BRCA2: tumor suppressor, chromosome stability; BRCA1: tumor suppressor,DNA damage response/repair; HER2: proto-oncogene, nonregulated tissue growth

Inactive (parent drug)-> metabolized-> metabolites FdUMP block TS=interfere with DNA/RNA/protein formation

Proteins S & C work together to prevent your blood from clotting too much; if low S&C = clot too much; P&C inactivate factors V/VIII = slow down clot formation

Anemia -> lower oxygenation of blood->body compensates = pallor, dyspnea, tachycardia

corn starch is a glucose polymer that is broken down slowly = control glucose levels

degree of abnormality of APC-assay correlates to heterozygosity (higher APC ratio) or homozygosity (low APC ratio) factor V Leiden mutation

LDH: high turn over of cells-excess cell lysis; Uric Acid-breakdown of cellular nucleic acid contents of leukemia cells

location at the chromosome 22 breakpoint of the t(11;22)(q24;q12) translocation; EWS (EWSR1) gene is involved in translocations in Ewing's sarcoma

TTP->ADAMTS13 deficient->cleavage down, increase vWG multimers->hypercoagubale->prothombotic->aggregate->obstruct vessel->sheering RBCS=shistocytes

Type 1: partial deficiency-quantity, autosomal dominant; Type 2: qualitative variant, AD/some AR; Type 3-severe quantitative-missing vWF, Autosomal Recessive

immune cells trigger inflammation->cytokines->inflammatory markers->activate nociceptors throughout body

DNA damage->lamina disrupted->chromatin conformation distress->increase p53 signaling->increase cell/tissue senescence= accelerated aging

LMNA codes for Lamina A-protein that acts as scaffolding on the inner side of the nucleus->farnesyl stays on lamina A->piles on=abnormal nuclear envelop