UNAM Institute of Materials Science and Nanotechnology’s Post

AI reveals prostate cancer is not one disease. Cancer Research UK-funded study, published in Cell Genomics, revealed prostate cancer, affecting one in eight men, includes two different subtypes. 05 March 2024 Excerpt: The discovery was made by an international team led by University of Oxford, and University of Manchester. AI was applied on data from DNA to identify two different subtypes affecting the prostate. The team hope their findings could save thousands of lives and revolutionize how prostate cancer is diagnosed and treated. Ultimately, it could provide tailored treatments for each patient according to a genetic test implemented using AI. The ground-breaking research, involved additional funding from Prostate Cancer Research, Scientists from University of Oxford, University of Manchester, University of East Anglia and the Institute of Cancer Research, London, highlight how prostate cancer diagnosis can affect physical, emotional and mental wellbeing. Note: Lead researcher Dr Dan Woodcock, Nuffield Department of Surgical Sciences, University of Oxford, said: 'Our research demonstrates prostate tumors evolve along multiple pathways, leading to two distinct disease types. This understanding is pivotal to classify tumors based on how cancer evolves rather than solely on individual gene mutations or expression patterns.' Researchers worked together as part of an international consortium, The Pan Prostate Cancer Group, established at The Institute of Cancer Research (ICR) and University of East Anglia to analyze genetic data from thousands of prostate cancer samples across nine countries. The team's collaboration with Cancer Research UK (CRUK) plans to develop a genetic test, when combined with conventional staging and grading, can provide more precise prognosis for each patient, allowing tailored treatment decisions. Researchers used AI to study changes in DNA of prostate cancer samples (whole genome sequencing) from 159 patients. Two distinct cancer groups were identified using an AI neural network. The two groups were confirmed using two other mathematical approaches applied to different aspects of the data. This finding was validated in independent datasets from Canada and Australia. All the information was integrated to generate an evolutionary tree showing how two subtypes of prostate cancer develop, converging into two distinct disease types, called ‘evotypes’. Dr Rupal Mistry, CRUK's senior Science Engagement Manager, said: 'The work published by this global consortium has potential to make a difference to people affected by prostate cancer. The more we understand about cancer the better chance we have of developing treatments to beat it. Further information and a direct link to published research enclosed.

A new study led by University of Pittsburgh and UPMC Hillman Cancer Center researchers shows that an enzyme called PARP1 is involved in repair of telomeres, the lengths of DNA that protect the tips of chromosomes, and that impairing this process can lead to telomere shortening and genomic instability that can cause #cancer. PARP1's job is genome surveillance: When it senses breaks or lesions in DNA, it adds a molecule called ADP-ribose to specific proteins, which act as a beacon to recruit other proteins that repair the break. The new findings, published in Nature Structural & Molecular Biology, are the first evidence that PARP1 also acts on telomeric DNA, opening up new avenues for understanding and improving PARP1-inhibiting cancer therapies. "No one thought that ADP-ribosylation at DNA was possible, but recent findings challenge this dogma," said Roderick O'Sullivan, Ph.D., associate professor of molecular pharmacology Pitt and investigator at UPMC Hillman. "PARP1 is one of the most important biomedical targets for cancer research, but it was thought that drugs targeting this enzyme only acted at proteins. Now that we know PARP1 also modifies DNA, it changes the game because we can potentially target this aspect of PARP1 biology to improve cancer treatments." O'Sullivan hypothesizes that ADP-ribose affects telomere integrity by disrupting a protective structure called shelterin that safeguards telomeres, but more research is needed to confirm this. "Targeting PARP1 has been a big success story for cancer therapy, but some patients develop resistance to PARP1 inhibitors," said O'Sullivan. "I'm excited about this study because we've discovered something new about PARP1 biology, which generates a whole load of new questions that could help us develop novel approaches to target PARP1 or fine-tune therapies we already have. We're right at the beginning of something exciting, and there's a lot more to explore." Other authors on the study were Sandy Schamus-Haynes, Ragini Bhargava Ph.D., and Patty Opresko, Ph.D., all of Pitt and UPMC; Junyeop Lee and Jaewon Min, Ph.D., both of Columbia University; Robert Lu, Ph.D., and Hilda Pickett, Ph.D., both of the University of Sydney; and Marion Schuller, D.Phil., and Joséphine Groslambert, both of the University of Oxford. https://lnkd.in/e7pnhG3P

