KACTUS’ Post

“For the longest time, people thought this is not something that can be commercialized.” Chantale Bernatchez, head of Process Development at CTMC / A joint venture between Resilience + MD Anderson Cancer Center The FDA has recently approved Iovance Biotherapeutics’ tumor infiltrating lymphocyte (TIL) therapy Amtagvi® for patients with unresectable or metastatic melanoma – marking the first cell therapy of its class to target a solid tumor. In an interview with Labiotech.eu, Chantale shared her insights into TIL therapy and what the first approval means for the cell and gene therapy sector. As Amtagvi® paves the way for many more TIL therapy approvals, it is imperative that logistical and reimbursement challenges are overcome, so that these therapies are not just approvable but accessible and affordable too. Read more ➡️ https://lnkd.in/dDBfZ5PU #CellTherapy #GeneTherapy #Biotechnology #ManufacturingBrighterFutures #AdvancedTherapies

MicroRNA-451a: A Potential Therapeutic Avenue Against Gemcitabine-Resistant Biliary Tract Cancers The study investigated miR-451a's impact on gemcitabine-resistant biliary tract cancers (BTCs), highlighting its significant inhibition of proliferation and induction of apoptosis in gallbladder cancer (GBC) and cholangiocarcinoma (CCA) cells, including those resistant to gemcitabine. Through its suppression of chemoresistant traits and regulation of the PI3K/AKT pathway by targeting macrophage migration inhibitory factor, miR-451a emerged as a promising therapeutic avenue for addressing gemcitabine-refractory BTCs. Employing 3D cell culture systems and GBC organoids, this research underscores the potential of miR-451a supplementation as a viable strategy against resistant BTCs. Read more: https://lnkd.in/d4YuFpbt #Ariti #Cancer #Research #resistance #Study #univeristy #people #peoplefirst #pharmaceuticals #health #healthcare #medical #carcinoma #oncology #therapy

Annexins and cancer Antibody to annexin A1 (AnxA1) halts cancer cell proliferation in vitro and in vivo. Cell cycle arrested in G1 phase. Already established that Knockout of AnxA2 gene targets metastasis by reducing membrane repair of cells in the circulation. Annexin “therapies” look more and more interesting .. #annexin #AnxA1 #proliferation #metastasis #cellcycle #therapies

🎉Pfizer's TALZENNA® Receives Novel EU #Approval for Prostate Cancer Treatment! 🎉 ℹ Pfizer's oral PARP inhibitor, TALZENNA®, in combination with XTANDI®, has been approved by the #europeancommission for metastatic castration-resistant prostate cancer (mCRPC). This marks the #first and only PARP inhibitor licensed in the EU for use with XTANDI for patients with mCRPC, with or without gene mutations. The approval is based on data from the Phase III TALAPRO-2 trial, which showed that TALZENNA plus XTANDI reduced the risk of disease progression or death by 37 percent versus placebo plus XTANDI. The #combination offers an effective #treatment that addresses disease progression in patients with or without any specific gene mutation. 💡 This significant advancement underscores Pfizer's #commitment to providing #innovative treatments for patients with prostate #cancer. #Pfizer #TALZENNA #XTANDI #ProstateCancer #innovation #EUApproval #medicaladvancements #cancertreatment #SymmetricTraining

#ScientificSaturday 🔬Gefitinib ― is a targeted cancer therapy drug, specifically a tyrosine kinase inhibitor, used primarily to treat non-small cell lung cancer (NSCLC) with certain mutations in the epidermal growth factor receptor (EGFR) gene. By inhibiting EGFR, gefitinib helps slow or stop the growth of cancer cells that overexpress this protein. It is administered orally and is most effective in patients whose tumors have specific EGFR mutations, determined through genetic testing. While gefitinib has improved treatment outcomes for some patients, it can also cause side effects such as skin reactions and diarrhea, and its effectiveness may diminish over time due to drug resistance. ❗This study explores the mechanisms behind gefitinib resistance in lung adenocarcinoma (LUAD) patients with EGFR mutations, focusing on the role of ferroptosis, a form of programmed cell death. The researchers discovered that gefitinib resistance in EGFR-mutated LUAD cells is partly due to the inhibition of ferroptosis, with the aldo-keto reductase family 1 member C1 (AKR1C1) identified as significantly upregulated in resistant cell strains, correlating with poorer patient outcomes. Further, they revealed that AKR1C1 upregulation is mediated by the decreased expression of miR-338-3p and the involvement of the long non-coding RNA NEAT1_1, which sponges miR-338-3p, neutralizing its suppression of AKR1C1. To read what else this study uncovered, click the link below. BioPharma Services Inc. has previously completed multiple clinical trials on Gefitinib. Trust our world-class Pharmacokinetic team with your next #Phase1, BA/BE or Human Abuse Liability (#HAL) drug development project. Read the full blog here: 👇 https://hubs.li/Q02qqyMT0 Discover our Services: 👇 https://hubs.li/Q02qqDKs0 #clinicalresearch #biopharma #drugdevelopment #drugresearch #cro #clinicaltrials

