JMSACL (Journal of Mass Spectrometry & Advances in the Clinical Lab)’s Post

In their recent article for Cell & Gene, Sanofi's Sarah Cooley and Kyle Jensen explain the potential advantages of NK cell engagers (NKCEs), a novel class of multifunctional biologics, which have emerged as an exciting innate immune-based mechanism in #oncology research. #nkcells #immunotherapy #cartcelltherapy #cellandgenetherapy #cgt #NKCE https://lnkd.in/e7NRuNTM

🎉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

🔬💊 Revolutionizing Pancreatic Cancer Treatment: The Power of Patient-Derived Organoids Pancreatic cancer poses a formidable challenge in the medical world, having the highest mortality rate among major cancers. But what if miniature models of a patient's tumor could change the game? Enter patient-derived organoids, a cutting-edge biotechnology offering a personalized approach to treatment. Researchers at the Salk Institute recently shed light on the reliability of these organoids in mimicking pancreatic tumors. Their study, published in JCI Insight, revealed that the choice of extracellular matrix—the scaffold for growing these organoids—didn't significantly alter gene expression or drug responses. However, one brand did accelerate organoid growth, an advantage for the urgency in pancreatic cancer treatment. Dr. Dannielle Engle, the study's senior author, emphasizes the importance of personalized medicine. With organoids, clinicians gain a predictive model to tailor treatments effectively, sparing patients from the "guessing game" of traditional approaches. While variations in culture media can influence organoid behavior, differences in extracellular matrices had minimal impact. This discovery strengthens confidence in organoid technology's accuracy and reliability for evaluating patient drug responses. With continued optimization and validation, these organoids hold promise in improving patient outcomes.   « Together, we're inching closer to a future where pancreatic cancer is no longer a death sentence » For further information, check the following paper.  https://lnkd.in/eKP-wwJ4

#cancerresearch #genetics #oncology #mutations https://lnkd.in/gQAeA297 Abstract The RAF family of #kinases includes key activators of the pro-tumourigenic mitogen-activated protein kinase pathway. Hyperactivation of #RAF #proteins, particularly BRAF and CRAF, drives #tumour #progression and drug resistance in many types of cancer. Although BRAF is the most studied RAF protein, partially owing to its high mutation incidence in melanoma, the role of CRAF in tumourigenesis and drug resistance is becoming increasingly clinically relevant. Here, we summarize the main known regulatory mechanisms and gene alterations that contribute to CRAF activity, highlighting the different oncogenic roles of CRAF, and categorize RAF1 (CRAF) mutations according to the effect on kinase activity. Additionally, we emphasize the effect that CRAF alterations may have on drug resistance and how precision therapies could effectively target CRAF-dependent tumours. Here, we discuss preclinical and clinical findings that may lead to improved treatments for all types of oncogenic RAF1 alterations in cancer.

Burning Rock Dx Spotlight: OncoScreen®Plus A study explored tumor-immune Microenvironment and NRF2 Associate with Clinical Efficacy of PD-1 Blockade Combined with Chemotherapy in Lung Squamous Cell Carcinoma. OncoScreen®Plus was been used to assess the Genomic profiling and tumor mutational burden (TMB). Result： As an immune signature, the immune-related gene expression signature (GES) might identify LUSC patients likely to benefit from first-line tislelizumab plus chemotherapy. Highlights: 1) Tislelizumab plus chemotherapy prolongs PFS in lung squamous cell cancer 2) An 11-gene immune gene expression signature correlates with the PFS benefit 3) In contrast, the PFS benefit is observed regardless of PD-L1 expression or TMB 4) NRF2 pathway activation negatively impacts predictive potential of PD-L1 and TMB Read the full study: https://lnkd.in/gntM7_BD #NSCLC #TMB #BurningRockDx #OncoScreen®Plus