A research team led by Professor Kwang-Hyun Cho from the KAIST Department of Bio and Brain Engineering has developed a technology that can treat colon cancer by converting cancer cells into a state resembling normal colon cells without killing them, thus avoiding side effects. The study is published in the journal Advanced Science. The research team focused on the observation that during the oncogenesis process, normal cells regress along their differentiation trajectory. Building on this insight, they developed a technology to create a digital twin of the gene network associated with the differentiation trajectory of normal cells. Through simulation analysis, the team systematically identified master molecular switches that induce normal cell differentiation. When these switches were applied to colon cancer cells, the cancer cells reverted to a normal-like state, a result confirmed through molecular and cellular experiments as well as animal studies. This research demonstrates that cancer cell reversion can be systematically achieved by analyzing and utilizing the digital twin of the cancer cell gene network, rather than relying on serendipitous discoveries. The findings hold significant promise for developing reversible cancer therapies that can be applied to various types of cancer. Professor Kwang-Hyun Cho said, "The fact that cancer cells can be converted back to normal cells is an astonishing phenomenon. This study proves that such reversion can be systematically induced. This research introduces the novel concept of reversible cancer therapy by reverting cancer cells to normal cells. It also develops foundational technology for identifying targets for cancer reversion through the systematic analysis of normal cell differentiation trajectories." #👍👍👍

On Tuesday May 7th, our Clinical and Translational Oncology PhD Programme participant Vivien Veninga will defend her theses, entitled: "𝑮𝒓𝒂𝒔𝒑𝒊𝒏𝒈 𝒕𝒉𝒆 𝒄𝒐𝒎𝒑𝒍𝒆𝒙𝒊𝒕𝒚 𝒐𝒇 𝒂𝒏𝒕𝒊-𝒕𝒖𝒎𝒐𝒓 𝒊𝒎𝒎𝒖𝒏𝒊𝒕𝒚." 𝐖𝐡𝐚𝐭 𝐢𝐬 𝐭𝐡𝐞 𝐦𝐚𝐢𝐧 𝐫𝐞𝐬𝐞𝐚𝐫𝐜𝐡 𝐭𝐨𝐩𝐢𝐜 𝐨𝐟 𝐲𝐨𝐮𝐫 𝐭𝐡𝐞𝐬𝐢𝐬? 👩🔬 Cancer immunotherapies, such as immune checkpoint inhibitors (ICI), have shown significant success in the treatment of cancer patients. This thesis aimed to analyze underlying cellular mechanisms of anti-tumor immunity using patient-derived tumor organoids as a model system. Next to focusing on T cell mediated tumor responses, we broadened the scope to NK cell and gamma delta T cells. Doing so enriched our understanding of responses to ICI in tumors that cannot be recognized by T cells and underlines the value of future therapies targeting immune cells of the adaptive and innate immune system. 𝐖𝐡𝐚𝐭 𝐢𝐬 𝐭𝐡𝐞 𝐟𝐢𝐧𝐝𝐢𝐧𝐠 𝐲𝐨𝐮 𝐚𝐫𝐞 𝐦𝐨𝐬𝐭 𝐩𝐫𝐨𝐮𝐝 𝐨𝐟 𝐚𝐧𝐝 𝐰𝐡𝐲? 💡 We discovered that a specific type of gd T cells can recognize and eliminate mismatch repair deficient (MMR-d) colon cancer cells harboring a mutation that makes them invisible to conventional T cells. Our experiments provided the field with a more comprehensive understanding of how a tumors response to immune checkpoint inhibitor anti-PD1 is not only mediated by conventional T cells. Following that lead, we tested if we could exploit the mechanism to enhance gamma delta T cell reactivity towards another colon cancer type, mismatch repair proficient (MMR-p), which currently remains difficult to treat. Not only did we show improved tumor reactivity towards MMR-p colorectal cancer in our model system by mutation of beta-2-microglobulin (B2M) but furthermore discovered a potential influence of gamma delta T cells by the MMR status of cancer cells. Those findings are a fantastic starting point to improve future cancer immunotherapies and highlight the value of scientific collaborations and team work without none of this would have been achievable. 𝐖𝐡𝐚𝐭 𝐚𝐫𝐞 𝐲𝐨𝐮𝐫 (𝐜𝐚𝐫𝐞𝐞𝐫) 𝐩𝐥𝐚𝐧𝐬, 𝐧𝐨𝐰 𝐭𝐡𝐚𝐭 𝐲𝐨𝐮’𝐯𝐞 𝐟𝐢𝐧𝐢𝐬𝐡𝐞𝐝 𝐲𝐨𝐮𝐫 𝐏𝐡𝐃? 🎓 I'll be working as a postdoc in Ansuman Satpathy’s lab at Stanford University. We want to congratulate Vivien Veninga and her (co)promotors Emile Voest and Noel de Miranda with this important work and wish Vivien Veninga lots of luck ánd fun during her defense! 📕 👏 UMC Utrecht Cancer Research UMC Utrecht Clinical and Translational Oncology PhD Programme Sjoerd Elias Susanne Lens