Mechanism of drug reactivating tumor suppressors . Researchers have revealed the mechanism of the drug valemetostat shown to be effective in treating certain types of cancer by targeting a protein modification (histone methylation) silencing the expression of tumor suppressor genes and restoring their function. The researchers also demonstrated in clinical trials the efficacy of the drug in treating blood cancers by reducing tumor growth. The findings could lead to sustainable, longer-term treatments for the disease, as well as therapies for other types of cancer with similar underlying causes. #ScienceDailynews #InnovativeResearch #NextGenScience #ExploringFrontiers

Exciting Research Update on Pancreatic Ductal Adenocarcinoma (PDAC)! I'm thrilled to share our latest preprint on bioRxiv, where we explore a promising combination therapy for PDAC, a cancer notorious for its resistance to current chemotherapies. Our study tackles the challenge of personalized therapy in PDAC by focusing on tumors dependent on KRAS for survival (dKRAS). We discovered that gene expression signature scores can effectively assess KRAS dependency, opening doors to tailored treatments. Findings: KRAS Dependency: Nearly 90% of PDAC cases harbor KRAS mutations. Our transcriptomic-based KRAS dependency scores can predict the efficacy of targeted therapies. Combination Therapy: We found that combining low-dose decitabine (DEC) with the PARP inhibitor olaparib (OLA) significantly enhances antitumor activity in dKRAS-PDAC. This synergy is due to DEC inducing DNA damage and activating a DNA damage response, which is further exploited by inhibiting PARP with OLA. Broader Efficacy: This combination is effective even in BRCA1/2 wild-type and homologous recombination-proficient tumors, extending the clinical benefit of OLA beyond BRCA status. Metastasis Inhibition: In dKRAS-PDAC tumors with a BRCA2 mutation, DEC+OLA inhibited metastasis growth, outperforming single-drug treatments. These findings underscore the potential of DEC+OLA combination therapy in PDAC, highlighting DNA damage response as a critical mechanism and advocating for its clinical evaluation irrespective of BRCA1/2 status. Read the full preprint here: https://lnkd.in/dTsM8kri Thank you to my incredible team and collaborators for contributing to this research. We believe this approach could pave the way for more effective and personalized treatments for PDAC patients. #PancreaticCancer #PDAC #KRAS #CancerResearch #PersonalizedMedicine #bioRxiv #Research #Oncology #CancerTherapy

🌟 Exciting New Mini Review Alert! 🌟   🔍 Delving into the Potential of Targeting Signal-Transducing Adaptor Protein-2 in Cancer Therapeutic Applications.   Adaptor proteins are key players in numerous intracellular signaling pathways. This review sheds light on the inhibitory peptide's role as a promising candidate for combatting prostate and lung cancers.   📝 Authors: Taiga Maemoto, Tadashi Matsuda, and more. 🔬 #SignalTransducingAdaptorProtein #SignalTransduction #EGFR #ProstateCancer #LungCancer #Peptides   Let's stay informed and empowered in the world of cancer therapeutics! 💪🚀  https://lnkd.in/eqCtvV7i Object]

