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47 Cards in this Set

  • Front
  • Back
what is a neoplasm/neoplasia?
- "new growth"
- abnormal mass of tissue where cells are proliferating beyond the stimuli that caused it;
- often called "tumor" or bump
- can be b9 or malignant
describe b9 neoplasm
1- grows w/in pseudocapsule w/well demarcated borders that exerts pressure on surrounding tissue causing it to atrophy
2- has no capability to metastasize
3- named by taking parenchyma and adding "-oma"
4- well differentiated & may resemble structure of normal tissue
5- overcrowded but architecturally organized
6- rate of growth is slowly progressive & may regress where dystrophic calcification might occur
7- adenoma term used to describe epithelial neoplasms growing in glandular pattern
8- contain normal bipolar mitotic figures
what are examples of b9 neoplasms?
- fibroma: b9 neoplasm of fibroblasts
- chondroma: b9 neoplasm of cartilage
- osteoma: b9 neoplasm of bone
describe malignant neoplasm
1- grows locally w/in pseudocapsule, invades by breaking thru pseudocapsule into surrounding tissue, then metastasizes
2- borders are not demarcated; very poorly differentiated so difficult to tell cell origin w/anaplasia
3- crowded w/unorganized architecture
4- rate of growth is off course; maybe slow to rapid but typically faster growing than b9 neoplasms
5- typically called "cancers"
6- if derived fm mesenchymal tissue called "sarcoma"
7- if derived fm 3 germ layers: ecto, endo, mesoderm tissue called "carcinoma"
8- exceptions to naming convention: mesothelioma, lymphoma, melanoma, hamartoma
9- contain multipolar mitotic figures
examples of malignant neoplasms?
- fibrosarcoma
- chondrosarcoma
- osteogenic sarcoma
- adenocarcinoma
- squamous cell carcinoma
what is a hamartoma?
- mass of non-neoplastic disorganized tissue
describe hyperplasia
- cells are under hormonal control and proliferate in response to increased hormonal levels
- can be pathologic or physiologic
examples of pathologic hyperplasia?
- BPH hormone in excess causes prostate enlargement due to cellular proliferation
- hyperplastic endometrium
describe metaplasia
- when one cell type is replaced for another
- N/C ratio is low meaning cells towards the surface are mature like they shd be
- crowded but architecturally organized
- metaplasia named by taking name of cell it turned into and adding "metaplasia"
ex of metaplasia?
- squamous metaplasia where original pseudostratified cilitated columnar cells were turned into squamous cells
describe dysplasia
- disorderly proliferation bc of fast replication rate w/increased no. of mutations
- unorganized architecture
- high N/C ratio
- antedates cancer
- pleomorphic
- mitotic figures present
ex of dysplasia?
- carcinoma in situ: where dysplasia takes entire thickness of epithelium
- considered most severe form of dysplasia just before CA
what is overall progression to CA?
metaplasia => dysplastic => b9 => malignant tumor
what are 2 components of tumors?
- stroma: supports parenchyma and contains lots of BVs
- parenchyma: contain the neoplastic cells of monoclonal origin which eventually become pleomorphic due to crowding and increased rate of mutation
what are the 3 routes of metastasis or dissemination?
1- seeding w/in bodily cavities: favored by carcinomas
2- lymphatic spread
favored by carcinomas
3- hematogenous spread
favored by sarcomas
what is angiolymphatic invasion?
- when malignant neoplasm spreads to lymphatics and blood vessels
ex of seeding w/in body cavities
- ovarian cancer: which can spread to abdominal cavity
ex of lymphatic spread
- breast cancer spreads to axillary lymph nodes
describe retinoblastoma
- CA by heredity;
- autosomal dominant
describe adeonomatous polyposis coli
- CA by heredity
- autosomal dominant
- several small polyps form
describe xeroderma pigmentosum
- CA by heredity
- autosomal recessive
- sun-induced skin CA
- defect in DNA repair enzyme
what are some CA influenced by the environment?
- stomach CA
- hepatocellular CA
- Cervical CA; HPV associated
but what are most CAs?
- non-familial & occur sporadically
what are oncogenes?what do they produce?
- are proto-oncogenes that have mutated
- they promote autonomous cell growth in CA
- they produce oncoproteins that resemble normal products of oncogenes
what is carcinogenesis?
- is non-lethal genetic damage/mutation
what causes carcinogenesis?
- virus
- radiation
- chemical
- inherited
- cumulative replication errors
how does CA originate?
- fm single progenitor(origin) that undergoes monoclonal expansion later on turning into pleomorphic cells due to crowding and mutation
- CA can evolve phenotypically & genotypically
what are the genes damaged in order to CA?
- growth promoting proto-oncogenes
- cancer suppressor genes
- apoptosis regulating genes
- genes encoding DNA repair proteins
what are proto-oncogenes?
- are genes that dont directly affect cell proliferation but an indirect effect so that when mutated they have effect on cell proliferation
what are non-oncogenic genes?
- are genes that have nothing to do w/cellular proliferation
Ex: keratin
what are the oncoproteins produced by oncogenes?
-oncoproteins resemble the normal products produced by proto-oncogenes but difference there's no regulation

- growth factors
- growth factor receptors
- signal transducing proteins critical for mitosis
describe growth factors as oncoproteins
- where growth factors continuously bind one after another causing over expression of the gene
describe growth factor receptors as oncoproteins
- where receptor gets stuck "on" and generates continuous mitotic signal
ex of growth factor receptors as oncoproteins
- EGF gene, c-erb B-1
what are signal transducing proteins?
- are intermediates btw receptor and nucleus
- responsible for transducing the signal that will be sent to nucleus for it to divide/undergo mitosis
describe c-ras gene
- aka"GTP/G binding protein"
- located on inside of membrane
- encodes GTP binding protein which signal mitosis
- contains a GTPase that becomes active w/help of GAP protein to shut off
what happens when there is a point mutation in ras gene?
- makes GTPase useless causing unregulated mitosis and cause nasty CAs ie colon CA, pancreas, lung CA)
what are the ways oncogenes become activated?
1- point mutations : ie ras protein
2- chromosomal translocations: Ex specifically reciprocal translocation of chromosomes 9 & 22 which causes makes a hybrid gene that makes tyrosine kinase which leads to chronic myelogenous leukemia
3- gene amplification
Ex: N-myc protein causes neuroblastoma
what are some cancer suppressor genes?
- growth inhibitory factors
- molecules that regulate cell adhesion
- molecules that regulate signal transduction
- molecules that regulate nuclear transcription & cell cycle
ex of molec that regulates cell adhesion
- E-cadherin
ex of molec that regulates signal transduction
- NF-1 gene
ex of molec that regulates cell cycle & transcription
- rbg protein
unphosphorylated state = hypophosphorylated active state
how does HPV take advantage?
- when mutation occurs to rbg protein it no longer binds to transcription proteins, so HPV grabs these floating and makes its virus
what genes regulate apoptosis?
- bcl-2 and bax favors genes
- bcl-2 favors immortality
- bax favors apoptosis
what results fm over expression of bcl-2, and bax?
- bcl-2 causes large B-cell lymphoma
- overexpression bax=cell death
what is meant by mulitstep carcinogenesis?
- meaning no single oncogene can directly cause CA its just the accumulation of mutations
what are elements involved in kinetics of tumor cell growth?
- tumor cell doubling time
- growth fraction: are portion of cells in the mitotic cycle
- cell production vs cell loss