Penny Triantafillou’s Post

Decoding the Future of Cancer Care: Reflections from GOPEN I recently had the privilege of attending the GOPEN meeting hosted by Illumina in Cambridge. It was an incredible experience to be surrounded by brilliant minds and cutting-edge research in the field of genomics and precision medicine. 👉 One of the key themes that emerged was the transformative power of multinomics in cancer care. By integrating various ``omics`` data we can gain a more comprehensive understanding of the underlying biology of cancer. This knowledge can be leveraged to develop more targeted and effective therapies. 👉 However, as we delve deeper into the world of genomics, it's crucial to address the ethical and societal implications of these advancements. Understanding the benefits and risks of genomics in oncology is essential for making informed decisions and ensuring equitable access to these technologies. 📌 During my participation in the meeting, I advocated for the importance of QUALY (Quality-Adjusted Life Years) and DALY (Disability-Adjusted Life Years) as metrics to assess the impact of cancer management. By considering both the quantity and quality of life, these measures can help us prioritize interventions that truly improve patient outcomes. 📌 I believe that continuous education for all stakeholders is crucial to harness the full potential of genomics in cancer care. This includes healthcare providers, researchers, policymakers, and patients themselves. By fostering a culture of knowledge sharing and collaboration, we can ensure that genomic advancements translate into tangible benefits for patients. I'm excited to see how these innovations will shape the future of cancer care and improve the lives of countless patients.

#Cancer #cells are depicted as SELF-ABNROMAL cells to make chaotic and bluffed tissue microenvironment. In this line, cancer cells are SELF-SMART cells that transmit signals to neighboring healthy cells within tumor microenvironment and to the tumor niche for distress signals to bring metabolic arrest and PCD to anti-tumor healthy cells. At the same time, cancer cells will ignore such signals and continue to proliferate abnormally within the same tumor microenvironment and extending to #tumor niche. This could be analogous to a society, where fake news on the disturbances spread by some #MALIGNANT members to enjoy the free rides of their own malignant activities. Hence, cancer cells enjoy the free rides within tumor microenvironment and surrounding tumor niche by sending distress signals and at the same time sparing cancer cells. Firstly, describing cancer cells as "SELF-ABNORMAL" cells creating a chaotic microenvironment is a widely accepted concept in cancer biology. Cancer cells indeed exhibit abnormal growth patterns and disrupt normal tissue architecture, leading to a disorganized microenvironment. However, labeling cancer cells as "SELF-ABNORMAL" might imply that they have some inherent awareness or intentionality, which could be misleading. The idea that cancer cells are "SELF-SMART" cells capable of sending signals to neighboring healthy cells to induce distress and metabolic arrest is intriguing and reflects the complex interplay within tumors. Cancer cells can indeed communicate with neighboring cells through various mechanisms, including signaling molecules and extracellular vesicles, influencing the tumor microenvironment. Comparing cancer cells to members of society spreading fake news to serve their own interests is an interesting analogy, highlighting the selfish nature of cancer cells within the tumor microenvironment. Cancer cells can indeed exploit signaling pathways to manipulate surrounding cells for their benefit, such as promoting tumor growth and evading the immune system. However, it's important to recognize that this analogy has its limitations. Unlike conscious individuals spreading misinformation, cancer cells operate based on biological imperatives driven by genetic mutations and selection pressures. Overall, while the viewpoints presented could offer thought-provoking analogies between cancer cells and societal dynamics, they should be interpreted with caution. Cancer biology is complex, and describing cancer cells in anthropomorphic terms risks oversimplification and misunderstanding of their behavior. It's essential to maintain a nuanced understanding of cancer as a biological phenomenon driven by genetic and environmental factors.

Artificial intelligence has helped scientists reveal a new form of aggressive prostate cancer, revolutionising how the disease is diagnosed and treated in the future. The Bob Champion Cancer Trust Research & Education Building at The University of East Anglia formed part of a European Consortium making the significant discovery that prostate cancer tumours evolve along multiple pathways, leading to two distinct disease types. The team hope their findings could save thousands of lives in future and revolutionise how prostate cancer is diagnosed and treated. Ultimately, it could provide tailored treatments to each individual patient according to a genetic test which will also be delivered using AI. Prof Colin Cooper head of the Bob Champion Cancer Trust Research & Education Building at University of East Anglia Medical School, highlighted that while prostate cancer is responsible for a large proportion of all male cancer deaths, it is more commonly a disease men die with rather than from. This means that unnecessary treatment can often be avoided, sparing men from side-effects such as incontinence and impotence. He added: “This study is really important because until now, we thought that prostate cancer was just one type of disease. But it is only now, with advancements in artificial intelligence, that we have been able to show that there are actually two different subtypes at play. “We hope that the findings will not only save lives through better diagnosis and tailored treatments in the future, but they may help researchers working in other cancer fields better understand other types of cancer too.” Prostate cancer is the most common cancer affecting men in the UK with around 52,000 cases a year with cases set to keep rising. A number of leading research organisations were involved in the study including The Institute of Cancer Research where the Bob Champion Cancer Trust also fund pioneering research into prostate cancer at a dedicated research unit. #prostatecancer #cancerresearch #cancercharity #ResearchStudy #ResearchNews