💎💎💎Whatsapp!! 💎💎💎Cell Suicide Pathway & Chemotherapy& Cancer New #Chemotherapy-Induced #Cancer_Cell #Suicide_Pathway Uncovered. #Chemotherapy kills cancer #cells, but researchers headed by a team at the Netherlands Cancer Institute have now found that the way these cells die appears to be different than previously understood. Their in vitro studies uncovered a completely new way in which cancer cells die, which is linked to the #Schlafen 11 (SLFN11) #gene, and #ribosome stalling. “This is a very unexpected finding,” said research co-lead Thijn Brummelkamp, PhD. “Cancer #patients have been treated with chemotherapy for almost a century, but this route to #cell_death has never been observed before. Where and when this occurs in patients will need to be further investigated. This discovery could ultimately have implications for the treatment of cancer patients.” Brummelkamp and colleagues reported on their findings in Science. In their paper, titled “DNA damage induces p53-independent apoptosis through ribosome stalling,” the team noted, “These results provide an explanation for the frequent #inactivation of SLFN11 in chemotherapy-unresponsive #tumors and highlight #ribosome #stalling as a #signaling event affecting #cell #fate in response to #DNA #damage. Many cancer treatments damage cell DNA. After too much #irreparable damage, cells can initiate their own death. The #p53 #protein is well known for taking charge of this process. This protein “referred to as the ‘#guardian of the genome’” the authors wrote, ensures repair of damaged DNA, but initiates cell suicide when the damage becomes too severe. This prevents #uncontrolled #cell #division and #cancer_formation. “The p53 protein can be activated by DNA damage and functions as a transcription factor to induce a cell cycle #arrest, allowing damage repair, or to induce #apoptosis,” the team further stated. Cells #lacking p53 can still undergo apoptosis when their DNA is damaged, but the responsible pathways aren’t known, the authors continued. So while cancer treatments such as #radiotherapy or #chemotherapy that eliminate tumor cells by damaging their DNA can activate the p53 protein, it’s still possible for cells with a #defective p53 pathway to undergo apoptosis in response to DNA damage, “although a clear understanding of the pathways involved isn’t unavailable,” the team pointed out. “Understanding these pathways could be relevant because 30 to 50% of all cancers contain #mutant TP53, and such tumors are still treated using #genotoxic #therapies irrespective of these #mutations. Brummelkamp continued, “In more than half of tumors, p53 no longer functions. The key player p53 plays no role there. So why do cancer cells without p53 still die when you damage their DNA with chemotherapy or #radiation? To my surprise, that turned out to be an unanswered question. ➡ 💎 You can find more pieces of work by clicking here. https://lnkd.in/eSG67K5G https://lnkd.in/dB3s88ei

