What a break-through!

Spanish scientists completely cure pancreatic cancer (PDAC) in mice.

The group focused on KRAS, a gene mutated in 90% of people with pancreatic cancer. The team employed a triple therapy, which combined an experimental KRAS inhibitor (daraxonrasib) with an approved drug for certain lung adenocarcinomas (afatinib) and a protein degrader (SD36).

#PDAC #PancreaticCancer #Science #Medicine #Oncology #CancerTreatment

https://www.cnio.es/en/news/the-group-led-by-barbacid-at-cnio-completely-eliminates-pancreatic-tumours-in-mice-with-no-resistance-developing/

The group led by Barbacid at CNIO completely eliminates pancreatic tumours in mice with no resistance developing

In Spain, more than 10,300 cases of pancreatic cancer are diagnosed each year, making it one of the most aggressive forms of cancer. Its detection in the late stages of the disease and the lack of effective therapies mean that the five-year survival rate after diagnosis is less than 10%. But research is finally taking […]

CNIO
🟣 November is Pancreas Cancer Awareness Month 🟣 🟪 It doesn't end in November. 🟪 Sending hope & support to all patients, #PDAC scientists, physicians & caregivers. 💜: PanCan Lustgarten Found. MSKCC Columbia’s Pancreas Ctr. Hirshberg Found. Nat. Pancreas Found. SIGNS & SYMPTOMS:
🟣 November is Pancreas Cancer Awareness Month 🟣 Symptoms of #PancreaticCancer can be vague. J was tired & depressed for about 6 mos; then had pain in his upper belly. Original diagnosis was gastritis. We persisted & he was eventually diagnosed with #PDAC, staged at 2B. Trust your instincts!

After three intensive days of scientific excellence, our course has come to an end. It has been an honor to have such committed and passionate students participating in pancreatic ductal adenocarcinoma (PDAC) research. Thank you to all our students for making this course a resounding success!

See you at the next edition!
#PancreaticCancer #Oncology #MedicalResearch #PDAC #SummerCourse

@Impossible_PhD I remember reading about Pfizer/BioNTech clinical trials for mRNA vaxx PDAC treatment in 2023, shortly after my mom was diagnosed.
This is immensely important and a huge breakthrough.
Extraordinary work by both BioNTech and MSKCC researchers.

https://www.mskcc.org/clinical-updates/custom-mrna-vaccines-pancreatic

#PDAC #mRNA

Custom mRNA Vaccines for Pancreatic Cancer

Cancer vaccines that use messenger RNA (mRNA) technology are an exciting new approach to develop immunotherapies for cancers with poor prognoses, such as pancreatic cancer.

Memorial Sloan Kettering Cancer Center

We’re excited to share our latest research: “ELOVL6 as a Therapeutic Target: Disrupting c-MYC-Driven Lipid Metabolism to Enhance Chemotherapy in Pancreatic Cancer.”

https://www.biorxiv.org/content/10.1101/2024.11.11.622928v1

Targeting metabolic dependencies like ELOVL6 in c-MYC-driven cancers could open new avenues in PDAC treatment, offering hope for better patient outcomes. Follow us for updates as we continue exploring the therapeutic potential of lipid metabolism in cancer

#PDAC

Today, I gave a lesson on tyrosine kinase receptors and serine/threonine kinase receptors, focusing on their signaling pathways and mutations in cancer. Two notable examples are EGFR and TGFBR. #PDAC
Probiotics functionalized with a gallium-polyphenol network modulate the intratumor microbiota and promote anti-tumor immune responses in pancreatic cancer #pancreaticcancer #PDAC https://www.nature.com/articles/s41467-024-51534-z
Probiotics functionalized with a gallium-polyphenol network modulate the intratumor microbiota and promote anti-tumor immune responses in pancreatic cancer - Nature Communications

The intratumor microbiota in pancreatic cancer has been described as pro-tumorigenic. Here the authors modify the probiotic Lactobacillus rhamnosus GG with a gallium-polyphenol network and chitosan nanocoating, showing accumulation in pancreatic lesions and modulation of the intratumor microbiota, eliciting anti-tumor immune response in preclinical models.

Nature
#Pancreatic ductal #adenocarcinoma (PDAC) is a deadly #cancer. @RoLiefke &co show that chromatin regulator SAMD1 represses EMT-related genes, inhibiting cellular migration, and is downregulated during #PDAC progression by #E3ligase FBXO11 #PLOSBiology https://plos.io/4crkx94
SAMD1 suppresses epithelial–mesenchymal transition pathways in pancreatic ductal adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer usually only detected at an advanced and metastatic state. This study shows that the chromatin regulator SAMD1 represses genes related to the epithelial-mesenchymal transition (EMT), thereby inhibiting cellular migration, and is downregulated during PDAC progression by the E3 ligase FBXO11.

LIM domain only 7: a novel driver of immune evasion through regulatory T cell differentiation and chemotaxis in pancreatic ductal adenocarcinoma #pancreaticcancer #PDAC https://www.nature.com/articles/s41418-024-01358-7
LIM domain only 7: a novel driver of immune evasion through regulatory T cell differentiation and chemotaxis in pancreatic ductal adenocarcinoma - Cell Death & Differentiation

With advancements in genomics and immunology, immunotherapy has emerged as a revolutionary strategy for tumor treatment. However, pancreatic ductal adenocarcinoma (PDAC), an immunologically “cold” tumor, exhibits limited responsiveness to immunotherapy. This study aimed to address the urgent need to uncover PDAC’s immune microenvironment heterogeneity and identify the molecular mechanisms driving immune evasion. Using single-cell RNA sequencing datasets and spatial proteomics, we discovered LIM domain only 7 (LMO7) in PDAC cells as a previously unrecognized driver of immune evasion through Treg cell enrichment. LMO7 was positively correlated with infiltrating regulatory T cells (Tregs) and dysfunctional CD8+ T cells. A series of in vitro and in vivo experiments demonstrated LMO7’s significant role in promoting Treg cell differentiation and chemotaxis while inhibiting CD8+ T cells and natural killer cell cytotoxicity. Mechanistically, LMO7, through its LIM domain, directly bound and promoted the ubiquitination and degradation of Foxp1. Foxp1 negatively regulated transforming growth factor-beta (TGF-β) and C-C motif chemokine ligand 5 (CCL5) expression by binding to sites 2 and I/III, respectively. Elevated TGF-β and CCL5 levels contribute to Treg cell enrichment, inducing immune evasion in PDAC. Combined treatment with TGF-β/CCL5 antibodies, along with LMO7 inhibition, effectively reversed immune evasion in PDAC, activated the immune response, and prolonged mouse survival. Therefore, this study identified LMO7 as a novel facilitator in driving immune evasion by promoting Treg cell enrichment and inhibiting cytotoxic effector functions. Targeting the LMO7-Foxp1-TGF-β/CCL5 axis holds promise as a therapeutic strategy for PDAC.

Nature