#Nature: Do stem-cell transplants increase cancer risk? Long-lived recipients offer clues People who have received transplants for blood cancer, some more than 40 years ago, do not have high rates of potentially cancer-causing mutations. Ever since the first blood-forming stem cells were successfully transplanted into people with blood cancers more than 50 years ago, researchers have wondered whether they developed cancer-causing mutations. A unique study1 on the longest-lived transplant recipients and their donors has revealed that people who receive donor stem cells don’t seem to have an increased risk of developing such mutations. The results are surprising but reassuring, says Michael Spencer Chapman, a haematologist at the Barts Cancer Institute in London. “It’s fantastic news for people undergoing these therapies,” says Alejo Rodriguez-Fraticelli, a quantitative stem-cell biologist at the Institute for Research in Biomedicine in Barcelona, Spain. Blood-forming, or ‘haematopoietic’, stem cells are precursor cells that reside in the bone marrow and give rise to all types of blood cell. They have been used to treat hundreds of thousands of people with blood cancers and bone-marrow diseases. The transplants involve depleting a person’s entire blood stem-cell reserves and replacing them with cells from a healthy donor. But researchers have long worried that putting the cells under such pressure could increase the risk of cancer. In rare cases, about 1 in every 1,000 transplants, donor cells develop into a cancer in the recipients. https://lnkd.in/eKKc_-Wp

There are so many talented students pursuing research in cancer data science, and today, we get to spotlight 3 of them! Help us congratulate Moinak Bhattacharya, Sriya Potluri, and Kartik Singhal, for winning the poster competition at the National Cancer Institute’s Informatics Technology for Cancer Research (ITCR) Program annual meeting. • 1st place - Moinak (as part of Prateek Prasanna’s lab) presented on a machine learning model to help determine the association between the geometric structure of a patient’s pulmonary arteries and their response to treatment, survival, and other clinical features. Poster Title: Immunotherapy Treatment Outcome Prediction in Small Cell Lung Cancer through Topo-Geometric Characterization of Pulmonary Artery Vasculature: A Proof-of-Concept Study. Read the paper this poster was based off of: https://lnkd.in/eBHcApGY • 2nd place - Sriya (working as part of Dr. Pablo Gonzalez-Camara’s lab) presented on an upcoming paper about leveraging the Immunopheno software package to analyze antigens or markers on cancerous surfaces. Poster Title: Data-driven Analyses of Immunophenotyping Data Using ImmunoPheno You can try out the tool mentioned in the poster: https://lnkd.in/eNSu5Ju9 • 3rd place - Kartik (a member of Drs. Malachi and Obi Griffiths’s lab) presented on a recent publication exploring the feasibility of personalizing cancer vaccines through genomic and RNA sequencing techniques. Poster Title: Immune Validation of Neoantigen Vaccines Through Clonal ITCR Analysis in Patients with Pancreas Cancer. Read the paper this poster was based off of: https://lnkd.in/e25sdHx6 And thank you to our ITCR-funded Principal Investigators for helping mentor and provide opportunities to train the next generation of cancer data science researchers! #Every1HasARole

NEWS: 🙌 Exciting news from researchers at the The Francis Crick Institute and UCL, working with Genomics England. They have shown that rogue 🧬 genetic material called extrachromosomal DNA (ecDNA) can drive the survival of many of the most aggressive cancers. This means the team are closer to understanding how cancer tumours grow and how to disrupt them and encourage the immune system to fight cancer.  Chris Bailey, first author and clinician 🧪 scientist at the Crick and University College London Hospital, said: "If we could target ecDNA specifically, we might be able to boost response to standard cancer therapies. Our work has opened up new questions, such as how ecDNA forms in the first place, and when would be best to target it." 🔬To learn more, read the new research in 1 of 3 papers published in Nature from the eDyNAmiC Cancer Grand Challenges team. The paper shows that ecDNA is linked to shorter patient survival and could represent a new treatment target to improve responses to cancer therapies.   Discover more about this research: https://lnkd.in/dD6CgDhp Nature journal: Origins and impact of extrachromosomal DNA https://lnkd.in/e8bKnKax   #francriscrickinstitute #fightingcancer #cancerresearch  #science #ecdna #dna #naturejournal

