HC1 - The nature of cancer Flashcards
tumors
- arise from normal tissue
- cannot maintain tissues of normal form and function
histological features tumors
resemble tissue of origin
begign
grow locally without invading adjecent tissue
thyroid adenomas
- pre-malignant epithelial growth
- excessive release of thyroid hormone = hyperthryriodism
pituitary adenoma
growth hormone > excessive growth = acromegaly
malignant
invade nearby tissues and spawn metastases = 90% of deaths
majority of tumors
epithelial cells
epithelia
sheets of cells that line the walls of cavities and channels or cover the body
lamina basalis
extracellular matrix, separates epithelial cells from stroma
caricinomas (epithelia)
malignant
squamous cell carcinomas
cells forming the protective layer
adenomacarcinomas
specialized cells that secrete
sarcomas (connective tissue)
-1% of cancers
- fibroblasts, collegen-secreting cells, adipocytes, osteoblasts, chondroblasts, myocytes
hematopoietic tissue
precursors of erythrocytes, antibody-secreting plasma cells, T and B lymphocytes
leukemia
spawned by malignant non-pigmented hematopoietic cells, freely moving through circulation
lymphomas
malignant T or B lymphocytes that aggregate and form solid tumors, usually found in lymph nodes
nervous system
gliomas, glioblastomas, neuroblastomas, schwannomas, medulloblastomas
difficulty with classification
- transdifferentiation > from one lineage to another
- epithelial mesenchymal transformation (EMT)
teratomas
- arise from germ cell precursors that persist at inappropriate sites in the developing fetus
- retain ability to generate most tissues
- genetic wildtype = no mutations
dedifferentiation
shed virtually all tissue-specificity
anaplastic tumors
no longer possible to identify the tissue from which they have arisen
progressive cancer development
cancer cell populations evolve progressively to greater degrees of aggressive behavior = multi-step process
cancer progression
normal-hyperplasmic- metaplasmic- dysplasia- neoplasmic - metastasis
hyperplasmic growth
- excessive number of cells
- retain ability to assemble into a tissue that appear reasonably normal
metaplasmic growth
normally present tissue is replaced with cells from a nearby tissue
dysplasia
- transitional state between benign and malignant growth
- variablity in nuclear shape and size,increased nuclear staining, increased size nucleus vs cytoplasma,
increased mitotic activity, lack of normal cytoplasmic features - aberrant relative numbers of various cell types
- major effects on tissue architecture
adenomas, polyps, adenomatous polyps, papillomas, warts
- all contain cell types of normal epithelial tissue > greatly expended
- respect boundry lamina basalis
neoplasm
invasion into underlying tissues (stroma)
monoclonal tumors
- descent from a single ancestor
- myelomas = B cell precursors
- particular chromosome rearrangement or mutation
monoclonality
competition between multiple populations with different proliferation rates
genetic heterogeneity
may mask monoclonal origin, genetic markers present in descendents
normal cells in aerobic conditions
glycolysis and citric acid cycle > 36 ATP
Warburg effect
many types of cancer cells use glycolysis even when exposed to oxygen
anaerobic/hypoxic conditions
glycolysis> reduction of pyruvate to lactate > secretion lactate> 2 ATP
hypoxia cancer
glycolysis for intermediates that can be used in biosynthesis
overexpression of glucose transporters (GLUT1)
PET-scan > accumulation of radiolabeled glucose
imported glucose
- normal cells = 30%
- cancer = 1%
cancer frequencies
- vary between populations
- caused by random unavoidable accidents
environment and genetics
determine cancer risk
Barrett’s esophagus
squamous cells are replaced by secretory cells of the stomach, esophageal adenocarcinomas
