Breast Cancer

Question 1

Neoplasma

Answer 1

Cells continually to divide

Question 2

Logs of Cancer cell growth

Answer 2

Question 3

Mutagens

Answer 3

Increases rate of DNA mutations, tabaco etc.

Question 4

Cancer origin

Answer 4

Started from mutations in one single cell;
Requires multiple mutations
Some mutations that occur in one cell can increase the likelihood of additional mutations occurring in the same cell.

Question 5

Growth factors (receptors) & pathway for cellular growth

Answer 5

Proteins that facilitate cellular growth and division
GFR binding of growth factor will cause the growth factor receptors to dimerize –> Dimerization of the GFRs will cause –> Intracellular domain of the receptors to go through enzymatic changes –> Being transphosphorylated by Tyrosine Kinases of the opposite receptor –> causes binding of Grb2 (adopter protein) –> causes binding of transmembrane proteins RAS –> promote transcription factors

Question 6

RAS pathway

Answer 6

Question 7

RAS

Answer 7

RAS can bind GDP and GTP;
Inactive when binding GDP

Active when binding GTP

There is a control dial to control RAS activity
GEFs: increases RAS activity
GAPs: decreases RAS activity

Question 8

GEFs

Answer 8

Guanine nucleotide exchange factor and increases RAS activity

Question 9

GAPs

Answer 9

GTPase activating proteins

Question 10

Mutations can cause cancers

Answer 10

1. Overproduction of growth factors (autocrine stimulation)
2. Ligand independent activation of growth factor receptor (HER2)
3. Loss of extracellular domain of the receptors (EFGR)
4. Overexpression of HER2 receptors
5. RAS mutations (take off the active site and causes to consistently active, mutations in Ras that destroy the GTPase activity and leave it bound to GTP and active permanently.)
6. Mutations of GAPs (loss of function)
7. Mutations in RAF (permanent active)
8. Chromosome translocation (CML)

Question 11

Proto-oncogene

Answer 11

A proto-oncogene is a normal cellular gene that plays a role in cell growth and division. Under certain conditions, such as mutations or changes in expression levels, proto-oncogenes can become oncogenes, which promote uncontrolled cell growth and can lead to the development of cancer.

Proto-oncogenes code for proteins that are involved in cell signaling pathways that control cell growth, differentiation, and survival. They can be activated by various mechanisms, such as point mutations, chromosomal translocations, gene amplification, and epigenetic modifications. When proto-oncogenes are activated or overexpressed, they can promote cell proliferation and survival, and inhibit cell differentiation and apoptosis.

Examples of proto-oncogenes include the c-Myc, Ras, and Bcl-2 genes, which are frequently mutated or overexpressed in many types of cancer. Mutations or changes in expression levels of proto-oncogenes can lead to the development of oncogenes, which promote the growth and survival of cancer cells. Therefore, understanding the role of proto-oncogenes in normal and cancerous cells is important for the development of cancer therapies that target oncogenic pathways.