inevitable result of multiple cell divisions. Specific DNA protein structures called telomeres sit at the end of chromosomes, and they shorten each time the cell divides. The ALT pathway helps cells counter telomere shortening via an unknown method, allowing them to maintain the length of their telomeres. Read more⬇️ 🔗https://lnkd.in/edRnMgd4 🔗https://lnkd.in/dZWbwxpi
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DNA methylation will become the most reliable method for early screening for cancer 👨🔬 Recently, Dr. Moshe Szyf, the founder of epigenetics, was interviewed by Zao Dx (a new media and industrial service platform focusing on the field of early screening and diagnosis ,early treatment of diseases) and said that DNA methylation will become the most reliable method for early screening of cancer. He said: DNA methylation is more closely related to changes in cancer cells than mutations, and occurs in almost every cancer. They create such big differences between cancer DNA and normal DNA that our next-generation sequencing technology can easily detect them. This is why I believe DNA methylation will become the most reliable method for early screening for cancer. #DNAmethylation #Cancerscreening #Cancerearlydetection #IColocomf #IColohunter #Colorectalcancer #CRC #bowelcancer
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DNA methylation will become the most reliable method for early screening for cancer 👨🔬 Recently, Dr. Moshe Szyf, the founder of epigenetics, was interviewed by Zao Dx (a new media and industrial service platform focusing on the field of early screening and diagnosis ,early treatment of diseases) and said that DNA methylation will become the most reliable method for early screening of cancer. He said: DNA methylation is more closely related to changes in cancer cells than mutations, and occurs in almost every cancer. They create such big differences between cancer DNA and normal DNA that our next-generation sequencing technology can easily detect them. This is why I believe DNA methylation will become the most reliable method for early screening for cancer. #DNAmethylation #Cancerscreening #Cancerearlydetection #IColocomf #IColohunter #Colorectalcancer #CRC #bowelcancer
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MYC is a protein that plays a significant role in the progression of cancer. It is responsible for exacerbating the majority of human cancer cases, with 75% of cancers being affected by this protein. In healthy cells, MYC assists with the process of transcription, which involves converting genetic information from DNA into RNA and proteins. However, in cancer cells, MYC becomes hyperactive and is not properly regulated, leading to rapid cancer growth. Researchers at UC Riverside aimed to find a way to control MYC’s hyperactivity to manage cancer. The challenge was that MYC lacks a structure, unlike most other proteins that could be manipulated to control hyperactivity. Eventually, the researchers developed a molecule (NT-B2R) that binds to MYC, inhibiting its cancer-promoting function without affecting MYC expression or phosphorylation levels. This discovery offers hope for new treatments and the potential to control cancer by dampening MYC’s hyperactivity. #MYC #Cancer #NTB2R https://lnkd.in/dKAP4p6R
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“With data from the Hartwig Medical Database, we have discovered a mutational signature that is caused by a gut bacterium. This is a common E. coli that is present in 20% of the population and has the potential to cause cancer. We first experimentally determined the pattern in vitro in the lab and then used the Hartwig dataset to determine how often we find it back in cancer, and how often it can cause cancer driver mutations”: Ruben van Boxtel, PI Prinses Máxima Centrum voor kinderoncologie and Oncode Institute Would you like to use this data, too? https://lnkd.in/excwE-kp The data is anonymized and made available free of charge to cancer research institutes and hospitals. It is used by research groups all over the world. Hartwig Medical Foundation is a not-for-profit organization that promotes scientific research in the fight against and treatment of cancer and other diseases, in the broadest sense and provided it is in the public interest. #cancerresearch #cancergenomics #bioinformatics Photo: e-coli bacteria
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As we're coming to the end of the work day, why not grab a cup of coffee... and a research paper? This new article from Dr Alan Prem Kumar and team will make for some intellectually stimulating reading. Here's the summary: SHP2 inhibitors show promise in treating certain types of cancer, but their effectiveness is hindered by a narrow therapeutic window and unclear resistance mechanisms. This study, co-led by N2CR member Dr Alan Prem Kumar, reveals that the SHP2 protein regulates the activity of another protein called SMURF2, which is involved in a signaling pathway called TGFβ. SHP2 depletion keeps SMURF2 inactive, sustaining TGFβ activity. TGFβ is important for cell migration, senescence (a state of cell aging), and cell survival. Combining SHP2 and TGFβ inhibitors may enhance the effectiveness of cancer treatments and improve patient outcomes. Read more: https://lnkd.in/eDwnVczg
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Gum disease may accelerate the development of pancreatic cancer, a new study in mice has shown, suggesting a direct link between oral health and the onset of this type of cancer. Research at EARA member The Hebrew University of Jerusalem investigated the potential of Porphyromonas gingivalis – a type of bacteria found in the mouth that can cause gum disease – in driving the most common pancreatic cancer (PDAC). P. gingivalis has previously been linked to PDAC development, and when the bacteria were given orally to genetically engineered mice that were predisposed to the disease, the team saw there was a faster progression of the cancer. Read more: https://lnkd.in/eT_A7Kv7 #AnimalResearch #GumDisease #OralHealth #PancreaticCancer #PDAC #CancerResearch #Mice
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In a recent fireside chat, our CEO Jeffrey Meckler and CSO Michael J. Newman, Ph.D. discuss how cancer grows and the challenges in treating advanced stages. It’s generally recognized that cancer typically emerges after 10-15 mutations accumulate in cells, a process that can span years. Treating advanced cancer is particularly difficult because there are hundreds of potential mutations, each contributing differently. Targeting a single mutation often leads to resistance or activation of alternative pathways. Our innovative Decoy technology contains a package of around a dozen immune-stimulating agents that activate both the innate and adaptive immune responses. We believe this broad stimulus enhances our chances of overcoming cancer’s ability to evade the body’s immune system. Watch to learn how we are tackling these challenges head-on with cutting-edge science. #IndaptusTherapeutics #CancerResearch #Immunotherapy #biology101
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