Carcinogenesis

Question 1

Four classes of normal regulatory genes?

Answer 1

1. Growth-promoting proto-oncogenes, 2. Growth-inhibiting tumor suppressor genes, 3. Genes that regulate programmed cell death (i.e.,
   apoptosis) , 4. Genes involved in DNA repair

Question 2

Consid­ered dominant because mutation of a single allele
can lead to cellular transformation

Answer 2

Growth-promoting proto-oncogenes

Question 3

Usually both normal alleles of tumor suppressor genes must be
damaged for transformation to occur.

Answer 3

Tumor suppressor genes

Question 4

May act like proto-­oncogenes (loss of one copy is

sufficient) or tumor suppressor genes (loss of both copies).

Answer 4

Genes that regulate apoptosis and DNA repair

Question 5

needs growth factors to proliferate ?

Answer 5

Normal cell

Question 6

How normal cell reacts to growth factors?

Answer 6

Growth factor (GF) binds to its receptor (GFR) – GFR activation results in several cytoplasmic signal
transduction molecules which transfers signals to nucleus – Activation of several nuclear regulatory factors that
initiates DNA transcription resulting in cell proliferation

Question 7

have the capacity to proliferate without external stimuli, which usually occurs as a consequence of oncogene activation.

Answer 7

Tumors

Question 8

Normal cellular genes whose products promote cell proliferation

Answer 8

Proto-oncogenes:

Question 9

Mutant proto-oncogenes that function autonomously without a requirement for normal growth-promoting signals.

Answer 9

Oncogenes

Question 10

Oncogenes they can work at the level of?

Answer 10

1/Growth Factors, 2/Growth Factor receptors, 3/Cytoplasmic proteins involved in signaling, 4/ Nuclear regulatory proteins 5/ Cell
cycle regulators.

Question 11

Examples of oncogenes?

Answer 11

AMPLIFICATION & OVEREXPRESSION / MUTATION

Question 12

Examples of oncogenes,

Answer 12

AMPLIFICATION & OVEREXPRESSION / MUTATION

Question 13

Examples of oncogenes/ AMPLIFICATION & OVEREXPRESSION ?

Answer 13

HER2

(growth factor receptor) in breast carcinoma

Question 14

Examples of oncogene/ MUTATION?

Answer 14

EGFR (epidermal growth factor receptor)
mutation in lung adenocarcinoma resulting in constitutional
activation of receptor

Question 15

encode proteins that inhibit cellular proliferation by

regulating the cell cycle. ?

Answer 15

Tumor suppressor

Question 16

which code for proteins involved in regulating the
cell cycle, repairing damaged DNA or, if the DNA is damaged beyond repair,
inducing programmed cell death ( apoptosis ) ?

Answer 16

Tumor suppressor genes

Question 17

Failure of tumor suppressor gene function leads to?

Answer 17

failure of growth inhibition which is characteristic of tumors

Question 18

Governor of the Cell Cycle

?

Answer 18

RB Gene:

Question 19

exerts anti proliferative effects by controlling the G1- to-S
transition of the cell cycle ?

Answer 19

Rb

Question 20

Almost all cancers have a disabled G1checkpoint due to

?

Answer 20

mutation of RB genes

Question 21

Guardian of the Genome?

Answer 21

TP53 Gene

Question 22

central monitor of stress in the cell • Can be activated by DNA damage.

Answer 22

p53 protein

Question 23

controls the expression and activity of genes involved

in cell cycle arrest, DNA repair, cellular senescence, and apoptosis. ?

Answer 23

Activated p53

Question 24

Eg of Tumor suppressor genes?

Answer 24

RB Gene/ TP53 Gene

Question 25

functions to prevent propagation of malignant cells by stimulation of apoptosis and cell cycle arrest in affected cells ?

Answer 25

P53

Question 26

Exposure to carcinogens and mutagens in normal cells (normal | 53) results in?

Answer 26

DNA damage by stimulation of apoptosis or cell | cycle arrest to allow DNA repair.

Question 27

Exposure to carcinogens and mutagens in cells with mutant | non functioning 53 results?