𝐂𝐮𝐫𝐫𝐞𝐧𝐭 𝐬𝐜𝐞𝐧𝐚𝐫𝐢𝐨 𝐨𝐟 𝐩𝐞𝐫𝐬𝐨𝐧𝐚𝐥𝐢𝐳𝐞𝐝 𝐭𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 💊 𝐢𝐧 𝐜𝐚𝐧𝐜𝐞𝐫 The emergence of 𝐛𝐢𝐨𝐦𝐚𝐫𝐤𝐞𝐫 𝐭𝐞𝐬𝐭𝐢𝐧𝐠 has led to the 𝐠𝐞𝐧𝐨𝐦𝐞-𝐰𝐢𝐝𝐞 𝐬𝐜𝐫𝐞𝐞𝐧𝐢𝐧𝐠 𝐨𝐟 𝐜𝐚𝐧𝐜𝐞𝐫. This can identify the causative genes’ mutation, amplification and fusions in various cancers. Based on the underlying genetic mechanism, personalized therapy including 𝐬𝐦𝐚𝐥𝐥 𝐦𝐨𝐥𝐞𝐜𝐮𝐥𝐞 𝐢𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬, 𝐠𝐞𝐧𝐞 𝐭𝐡𝐞𝐫𝐚𝐩𝐲, 𝐢𝐦𝐦𝐮𝐧𝐨𝐭𝐡𝐞𝐫𝐚𝐩𝐲 𝐬𝐮𝐜𝐡 𝐚𝐬 𝐛𝐢𝐨𝐬𝐢𝐦𝐢𝐥𝐚𝐫𝐬, 𝐂𝐀𝐑𝐬, 𝐜𝐡𝐞𝐜𝐤𝐩𝐨𝐢𝐧𝐭 𝐢𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬, 𝐯𝐚𝐜𝐜𝐢𝐧𝐞𝐬 𝐚𝐧𝐝 𝐜𝐲𝐭𝐨𝐤𝐢𝐧𝐞 𝐭𝐡𝐞𝐫𝐚𝐩𝐲 can be administered to the patients. Personalized therapy offers lesser side effects as it targets the contributing factor, however, is unable to reach the masses due to ☛ ✷ 𝑯𝒊𝒈𝒉 𝒄𝒐𝒔𝒕 𝒐𝒇 𝒅𝒊𝒂𝒈𝒏𝒐𝒔𝒊𝒔 𝒂𝒏𝒅 𝒕𝒓𝒆𝒂𝒕𝒎𝒆𝒏𝒕 ✷ 𝑻𝒊𝒎𝒆 𝒕𝒂𝒌𝒆𝒏 𝒇𝒐𝒓 𝒅𝒊𝒂𝒈𝒏𝒐𝒔𝒊𝒔 ✷ 𝑵𝒐𝒕 𝒂𝒗𝒂𝒊𝒍𝒂𝒃𝒍𝒆 𝒇𝒐𝒓 𝒂𝒍𝒍 𝒄𝒂𝒏𝒄𝒆𝒓𝒔, 𝒂𝒔 𝒔𝒐𝒎𝒆 𝒕𝒂𝒓𝒈𝒆𝒕𝒔 𝒂𝒓𝒆 𝒖𝒏𝒅𝒓𝒖𝒈𝒈𝒂𝒃𝒍𝒆 ✷ 𝑺𝒐𝒎𝒆 𝒕𝒉𝒆𝒓𝒂𝒑𝒊𝒆𝒔 𝒂𝒓𝒆 𝒊𝒏 𝒕𝒓𝒊𝒂𝒍𝒔 ✷ 𝑾𝒐𝒓𝒌𝒔 𝒃𝒆𝒔𝒕 𝒊𝒏 𝒄𝒐𝒎𝒃𝒊𝒏𝒂𝒕𝒊𝒐𝒏, 𝒐𝒘𝒊𝒏𝒈 𝒕𝒐 𝒕𝒉𝒆𝒓𝒂𝒑𝒚 𝒓𝒆𝒔𝒊𝒔𝒕𝒂𝒏𝒄𝒆 Points to improve ☛ ◆ 𝑴𝒐𝒍𝒆𝒄𝒖𝒍𝒂𝒓 𝒕𝒖𝒎𝒐𝒓 𝒃𝒐𝒂𝒓𝒅: Adopting multi-omics approach to understand the novel and lesser-known players ◆ 𝑷𝒂𝒕𝒊𝒆𝒏𝒕-𝒅𝒆𝒓𝒊𝒗𝒆𝒅 𝒐𝒓𝒈𝒂𝒏𝒐𝒊𝒅𝒔 𝒂𝒏𝒅 𝒙𝒆𝒏𝒐𝒈𝒓𝒂𝒇𝒕𝒔: cancer evolution, clonal selection and sensitivity upon drug exposure ◆ 𝑳𝒊𝒒𝒖𝒊𝒅 𝒃𝒊𝒐𝒑𝒔𝒚: Understanding tumor heterogeneity better relative to single biopsy The following news highlights the recent FDA approved targeted therapies in cancer in 2024 ☟ #cancer #targetedtherapy

Phenotypic plasticity is a cancer hallmark, and lung adeno-to-squamous transition (AST) triggered by LKB1 inactivation is significantly associated with drug resistance. Clinical data show that squamous transition occurs in certain lung adenocarcinoma patients who relapse from targeted therapy using EGFR tyrosine-kinase inhibitors (TKIs) or KRAS inhibitor. However, the epigenetic regulatory mechanisms involved in AST remain largely unknown. - TET2-STAT3-CXCL5 nexus promotes neutrophil lipid transfer to fuel lung adeno-to-squamous transition - Tet2 knockout in KrasG12D;Lkb1-/- (KL) model suppresses squamous transition through immune microenvironment remodeling - TET2 is recruited to Cxcl5 promoter region via the interaction with STAT3, resulting in Cxcl5 promoter demethylation and gene expression - Therapeutic strategies to control AST process include targeting STAT3 activation, reducing CXCL5 level, or blocking lipid transfer - Study uncovers epigenetic mechanism orchestrating phenotypic plasticity through regulating immune microenvironment and metabolic communication What are your thoughts on the potential therapeutic strategies identified in this study to inhibit lung cancer transition? #medicalinnovation #cancerresearch #lungcancer #sciencex