Van Der Woude Syndrome

– Leou Ismael Banla, MD, PhD, receives annual Conquer Cancer-Vaniam Group LLC Young Investigator Award, dedicated to Black, African, or African American cancer researchers – Erica Pimenta, MD, PhD, receives annual Conquer Cancer-Women Leaders in Oncology "Women Who Conquer Cancer" Young Investigator Award CHICAGO, June 5, 2024 /PRNewswire/ -- Conquer Cancer®, the ASCO Foundation, presented the 2024 Young Investigator Awards (YIAs) funded by Vaniam Group™ and Women Leaders in Oncology® (WLO) on May 31. Both annual awards recognize and promote greater diversity and equity across cancer research. Leou Ismael Banla, MD, PhD, of Massachusetts General Hospital and the Harvard Radiation Oncology Program, became the fourth recipient of the Conquer Cancer-Vaniam Group LLC YIA, which is dedicated to Black, African, or African American cancer researchers. Dr Banla, of Boston, Massachusetts, will use his funding for continued research on advancing imaging techniques to obtain a clearer picture of specific markers found on pancreatic ductal adenocarcinoma (PDAC) cells Erica Pimenta, MD, PhD, of Dana-Farber Cancer Institute, became the eighth recipient of the Conquer Cancer-Women Leaders in Oncology "Women Who Conquer Cancer" YIA for her innovative work investigating the key pathways in the de-differentiated subtype (DDLPS) of liposarcoma (LPS). Her continued research in Boston, Massachusetts, will explore how the lack of insulin-like growth factor-1 (IFG-1) may serve this at-risk population "The pursuit of an equitable future in oncology research and treatment inspires our work at Vaniam Group," said Deanna B. van Gestel, Founder and CEO of Vaniam Group and WLO, and Board Member of Conquer Cancer, the ASCO Foundation. "Championing young investigators, most especially women and people of color, will help pave the way to better health outcomes for patients living with cancer. It is our honor to support Dr Banla and Dr Pimenta in their important research." Both grants were presented by Conquer Cancer in conjunction with the 2024 ASCO Annual Meeting held in Chicago on Friday, May 31st, 2024. Conquer Cancer-Vaniam Group LLC YIA Presented by Conquer Cancer and funded by Vaniam Group, the Conquer Cancer-Vaniam Group LLC YIA provides annual research grants to Black, African, or African American researchers who specialize in oncology. The YIA was established in 2021 to encourage more people of color to apply for Conquer Cancer grants. Dr Banla is the fourth recipient of this YIA. In 2021, Quaovi H. Sodji, MD, PhD, of University of Wisconsin-Madison, received the inaugural grant while completing residency at Stanford University for his research exploring a novel immunotherapy approach to combat pancreatic cancer. Women Leaders in Oncology Created in 2014 by Ms. van Gestel, WLO is focused on growing a community and fostering meaningful connections for women in oncology drug development, clinical research, and medical practice. WLO facilitates networking, mentorship, and research funding for women across oncology at all levels, along with sponsorship opportunities that enable corporations to exceed their diversity, equity, and inclusion goals in a measurable and impactful way. In addition to raising funds to support the annual YIA, WLO community members also contribute toward the $1.35 million endowment that Ms. van Gestel has pledged to raise by 2026 to fund future Women Who Conquer Cancer YIAs. Anyone interested in supporting this cause can donate at CONQUER.ORG/WLO. Leou Ismael Banla, MD, PhD As a recipient of the Conquer Cancer-Vaniam Group LLC YIA, Leou Ismael Banla, MD, PhD, will continue his research into confirming the potential PDAC cancer biomarkers identified by his team. Although still in its early stages, success in Dr Banla's research could enable more targeted treatments for PDAC cancer, ultimately leading to improved patient options. "We're aiming to create more tailored treatments for PDAC," shared Dr Banla. "These new methods could lead to better drugs that are safer, have fewer side effects, and are more efficient at treating this deadly form of cancer." Dr Banla is a distinguished fourth-year resident and Holman research fellow with the Harvard Radiation Oncology Program. His research endeavors focus on advancing the precision of treatments for aggressive malignancies, particularly pancreatic cancer. With a keen interest in leveraging cutting-edge developments in cancer biology and bioengineering, Dr Banla's work spans from developing antibody-drug conjugates targeting specific surface proteins to pioneering methods for in vivo drug activation. Erica Pimenta, MD, PhD Dr Erica Pimenta, a medical oncology fellow at Dana-Farber Cancer Institute, is dedicated to understanding sarcoma pathogenesis and immune evasion. As a recipient of the WLO Women Who Conquer Cancer YIA, Dr Pimenta will further her work on LPS, a common form of soft tissue sarcoma. Through this funding, Dr Pimenta will continue her investigation into the shift from the well-differentiated subtype to DDLPS, uncovering the key pathways that may drive this transition. "We do not currently understand the cellular pathways that are involved in this transition," stated Dr Pimenta, "but uncovering these important processes is required