Brews & Brains (B&B): B&B is a series all about sparking meaningful conversations about the challenges, triumphs, and experiences that shape both the professional and personal lives of postdocs. Whether it’s navigating research hurdles, maintaining a work-life balance, or discussing the human side of academia, B&B gives postdocs a platform to share their stories, voice their concerns, and connect on a deeper level. 🎉 The first episode is out NOW! 🎉 B&B chapter1:  A dual between cancer and science, a journey to understand and find cure for Cancer: from the perspective of postdocs studying Cancer Biology In Brews & Brains Chapter 1, we explored cancer biology with postdocs leading cutting-edge research in CAR-T therapy, chemo-resistance, probiotics for cancer treatment, and DNA methylation. The panel discussed breakthroughs, emphasizing the importance of personalized medicine and the transformative role of AI. While cancer’s complexity—especially its heterogeneity—poses significant challenges, researchers are optimistic. AI’s ability to speed up drug discovery and optimize clinical trials could be a game-changer. The panel advised aspiring cancer biologists to hone computational skills, build networks, and carefully choose their labs to thrive in this competitive field. At WashU, unique opportunities, mentorship, and resources make it an ideal environment for advancing cancer research. Stay tuned for more exciting developments in Brains & Brews! Key Takeaways: Personalized Cancer Treatments: The future of cancer research is focused on personalized therapies, especially in CAR-T treatments. AI's Role: AI is expected to revolutionize cancer research, accelerating drug discovery, clinical trials, and data analysis. Challenges in Cancer Research: Cancer's complexity and heterogeneity remain major obstacles in diagnosis and treatment. Essential Skills: Future cancer biologists should focus on computational skills, networking, and selecting the right research lab. WashU’s Advantages: Washington University provides strong mentorship, state-of-the-art facilities, and collaborative opportunities for cancer researchers. Read the full chapter here:

The Future of Cancer Research – Mapping Tumor Terrain with Spatial Multiomics What if we could unlock the secrets of tumor biology by mapping the intricate landscapes within cancer itself? Emerging spatial multiomics technologies are doing just that, transforming our understanding of tumor microenvironments and offering unprecedented opportunities for targeted cancer treatments. A recent article in Nature explores the revolutionary potential of spatial multiomics. By integrating spatial data on RNA, proteins, and even metabolic signatures, scientists can now create detailed molecular maps of tumors. These insights reveal the heterogeneity within tumors and uncover pockets of drug resistance or vulnerability that were previously invisible. Spatial omics goes beyond identifying individual cells—it places them in context, highlighting how cellular neighborhoods interact. Techniques like Imaging Mass Cytometry (IMC) and platforms such as NanoString’s GeoMx or Vizgen’s MERSCOPE allow researchers to visualize and quantify biomolecules across tumor samples. This groundbreaking approach offers a deeper understanding of cancer progression, immune evasion, and treatment resistance. Key Takeaways: Tumor Heterogeneity Visualized: Spatial multiomics illuminates the diversity within tumors, showcasing how cellular communities influence disease progression. Integration of Multiomic Layers: Combining transcriptomics, proteomics, and metabolomics creates a holistic picture of tumor biology. Practical Applications: These maps help identify treatment targets, predict therapy outcomes, and design personalized interventions. Technological Challenges: High costs, complex data analysis, and integration across platforms remain barriers to widespread adoption. The Role of AI: Deep learning is poised to revolutionize the field by turning these molecular maps into predictive models for clinical applications. This transformative research holds immense promise for precision oncology. However, the barriers to entry—cost, complexity, and computational demands—underscore the need for collaborative efforts and technological refinement. What does this mean for professionals in precision medicine? The era of spatial multiomics invites a shift toward integrative, data-driven approaches that consider not just what cells are present but how they interact. For researchers and clinicians alike, it’s a call to embrace innovation and rethink cancer treatment strategies. What’s next? As AI begins to unlock the hidden patterns within these spatial maps, could we one day predict—and even preempt—tumor formation? How do you envision spatial multiomics shaping the future of oncology?