Answer 27

expansion of affected cells

Question 28

Evasion of Cell Death

Answer 28

The balance between pro-apoptotic (e.g., BAX, BAK) and anti-apoptotic molecules (BCL2, BCL-XL). • In 85% of follicular B cell lymphomas, the anti-apoptotic gene BCL2 is activated by the t(14;18) translocation.

Question 29

Normal cells after certain numbers of divisions reach?

Answer 29

terminally | non-dividing (replicative senescence)

Question 30

How cells count number of divisions?

Answer 30

Unknown but possibly by shortening of “telomeres” at the end of each chromosome, which when shortened beyond certain point leads to stimulation of P53-dependent cell cycle arrest

Question 31

Germ cells? | Dividing

Answer 31

They have enzyme (telomerase) leads to cell’s sustained | ability to replicate

Question 32

Cancer cells replication by?

Answer 32

By acquiring telomerase activity (detected in over | 90% of tumors), this gives the malignant cell a stem-cell like features

Question 33

caused by defects in DNA mismatch repair genes | ?

Answer 33

Familial colon carcinoma as well as endometrial and ovarian | carcinoma

Question 34

process through which new blood vessels form from | pre-existing vessels

Answer 34

Angiogenesis

Question 35

produced by | tumor cells is the main growth factor responsible for Angiogenesis?

Answer 35

Vascular Endothelial Growth Factor [VEGF]

Question 36

Ability to invade tissues, occurs in four steps: ?

Answer 36

1. Loosening of cell–cell contacts : 2. Degradation of ECM, 3. Attachment to novel ECM components, 4. Migration of tumor cells.

Question 37

Cell–cell contacts are lost by the inactivation of

Answer 37

E-cadherin

Question 38

Basement membrane and interstitial matrix degradation is | mediated by?

Answer 38

proteolytic enzymes secreted by tumor cells and | stromal cells.

Question 39

Migration/motility of tumor cells by ?

Answer 39

tumor-derived cytokines” | motility factor”.

Question 40

Patients with HNPCC syndrome (Hereditary Non-Polyposis | Colorectal Cancer) have defects in?

Answer 40

mismatch repair system, leading to development of carcinomas of the colon.

Question 41

Patients with xeroderma pigmentosum :increased risk for the development of cancers of the?

Answer 41

skin exposed to UV light.

Question 42

process which results in the transformation of normal cell to neoplastic cell by causing genetic alterations and cumulative genetic defects

Answer 42

Carcinogenesis

Question 43

is an agent that participates in causing the tumor, its ultimate site of action is mainly DNA ?

Answer 43

Carcinogen

Question 44

causing hepatocellular carcinma ?

Answer 44

HBV

Question 45

causing lung cancer | ?

Answer 45

Tobacco

Question 46

Over a period of time, many tumors become more aggressive and acquire greater malignant potential & less responsive to therapy ?

Answer 46

tumor progression

Question 47

Carcinogens types?

Answer 47

1) Chemical Carcinogens (2) Radiation Carcinogens (3) Microbial Carcinogens

Question 48

Chemicals?

Answer 48

ALKYLATING AGENTS / ACYLATING/AROMATIC AMINES, AMIDES, AZO DYES /Chemotherapy drugs (e.g., alkylating agents) : leukemia.

Question 49

``` Chemotherapy drugs (e.g., alkylating agents) : leukemia. ? ```

Answer 49

Chemicals carcinogen

Question 50

Therapeutic irradiation of the head and neck can give rise to ?

Answer 50

thyroid cancers years later.

Question 51

Skin cancers (melanomas, squamous cell carcinomas, and basal cell carcinomas). • Fair­ skinned people. • Melanomas are associated with intense intermittent exposure, as occurs with sunbathing From?

Answer 51

UV radiation

Question 52

human papilloma virus (HPV), | / HBV ?

Answer 52

2.Oncogenic DNA Viruses e

Question 53

3.Helicobacter pylori, is implicated in the?

Answer 53

genesis of both gastric | adenocarcinomas and gastric lymphomas.