Pancreatic+Cancer+Symptoms

Physical Symptoms vs Molecular Symptoms [] “ Regulation of //BRCA2 // Gene Expression by the SLUG Repressor Protein in Human Breast Cells” -BRCA2 Gene mutations indicate the strong possibility of pancreatic cancer (among other cancers) -Mutations cause the body to have a deficiency of the SLUG protein, which suppresses BRCA2 from being exhibited in non-dividing cells. Since cancerous cells in the breasts, ovaries, and pancreas do not show SLUG, they grow at uncontrolled rates. BRCA2 is fatal in uncontrolled quantities to cells so finding what stops this from killing cancerous cells could find a pancreatic cancer detector. [] =“PAM4-Reactive MUC1 Is a Biomarker for Early Pancreatic Adenocarcinoma“ = -Protein MUC1 binds to pathogens and is a good detector for cancer. -PanIN (pancreatic intraepithelial neoplasias) lesions of different levels, PanIN-1A, -1B, -2, -3, describe the stages leading to pancreatic cancer with PanIN-3 being the stage right before pancreatic cancer. -A pancreas without PanIN lesions has normally none of the protein MUC1. As the cancerous cells develop, MUC1 becomes overabundant in an attempt to signal antibodies to come and destroy these cells. -PAM4, an antibody, is signaled by MUC1 in the pancreas. Only reactive with abnormally large amounts of MUC1 - [] ==“Telomere Shortening Is Nearly Universal in Pancreatic Intraepithelial Neoplasia “ ==
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-Cells reproduce abnormally due to critically shortened telomeres (ends of chromosomes) - Detection [] “Pancreatic cancer—EUS and early diagnosis” - Endoscopic Ultrasounds can detect physical lesions -Along with Computer Tomography scans, EUS provides the greatest percentage of true positives with pancreatic cancer diagnosis -CT scans have the highest accuracy in diagnosing where the actual tumor is and how far it extends in the pancreas. Combined with the accurate tumor size detection of the EUS as well as the EUS’s ability to show how involved the lymph nodes are, the screening method of the combination of these two produces the most accurate result of pancreatic screening.

Demographics at Risk [] “Assessment of “Gene–Environment” Interaction in Cases of Familial and Sporadic Pancreatic Cancer” -25% of pancreatic cancer cases explained by hereditary cancers or high-risk familial syndromes -hereditary pancreatitis, hereditary non-polyposis colorectal cancer, hereditary breast and ovarian cancer, familial atypical multiple mole melanoma, Peutz–Jeghers syndrome (spots on the face, makes the victim predisposed to cancers), and ataxia–telangectasia (degenerative neurological disease) -Age >60 -Only 13% of those who develop pancreatic cancer are below 60 years of age, with 50% being above 75 years old -Sedentary lifestyle, obesity, diabetes, metabolic diseases -Ashkenazi Jews’ -Subset of Ashkenazi Jews: those who never smoked were diagnosed significantly later (6 years later) than those who did -Exposure to residential radon and occupational asbestos -White color worker subset  -Those that were exposed to external tobacco smoke at less than 21 years of age were on average diagnosed with pancreatic cancer 5 years before those who were not

MUC1 Protein Screening [] “Experimental trial for diagnosis of pancreatic ductal carcinoma based on gene expression profiles of pancreatic ductal cells” -Study of MUC1 positive cells yielded the possibility to isolate genes that may cause pancreatic cancer, or genes that prevent the cancer from forming beyond benign lesions -18 genes that are prominently featured in patients with pancreatic cancer and NOT in those with a healthy pancreas: H2BFB, RASAL2, PLOD2, as well as others with less determinable markers. -H2BFB is a histone, a protein that compresses DNA into the nucleosome. A nucleosome is the building block of a chromosome, carrying genetic information to dividing cells. H2BFB is believed to be correlated to the increased division of cancerous cells -PLOD2 is an enzyme that forms and stabilizes collagen.

[] “Lipopolysaccharide (LPS) Increases the Invasive Ability of Pancreatic Cancer Cells Through the TLR4/MyD88 Signaling Pathway” -LPS promotes NF-kB in cancer cells. NF-kB promotes inflammation which in turn aids in the development of cancer cells -Unclear on the reason for inflammation affecting cancer growth.