🌟 *The Crucial Role of Clonal Hematopoiesis of Indeterminate Potential (CHIP) in Cancer Genomics* 🌟 In the intricate world of cancer genomics, Clonal Hematopoiesis of Indeterminate Potential (CHIP) stands out as a significant factor. CHIP is a condition where somatic mutations in hematopoietic stem cells give rise to clones of blood cells with specific mutations, but without an overt hematologic malignancy. Why does CHIP matter so much in cancer genomics? Let’s dive in: 🧬 *Variant Allele Frequency (VAF)* in *CHIP* One of the key ways to monitor CHIP is by measuring *Variant Allele Frequency (VAF)*. 💡 *Key Insights into VAF in CHIP:* - *Typical VAF Range*: In CHIP, the VAF generally ranges from *2% to 10%*. This indicates that only a small subset of blood cells carry the mutation. - *Higher VAF & Clonal Expansion*: As the clone expands, VAF can increase. A higher VAF (>10%) may signal a more substantial clonal burden, suggesting a potential progression towards a hematological malignancy like leukemia. ✨Importance of *CHIP* in *Cancer Genomics* 🔍 *Precursor to Hematological Malignancies*: CHIP can evolve into serious blood cancers such as AML and MDS. Tracking these mutations allows for early detection and intervention. 🧬 *Impact on Solid Tumor Development* : Emerging evidence shows CHIP mutations may influence solid tumors. Genes like TP53 and JAK2, common in CHIP, might enhance risks for cancers like lung and colorectal cancer. 🛡️ *Alterations in the Immune System* : Mutations in genes like TET2 may impair immune functions, allowing tumors to evade detection and affecting the efficacy of cancer therapies. 📈 *Cancer Risk Assessment* : CHIP mutations are early indicators of increased cancer risk, especially in older adults or those with high genetic predisposition. 🔍 *Role in Cancer Screening* : CHIP mutations are becoming invaluable in non-invasive cancer screenings, potentially signaling early tumorigenesis through liquid biopsies. 💊 *Biomarker for Treatment Resistance* : CHIP-associated mutations can indicate resistance to therapies, guiding clinicians toward more effective treatment plans. 🔄 *Impact on Cancer Epigenetics* : CHIP mutations often affect epigenetic regulation, contributing to genomic instability and increasing the chances of malignant transformations. By integrating CHIP profiling into clinical practice, we can enhance cancer screening, risk stratification, and precision oncology, improving patient outcomes through early intervention and personalized therapies. As our understanding of CHIP deepens, its role in predictive genomics and precision medicine will continue to evolve, underscoring the importance of ongoing research. Let’s embrace the potential of CHIP in transforming cancer care and creating a future where early detection and intervention become the norm. 🌟 #CancerGenomics #CHIP #PrecisionMedicine #VAF #Oncology #HealthcareInnovation #EarlyDetection #CancerResearch

Big breakthrough in medical treatment: Korean scientists find undo button that turns tumour cells into normal ones Yes, Korean scientists at the Korea Advanced Institute of Science and Technology (KAIST) have developed a technology that can transform colon cancer cells into normal cells: How it works The technology uses computer modeling to identify molecular switches that can reverse cancer cells back to a normal-like state. Benefits This approach could lead to safer, side-effect-free cancer therapies. It could also help address the risk of recurrence that's associated with traditional cancer treatments. Research The research team studied the process of oncogenesis, which is when normal cells lose their differentiation during cancer formation. They used advanced simulation tools to create a digital twin of the gene network linked to cell differentiation. Next steps The findings suggest that similar strategies could be used to treat different types of cancer. Researchers in Korea have discovered a way to reverse cancer and change tumour cells back to normal. A groundbreaking development in cancer treatment has been made by researchers at Korea Advanced Institute of Science and Technology (KAIST), who have created a technology that changes colon cancer cells into healthy cells without killing them. The Department of Bio and Brain Engineering's Professor Kwang-Hyun Cho is spearheading this novel approach, which marks a substantial shift from conventional cancer treatments that depend on eradicating cancer cells, which frequently result in serious side effects and recurrence risks. The ability of cancer cells to transform back into healthy cells is a remarkable phenomenon. This study demonstrates that it is possible to systematically induce such reversion, Cho said. Short Researchers in South Korea have developed a technology to cure cancer It converts colon cancer cells back to normal cells It also reduces the risk of side effects unlide traditional treatments In a groundbreaking development, researchers at KAIST (Korea Advanced Institute of Science and Technology) unveiled a new technology that treats colon cancer without killing cancer cells. Instead, the technology converts cancer cells into a state resembling normal colon cells, effectively avoiding harmful side effects. This innovative approach challenges the traditional notion of cancer treatment where many therapies come with limitations, remission risk and side effects.