📃Scientific paper: Expression Profile and Diagnostic Significance of MicroRNAs in Papillary Thyroid Cancer Abstract: SIMPLE SUMMARY: In recent years, the incidence of papillary thyroid cancer (PTC) has increased in many countries worldwide. MicroRNAs appear to be important regulators of PTC, but a better understanding of their role is needed to develop novel diagnostic tools and identify potential vulnerabilities. In this study, we aimed to gain insight into the microRNA profile of PTC tissue. Consequently, crucial pathways in PTC were highlighted. A panel of four microRNAs (miR-152-3p, miR-221-3p, miR-551b-3p, and miR-7-5p) was proposed as a PTC diagnostic biomarker. Our analysis indicated that microRNAs are a potential diagnostic tool for PTC patients. ABSTRACT: The incidence of papillary thyroid cancer (PTC) has increased in recent years. To improve the diagnostic management of PTC, we propose the use of microRNAs (miRNAs) as a biomarker. Our aim in this study was to evaluate the miRNA expression pattern in PTC using NanoString technology. We identified ten miRNAs deregulated in PTC compared with reference tissue: miR-146b-5p, miR-221-3p, miR-221-5p, miR-34-5p, miR-551b-3p, miR-152-3p, miR-15a-5p, miR-31-5p, and miR-7-5p (FDR < 0.05; |fold change (FC)| ≥ 1.5). The gene ontology (GO) analysis of differentially expressed miRNA (DEM) target genes identified the predominant involvement of epidermal growth factor receptor (EGFR), tyrosine kinase inhibitor resistance, and pathways in cancer in PTC. The highest area under the receiver operating characteristic (ROC) curve (AUC) for ... Continued on ES/IODE ➡️ https://etcse.fr/ljgy ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: Expression Profile and Diagnostic Significance of MicroRNAs in Papillary Thyroid Cancer Abstract: SIMPLE SUMMARY: In recent years, the incidence of papillary thyroid cancer (PTC) has increased in many countries worldwide. MicroRNAs appear to be important regulators of PTC, but a better understanding of their role is needed to develop novel diagnostic tools and identify potential vulnerabilities. In this study, we aimed to gain insight into the microRNA profile of PTC tissue. Consequently, crucial pathways in PTC were highlighted. A panel of four microRNAs (miR-152-3p, miR-221-3p, miR-551b-3p, and miR-7-5p) was proposed as a PTC diagnostic biomarker. Our analysis indicated that microRNAs are a potential diagnostic tool for PTC patients. ABSTRACT: The incidence of papillary thyroid cancer (PTC) has increased in recent years. To improve the diagnostic management of PTC, we propose the use of microRNAs (miRNAs) as a biomarker. Our aim in this study was to evaluate the miRNA expression pattern in PTC using NanoString technology. We identified ten miRNAs deregulated in PTC compared with reference tissue: miR-146b-5p, miR-221-3p, miR-221-5p, miR-34-5p, miR-551b-3p, miR-152-3p, miR-15a-5p, miR-31-5p, and miR-7-5p (FDR < 0.05; |fold change (FC)| ≥ 1.5). The gene ontology (GO) analysis of differentially expressed miRNA (DEM) target genes identified the predominant involvement of epidermal growth factor receptor (EGFR), tyrosine kinase inhibitor resistance, and pathways in cancer in PTC. The highest area under the receiver operating characteristic (ROC) curve (AUC) for ... Continued on ES/IODE ➡️ https://etcse.fr/ljgy ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

Lung Cancer Clinical Trials Yield Positive Patient Outcomes in Genprex, Inc.'s New Video Update Featuring Chief Medical Officer Genprex, Inc. shared promising updates from its Acclaim-1 and Acclaim-3 Phase 1/2 clinical trials for lung cancer in a video featuring Chief Medical Officer Dr. Mark Berger. The Acclaim-1 trial evaluates Genprex, Inc.'s Reqorsa® Gene Therapy in combination with AstraZeneca's Tagrisso® for patients with late-stage non-small cell lung cancer who have EGFR mutations. The Acclaim-3 trial examines Reqorsa with Genentech's Tecentriq® as maintenance therapy for patients with extensive-stage small cell lung cancer. Genprex, Inc. has refined its clinical development strategy by streamlining the Acclaim-1 trial and closing the Acclaim-2 study to focus on the most promising outcomes. Dr. Berger emphasized the potential of Reqorsa to improve lung cancer treatment and enhance patient quality of life, as the company advances toward bringing this innovative therapy to market. For more details please click the link! https://lnkd.in/d6xP4zxr #marketaccess #reimbursement #pricing #hta #heor #healtheconomics #medicaldevices #pharmaceutical 

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