to improve outcomes for patients with LPS." Dr Pimenta's unique training, bridging adult and pediatric medicine, as well as computational and molecular biology, positions her to conduct clinically meaningful, patient-derived, and biologically relevant research into sarcoma biology. She plans to pursue an independent career as a physician-scientist, focusing on mesenchymal tumor biology and immune evasion, with the overall goal of improving the lives of patients living with sarcoma. About Vaniam Group Vaniam Group is a people-first, purpose-driven, independent network of healthcare and scientific communications agencies committed to helping biopharmaceutical companies realize the full potential of their compounds across oncology, virology, and rare disease. Founded in 2007 as a virtual-by-design organization, Vaniam Group harnesses the talents and expertise of team members around the world. For more information, visit VaniamGroup.com. ASCO® and Conquer Cancer®, the ASCO Foundation, are registered trademarks of the American Society of Clinical Oncology. Used with permission. ASCO and Conquer Cancer® are not partners or affiliates of WLO or Vaniam Group and do not recommend or endorse any organization, product, or service. SOURCE Vaniam Group LLC

Data published today by Dana-Farber Cancer Institute and Hebrew University-Hadassah Medical School to be presented at the American Association of Cancer Research (AACR) Annual Meeting 2024 BROOKLINE, Mass.--(BUSINESS WIRE)-- Edgewood Oncology, a clinical-stage biotechnology company focused on delivering BTX-A51 to patients with hematologic malignancies and genetically-defined solid tumors, today announced the publication of new preclinical data from a study of BTX-A51 in human liposarcoma (LPS) conducted by Dana-Farber Cancer Institute and Hebrew University-Hadassah Medical School to be presented at the AACR Annual Meeting 2024 in San Diego. BTX-A51 is a first-in-class, small molecule, multi-selective kinase inhibitor of casein kinase 1 alpha (CK1α) as well as the transcriptional regulators cyclin-dependent kinases 7 and 9 (CDK7 and CDK9) that synergistically co-targets master regulators of cancer to promote programmed cell death, or apoptosis. The presentation (Abstract 604), “Targeting casein kinase 1 alpha (CK1alpha) and transcriptional CDKs (CDK7/9) in human liposarcomas,” highlighted findings for BTX-A51 in preclinical human models of LPS. The data demonstrate that BTX-A51 has preclinical efficacy in treating patient-derived LPS in cell lines and human xenograft models and provides insight into the synergy gained by inhibiting both CK1α and CDK9. “Dedifferentiated liposarcomas (DDLPS) are rare tumors derived from precursors of fat cells which can occur anywhere in the body. Patients with metastatic DDLPS face a life-threatening disease in need of more effective therapeutic options, which we hope to develop by taking advantage of vulnerabilities in LPS that have been uncovered by recent research on the abnormal DNA and other molecular characteristics of LPS,” said George Demetri, M.D., Professor of Medicine and director of the Sarcoma Center at Dana-Farber. “Based on these data, we believe that it is justified to move BTX-A51 into a clinical trial for patients with LPS, which we will plan to open soon for enrollment.” Liposarcomas are universally characterized by amplification of the mouse double minute 2 homolog (MDM2) gene, which leads to destruction of the normal (non-mutated, also known as “wild type”) p53. The data demonstrate that BTX-A51 significantly reduces the abnormal overexpression of MDM2 in multiple patient-derived LPS cell lines, leading to upregulation of p53 expression and ultimately apoptosis. Finally, BTX-A51 was demonstrated to be well-tolerated and effective in an LPS patient-derived xenograft model. “We’re pleased that investigators at Dana-Farber have taken an interest in BTX-A51, which is currently being evaluated in a Phase 2 combination study with azacitidine in patients with relapsed or refractory (R/R) AML,” said David N. Cook, Ph.D., chief executive officer of Edgewood Oncology. “These data also suggest the potential for BTX-A51 in cancers with MDM2 amplifications, a group of genetically defined tumors that span multiple tissue types suggesting broader potential.” Additional Details about the Study Using three different CDK9-selective inhibitors in human LPS cell lines, the authors showed that CDK9 inhibition suppressed cell growth and induced apoptosis by decreasing MDM2 levels while inducing expression of p53. It was also demonstrated that the potency of CDK9 inhibitors is significantly enhanced upon CK1α depletion. These data led to the investigation of BTX-A51, which targets CK1α and CDK9 as well as CDK7, in LPS cells and has previously been shown to inhibit these kinases with nanomolar efficacy in AML models. BTX-A51 potently reduced expression of MDM2 with marked induction of p53, resulting in apoptosis of LPS cells. BTX-A51 also reduces expression of MCL1 and primes LPS cell lines and primary LPS cells for BIM-induced apoptosis, as demonstrated by BH3 profiling. Importantly, preliminary in vivo data in an LPS patient-derived xenograft model reveal that BTX-A51 is well-tolerated under conditions that inhibit tumor growth. About Edgewood Oncology Edgewood Oncology is a clinical-stage biotechnology company that was founded to deliver on the promise of BTX-A51 for patients with hematologic malignancies and genetically-defined solid tumors. BTX-A51 is a novel small molecule, multi-kinase inhibitor that synergistically co-targets master regulators of cancer to activate programmed cell death, or apoptosis. BTX-A51 holds promise in acute myeloid leukemia and genetically-defined solid tumors, which are the focus of ongoing clinical programs. For more information, please visit , and follow us on LinkedIn. View source version on businesswire.com: Contacts Tracy Lessor TLOW Communications, LLC 617-519-9827 tracy@tlowcommunications.com Source: Edgewood Oncology View this news release online at:

