Unit 2 Pathophysiology - Chapter 12 Cancer Biology Flashcards
(65 cards)
Benign tumors
- encapsulated
- contain differentiated cells
- organized stroma
- do not spread
Malignant tumor
- rapid growth
- anaplasia (loss of maturity + functions)
- loss of differentiation
- no cell organization
- no capsule
- invade blood vessels + lymphatics + distant metastases
Carcinomas and leukemias arise from?
Epithelial tissues // leukemias
CIS or carcinoma in situ
preinvasive epithelial tumors of glandular or squamous cell origin
early stage cancers localized to epithelium and did not penetrate local basement membrane (right under epithelium) and did not invade surrounding stroma
Genetic changes - cancer
small, large DNA mutations in genes, chromosomes, non-coding RNAs, altered chemical modifications of DNA + histones (epigenetics)
Chromosome translocation
partial or whole chromosome breaks off and attaches to another
gene amplification
Increase in number of genes; maybe also more RNA and protein production from gene
DNA methylation
methylation of the DNA sequence of a gene may turn the gene off so it does not make a protein.
histone acetylation
By modifying chromatin proteins and transcription-related factors, these acetylases are believed to regulate the transcription of many genes.
altered expression of non–coding RNA
chromatin remodeling, regulate gene expression at transcriptional or post-transcriptional
Driver mutations
drive progress of cancer
Passenger mutations
random events; along for the ride hehe
Cancer cell can develop own mutations?
Yes, resulting in genomic heterogenous mixture of cancer cells w/ subsets that accumulate more mutations => increase malignant potential
Development of cancer analogus to what?
Wound healing
initial proliferation of cancer cells and enlarging tumor => creates proinflammatory mediators by cancer cells + adjacent nonmalignant cells
These mediators => recruit inflammatory/immune/tissue repair cells forming the stroma (connective, functionally supportive framework of a biological cell, tissue, or organ) that surround and infiltrate tumor
Stromal and cancer cells relation
D/t extensive paracine signaling amongst both populations
- increased proliferation and heterogenous growth during tumor growth
- stromal cell phenotypes that promote more cancer progressio nand metastatic potential
Hallmarks/enablers of genomic alterations for cancer
- sustained proliferative signaling
- evade growth suppression
- genomic instability
- replicative immortality
Hallmark secondary to genomic change
cellular adaptations, including angiogenesis (formation of new blood vessels) and reprogramming energy metabolism
Hallmark/enablers - protective mechanisms
apoptotic cell death, promote tumor inflammation, avoid immune destruction
last hall mark - most important?
culmination of all previously mentioned: activating invasion and metastasis
Cancercous cells express specifically what?
mutated or overexpressed proto-oncogenes (oncogenes), they are independent of normal regulators and signal uncontrolled proliferation
RAS oncogene
result from point mutation, all Ras proteins are GTPases which act as molecular switches in the cell, regulating signaling pathways and other interactions until they mutate and for cancer
Philadelphia chromosome in CML or chronic myeloid leukemia
Comes about d/t translocation that creates novels protein fusion of BCR + ABL genes and expression for unregulator promotor of cell growth
Abl is tumor suppressor gene
BCR protein may act as a GTPase activating protein (GAP). GAPs turn off (inactivate) proteins called GTPases, which play an important role in chemical signaling within cells.
How do Tumor suppression genes work in cancer
mutations of each allele, for each parent in terms of inactivating said gene
Common mutation in cancer cells
inactivation of tumor suppressor gene, tumor protein P53 (TP53) important in contrlling gene expression for DNA damage repair, suppression of cellular proliferation during genomic repair, and apoptosis initiation => resulting mutation rates and cancer
