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Flashcards in Neoplasia Lectures Deck (37):
1

initiation

mutation in one or more genes controlling key regulatory pathways of the cell (irreversible)- must be a heritable DNA alteration

2

promotion

selective growth and uncontrolled proliferationin the initiated cell and its progeny by the continuous exposure to a promoting agent

3

progression

results from continuing evolution of o unstable chromosomes; further mutations from genetic instbility during promotion results in further degrees of independence, invasiveness, metastasis, etc.

4

proto-oncogene

normal gene, which when altered by mutation becomes an oncogene hat can contribute to cancer. mutations typically dominant

5

Glioma

-most common primary tumors of the CNS affecting adults
-life expectancy = 14 months
-amplification of PDGF and PDGFR occurs in 11% of all gliomas

6

PDGF

-autocrine and paracrine stimulatory loops
-PDGF promotes cell survival and proliferation

7

HER2 (Erb2)

- amplified in breast cancer - results in increase in HER2 growth factor receptor which activated proliferation and survival

8

RAS

-most commonly mutatated proto-oncogene in human tumors
-point mutations prevent GTP hydrolysis which is essential to inativate RAS --> RAs is trapped in its activated, GTP bound form

9

ABl (protein kinase)

-chronic myelogenous leukemia
ABL1 encodes tyrosine kinase that regulates cell differentiation, division, adhesion and stress response
-break in chr 9 and 22
-c-able translocates to 22 --> philadelphia chromosome (Bcr-abl)
-result = gene that encodes a constitutively active, oncogenic BCR-ABL tyrosine kinase
-Imatinib blocks it

10

cyclins and CDKs

- complexes of cyclin and CDK drive the cell cycle
-CDKs controlled by inhibitors - mutations in genes encoding cyclins, CDKs and CDK inhibitors result in uncontrolled cell cycle progression

11

Myc

-myc activates transcription of several growth promoting genes including cyclin-dependent kinases
-c-myc mutation causes increasing expression of genes tht promote the cell cycle and repressing genes that deter the cell cycle --> tumorigenesis

12

Burkitt Lymphoma

-Reciprocal breaks in chr 8& 14
-c-myc translocates to 14
-juxtaposes c-myc with Ig heavy chain --> amplification and overproduction of the normal transciption factor, MYC

13

double minutes (dmin)

-circular, extrachromosomal amplification of specific acentric DNA fragments
-homogeneously staining regions (hsr)

14

Warburg effect

tumors are initially hypoxic and so they alter metabolism to shift from oxidative phosphorylation to aerobic glycolysis
-c-myc and p53 are both regulators of metabolism

15

tumor suppressors

-genes that encode proteins that inhibit cell proliferation by regulating the cell cycle
-BOTH copies of gene must be dysfunctional for tumorigenesis

16

sporadic carcinogenesis

-both copies are lost throughsomatic mutations

17

familial carcinogenesis

-affected persons inherit one defective copy of a tumor suppressor gene and lose the second one through somatic mutation

18

Retinoblastoma

-most common malignant cancer in children
-Rb control G1-S phase usually

19

p53

-determines response of cells to DNA damage and hypoxia
-promotes cell cycle arrest through CDK1 and apoptosis through Bax
-mutations in p53 implicated in over 70% of cancers

20

Li-Fraumeni syndrome

-inherit one defective copy of p53 and lose the second in somatic tissues

21

APC

- antiproliferative actions by regulating the destruction of the cytoplasmic protein B-cetenin
-signaling from WNT inhibits APC and drives proliferation
-loss of APC --> B-catenin translocates to nucleaus and acts as growth promoting transcription factor

22

Familial Adenomatous polyposis

- develop hundreds of thousands of colon polyps that will turn into cancer if untreated
-caused by mutations in APC gene
-if not caused by APC mutation then B-Catenin mutation

23

Epithelial Mesenchymal Transition

process by which epithelial cells lose their cell polarity and cell-cell adhesion and gain migratory and invasive properties to become mesenchymal cells

24

paraneoplastic syndrome

-signs and symptoms in a patient with cancer that cannot be attributed to either 1) the location of the primary tumor or is metasstases 2) the secretion of hormones indigenous to the tissue from which the tumor derived

25

Adenoma

benign tumor arising from glandular or secretory epithelium

26

papilloma

benign tumor arising from non-secretory epithelim

27

carcinoma

malignant epithelial neoplasm

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sarcoma

malignant mesenchymal neoplasm

29

dysplasia

disorderly growth of epithelium with pleomorphism and loss of architectural orientation

30

invasion

breaking the basement membrane

31

metastases

local or systemic dissemination

32

grade

refers to degree of differentiation (resemblance of tumor to normal tissue)

33

stage

referes to size and dissemination of tumor

34

grade I and II

well differentiated; low grade

35

grade II or III

moderately differentiated; intermediate grade

36

grade III or IV

poorly differentiated; high grade

37

anaplastic

undifferentiated; high grade