Intro

Question 1

Carcinoma

Answer 1

in situ or invasive. Cancer of epithelial cells: squamous and adenocarcinomas

Question 2

Sarcoma

Answer 2

Solid tumors of CT (musc, cartilage, fibrous)

Question 3

Leukemia and Lymphomas

Answer 3

Cancer of Immune cells

Question 4

Neuroectodermal

Answer 4

gliomas, blastomas, schwannoma’s

Question 5

Incidence

Answer 5

Number of new cases per year. Indicative of risk of developing the disease

Question 6

Prevalence

Answer 6

total number of cases = (diseased)/(dis and all). Indicative of how widespread the disease is

Question 7

Most likely cancers

Answer 7

Males = NMSC and prostate; Females = breast and NMSC. Lung cancer is the deadliest

Question 8

Cell bio and cancer

Answer 8

Problems in signal transduction via mutations lead to uncontrolled proliferation.

Question 9

Cell Cycle Overview

Answer 9

M phase (mitosis and cyto), Interphase (G1 responds to growth factors, S is DNA copy, G2 is another growth phase). Each controlled by checkpoints. Can enter G0 to stop growth.

Question 10

Mutations target what genes

Answer 10

Protooncogenes (gain of fx) or tumor suppressors (loss of fx)

Question 11

Tumor Suppressors - p53

Answer 11

p53 is activated in response to DNA dmg and is a transcription factor that is continuously made. If no problems present it will bind to mdm2 (p53 inhibited and poly-ubiq). If dmg occurs, p53 accumulates and can’t bind to inhibitor and is able to arrest cell cycle at any stage. It induces DNA repair enzymes and if that doesn’t work it induces apoptosis.

Question 12

Tumor suppresor - Rb

Answer 12

Phosphoprotein that when hypophos it inhibits G1 to S phase transition

Question 13

Properties of Tumor cells

Answer 13

Tumor is an abnormal proliferation of cells, monoclonal. Benign tumors resemble original cell and is localized. Malignant don’t resemble the original cells and are invasive/spread.

Question 14

Abnormal cell functions of a tumor

Answer 14

Monoclonal, genetic instability (increased mutation rate, selects for proliferative advantage), anchorage independent (no longer needs integrin to survive), loss of replication senescence, loss of contact inhibition, discards cell cycle control, avoids apoptosis, angiogenesis, invasive, metastatic.

Question 15

Three stages

Answer 15

1. Initiation - change in DNA
2. Promotion - clonal expansion
3. Progression - additional changes can lead to metastasis

Question 16

Direct carcinogens

Answer 16

electrophile compounds that react with DNA

Question 17

Indirect Carcinogens

Answer 17

Metabolized before reacting with DNA
Benzo-Pyrene in cig smoke forms DNA adducts (covalent bond to DNA therefore can’t replicate). Aflatoxin B1 from aspergillus can lead to liver cancers in china.

Question 18

DNA dmg - malignant transformation

Answer 18

UV radiation can lead to TT dimers. Alkylation and chain crosslinks due to bulky groups added leading to breaks and mismatches