Cancer cells are driven by the same imperative guiding all living things: to grow, survive and reproduce. Although cancer’s evolutionary underpinnings have been recognized since the 1950s, clinicians have been slow to apply the lessons of evolution to the fight against this deadly disease, which remains the second-leading cause of death, claiming 9.7 million lives worldwide in 2022. A new review by Arizona State University researcher Carlo Maley and Lucie Laplane from the University of Paris Pantheon-Sorbonne examines the prevailing theory of cancer evolution. The authors highlight both practical and theoretical limitations of the clonal model of cancer evolution and propose areas for improving the model’s relevance and accuracy. The study suggests that the model could be improved by acknowledging that cancer cells inherit not only genetic mutations but also other traits that allow them to rapidly adapt to their environment — even without genetic alterations. Cancer cells are highly responsive to their surrounding environment, which can promote or suppress their growth. Further, #cancer evolution often follows complex dynamics, leading to tangled and unpredictable growth patterns. Cancer biologists have traditionally defined a "clone" as a group of cells descending from a single ancestor cell and sharing the same genetic makeup. But cancer cells mutate so fast that no two cells have the same genetic makeup. The study proposes replacing the concept of a clone with a focus on the cell genealogies that record the history and define the structure of the cells in a tumor. The value of an effective model lies in its ability to explain how and why cancers evolve and respond to therapy. By refining the clonal evolution model, the study paves the way for more effective cancer therapies that consider the full complexity of cancer cell evolution. #ASU #ASUBiodesign #ASUResearch

The SAMBAI team, led from Morehouse School of Medicine by Melissa Davis, is a global, interdisciplinary team of researchers, including TOUCH, The Black Breast Cancer Alliance’s Ricki Fairley. Cancer Grand Challenges is a global funding platform, co-founded by Cancer Research UK and the National Cancer Institute in the US, that supports a community of diverse, global teams to come together, think differently and take on some of cancer’s toughest challenges. Inequities in cancer prevention, screening, and treatment lead to disparities in cancer incidence and mortality and are a major public health concern. Team SAMBAI aims to build an unprecedented resource, which will comprise a comprehensive measurement of social, environmental, genetic and biological factors that can be used to help define the causes of disparate outcomes in the selected populations. The team will focus on prostate, breast and pancreatic cancers spanning diverse cohorts of African descent from regions of Africa, the UK and the US. Find out more about our plan to drive progress in research: https://bit.ly/3wIZYWi We are blessed to be able to take TOUCH BBCA global for this iconic research that will advance cancer science. We are ecstatic to build a comprehensive, culturally agile patient engagement ecosystem driven by patients, survivors and caregivers with lived breast, prostate, and pancreatic cancer experience. We will humanize this pre-emptive cancer research with education, support, and resources. When patients are educated with words they can spell from voices of trust, they embrace it. It's not just science for us. It's hope. It's another birthday, a grandbaby, another sunrise. Our team of cancer thriver patient ambassadors will play a strategic role in recruiting and building an involved patient community to ensure that patients have utmost respect, safety, and support.

Tempus Donates Over 3,000 Cancer Patient Profiles to Fuel National Cancer Institute Research - HIT Consultant #TempusDonation: Tempus, a healthcare technology company, donates over 3,000 cancer patient profiles to the National Cancer Institute for research purposes. The donation aims to advance cancer research and improve patient outcomes. #DataDonation: The donated patient profiles include clinical and molecular data, providing valuable insights into cancer treatment and outcomes. This data will be used by researchers to develop personalized treatment plans for cancer patients. #ImpactOnResearch: The donation of patient profiles will significantly impact cancer research by enabling researchers to analyze large datasets and identify patterns that can lead to breakthrough discoveries in cancer treatment. #CollaborativeEffort: Tempus's donation highlights the importance of collaboration between healthcare technology companies and research institutions in advancing cancer research and improving ai.mediformatica.com #cancer #data #tempus #research #cancerresearch #acce #artificialintelligence #clinical #clinicalinformation #dataacce #datasets #insights #digitalhealth #healthit #healthtech #healthcaretechnology @MediFormatica (https://buff.ly/3veW3jG)

Joint research with Harvard reveals health inequalities in cancer Research by Queen Mary University of London and Harvard University shows that people with the Duffy-null phenotype – a trait found predominantly in people of African or Middle Eastern descent – may be erroneously excluded from clinical trials and some cancer treatments due to misinterpretation of their routine blood test results. Some clinical trials or cancer treatments require participants to have a certain level of white blood cells called ‘neutrophils’ to ensure that they’re healthy enough to participate in the trial, and this is measured by a standard blood test.  People with the Duffy-null phenotype have relatively lower levels of neutrophils when measured in the blood. In people without the Duffy-null phenotype, low neutrophil levels would be associated with a higher risk of infection, but this isn’t the case for people with Duffy-null phenotype – they are often perfectly healthy.  Dr Stephen Hibbs, lead author and HARP Fellow, said: “Health inequity in cancer treatment and research has many causes, and some are more difficult to address than others. Neutrophil criteria for clinical trials and dose modifications are a hidden contributor to inequity that can be rectified. Now, action to amend these criteria is needed to ensure Duffy-null patients are not disadvantaged”. The study, published today in JAMA Open Network, demonstrates the need to reevaluate what is considered ‘normal’ across healthcare to ensure that criteria and measures are not excluding races and ethnicities. Follow the link in the comment, below, for the paper. NHS Race & Health Observatory