A bitter taste in the mouth is often a symptom or side effect of illness, which may be the result of how the body reacts to pathogens. A new study sheds light on the mechanisms involved in the complex interplay between taste perception and immune function. Their work also highlights the potential of a sequencing tool for investigating epigenetic mechanisms that affect taste-cell gene expression. A bitter taste in the mouth is often a symptom or side effect of illness, which may be the result of how the body reacts to pathogens. A new study published in iScience, by Hong Wang, PhD, an Associate Member at the Monell Chemical Sense Center, and colleagues sheds light on the mechanisms involved in the complex interplay between taste perception and immune function. Their work also highlights the potential of a sequencing tool for investigating epigenetic mechanisms that affect taste-cell gene expression. Epigenetics is the study of how and when genes are expressed rather than alteration of the genetic code itself. In addition to being unpleasant, a bitter taste in the mouth or from food can contribute to a loss of appetite, an effect associated with ailments from the common cold to cancer. Bitter taste can also affect patients' willingness to take certain medications, especially when they are young children. Bitter receptors are encoded by Tas2r genes, which also provide an important defense against bacteria and parasites in the mouth and gut. However, this process is not well understood. For this study, the team explored how inducing inflammation would affect gene regulation of these taste receptors. Using lipopolysaccharide (LPS), a compound that induces inflammation similar to that caused by bacterial infections, they found that mice showed a distinct elevated aversion to bitter tastes. The team used nerve-recording experiments to confirm that this aversion originates in the taste buds of mice, rather than in their brains. "Our study had very clear data showing this is actually a change at the peripheral level, not deep in the brain," said Wang, confirming that genes in taste cells govern bitter taste distortion to this type of inflammation. This finding has interesting clinical implications for the study of behavioral aspects of illness, such as a loss of appetite. When people are sick they often do not feel like eating. This can affect even humans' love for sugary treats, as other studies have noted. Mice also have a decreased preference for sweet tastes during illness and forced intake of sugar can make them sicker. These results potentially indicate a protective behavior with a biological or evolutionary basis. To investigate the underlying gene expression mechanisms of the bitterness response, the team used several methods of analysis. Real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR) revealed a significantly increased response across the majority of the Tas2r taste-receptor genes, with peak gene expression ranging from three to five days during the sickness period. The researchers also used single-cell sequencing assay for transposase-accessible chromatin (scATAC-seq) to explore the expression of Tas2r genes in response to LPS -- the first reported instance of this method to study taste receptor gene expression. LPS markedly increased the accessibility of many Tas2r genes, indicating that the bitter taste distortion in this experiment is caused by an epigenetic mechanism, similar to how disease-causing bacteria can affect those genes. Finally, the study showed that LPS-induced inflammation globally affected gene expression in taste stem cells, suggesting a "remodeling" of the cells' genome. This may leave an epigenetic memory, enabling the cells to respond faster to future infections, but may also contribute to long-lasting effects on taste responses. This finding sheds light on why cancer treatment and certain chronic illnesses can cause a lingering bitter taste in the mouth or alter the taste perception of certain foods. This diverse response across taste receptors has potential implications for research on how to make more effective bitter blockers for medications and other edible health and wellness products. "The spectrum of the bitter taste receptor expression is not uniform," Wang said. "If we want to look at a bitter blocker for an individual taste receptor, we may want to take these factors into consideration, such as whether it's for after a sickness, during a sickness, or which of the taste receptor genes is most prominently expressed."