High fat diet breast cancer organoid

By | November 8, 2020

high fat diet breast cancer organoid

Mammary branching was quantified by identifying branch points from the primary ducts originating from the nipple. Ann Epidemiol. Following mammosphere formation, the colonies were then dissociated and plated again to form secondary colonies. Stem Cell Res Ther. Characterization of a stem-like subpopulation in basal-like ductal carcinoma in situ DCIS lesions. Yuan GC 2 ,. Overweight, obesity, and cancer risk. To facilitate invasion, the lower chamber contained 1. External link. Munoz J, et al. Larsson, S.

Saadatpour A 2 ,. Mouse strain-dependent variation in obesity and glucose homeostasis in response to high-fat feeding. Association of adipose tissue and liver fibrosis with tissue stiffness in morbid obesity: links with diabetes and BMI loss after gastric bypass. Castellano-Megias, V. Overall, here we propose organoid-based model systems to study in vivo the effects of obesity on the pancreatic carcinogenesis. Together, these results suggest that obesity did not induce long-term changes in ovarian cycling that may lead to changes in ductal branching observed in our HFD-fed 3-week groups. We thank Patti Wisniewski and Glenn Paradis of the Whitehead flow cytometry and Koch core facilities, respectively, for their expertise in cell sorting. B Expression levels of proteins associated with fibrosis and myofibroblast differentiation were analyzed using Western blotting. Mol Genet Metab 71 — Tomasetti C, Vogelstein B. The uterus is also very sensitive to the effects of ovarian steroids, and uterine weight is frequently used to assess increased exposure to circulating estrogens [ 51 ].

Pancreatic ductal adenocarcinoma PDAC is the third leading cause of cancer-related mortality among adults in developed countries. The discovery of the most common genetic alterations as well as the development of organoid models of pancreatic cancer have provided insight into the fundamental pathways driving tumor progression from a normal cell to non-invasive precursor lesion and finally to widely metastatic disease, offering new opportunities for identifying the key driver of cancer evolution. Obesity is one of the most serious public health challenges of the 21st century. Despite strong evidence indicates a link between obesity and cancer incidence, the molecular basis of the initiating events remains largely elusive. This is mainly due to the lack of an accurate and reliable model of pancreatic carcinogenesis that mimics human obesity-associated PDAC, making data interpretation difficult and often confusing. Here we propose a feasible and manageable organoid-based preclinical tool to study the effects of obesity on pancreatic carcinogenesis. Therefore, we tracked the effects of obesity on the natural evolution of PDAC in a genetically defined transplantable model of the syngeneic murine pancreatic preneoplastic lesion mP and tumor mT derived-organoids that recapitulates the progression of human disease from early preinvasive lesions to metastatic disease. Our results suggest that organoid-derived transplant in obese mice represents a suitable system to study early steps of pancreatic carcinogenesis and supports the hypothesis that inflammation induced by obesity stimulates tumor progression and metastatization during pancreatic carcinogenesis. Cancer and obesity are the two major epidemics of the 21st century Kaidar-Person et al. It is projected to become the second cause of cancer death in Western societies within a decade Siegel et al. PDAC is associated with several distinct precursor lesions that likely impact disease biology, efficacy of therapy, and prognosis.

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Fibroblasts in pancreatic ductal adenocarcinoma: biological mechanisms and therapeutic targets. Acta Oncol. Stem Cell Rep. Mammosphere formation.

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