Cancer and Cell Cycle Flashcards

Question

What is the role of additional mutations in the multi-hit model of colon cancer?

Answer 1

Permit the tumor cells to: * Exit from the blood vessels * Proliferate at distant sites leading to the formation of secondary tumors.

Answer 2

Loss of APC leads to the initial growth of small polyps

Answer 3

A catalogue of mutations found in cancer genes in human tumors.

Answer 4

Genes that function to promote cell growth in a controlled manner. * When these genes acquire mutations that result in continually active proteins they become oncogenes. * Cause uncontrolled cell growth and division -> leads to cancer

Answer 5

*Oncogenic mutations in proto-oncogenes that encode cell surface receptors* **HER2 receptor** * mutated in the transmembrane region * valine replaced by glutamine * results in over-production or unregulated activity **EGF receptor** * mutated through partial gene deletion, * results in the loss of the extracellular ligand binding domain.

Answer 6

Genes that function to inhibit cell proliferation and tumor development. They halt the cell cycle to: * Prevent unnecessary division * Promote DNA repair * Promote apoptosis.

Answer 7

* Best-known tumor suppressor gene. * "guardian of the genome" * Functions to prevent the formation of cancerous cells. p53 gene is mutated in more than 50% of all cancers

Answer 8

**Types 1 - 4** Mutant forms of proteins that normally promote cell growth can give rise to dominantly acting oncogenes **Types 5 - 6** Tumour-suppressor gene mutations **Type 7** Both tumour suppressors and oncoproteins *apoptotic proteins.*

Answer 9

* Non-specific * Targets rapidly dividing cells *(includes healthy cells)* This can lead to side effects such as * hair loss * low blood counts * nausea/vomiting

Answer 10

Drugs designed to target components responsible for, and unique to, the cancer. Results in: * fewer side effects * increased efficacy compared to conventional chemotherapy.

Answer 11

Trastuzumab is a targeted therapy drug used to treat HER2-positive breast cancer.

Answer 12

HER2 receptors on breast tumor cells.

Answer 13

Trastuzumab binds to the HER2 receptors preventing their activation interrupting the signaling cascade that drives tumor growth and progression.

Answer 14

Induces internalization and degradation of the cell

Answer 15

Can stimulate the immune system to recognize and target HER2-overexpressing cells, contributing to the elimination of tumor cells.

Answer 16

PI3K mTOR MAPK which regulate cell proliferation and survival.

Answer 17

* Blocks the phosphorylation of proteins involved in the downstream signaling pathways. * This prevents the activation of proteins that contribute to cell growth and division.

Answer 18

* By disrupting the inner phosphorylation cascade, * Trastuzumab prevents tumor cells from dividing and making copies of themselves, * leading to the regression and elimination of the tumor cells over time.

Answer 19

* Highly selective * Humanized monoclonal **IgG4-kappa** isotype antibody * Against PD-1 *Second most popular drug in the world*

Answer 20

**PD-1 receptor** A negative regulator of T cell effector mechanisms that limits immune responses against cancer. * When PD-1 is active, it turns off T cells * If T cells are not active, the immune system cannot function.

Answer 21

* It works by stopping the deactivation of T cells * Allowing them to remain active and carry out their anti-tumor functions.

Answer 22

* PD-1, when expressed on antigen-stimulated T cells, induces downstream signaling that inhibits T cell proliferation, cytokine release, and cytotoxicity. * This inhibition suppresses the immune response against tumors.

Answer 23

1. Many tumours suppress cytotoxic T-cell activity by expressing PD-1 ligand *(PD-L1)* on the cell surface. 2. PD-L1 activates PD-1 on the surface of a T cell 3. The T cell goes dead automatically 4. Cannot function once PD-L1 has blocked it.

Answer 24

Anti-PD-1 antibodies can reverse T-cell suppression induce long-lasting antitumor responses in patients with advanced solid tumours

Answer 25

* Blocking T cells prevents them from entering an anergic state and allows them to maintain their anti-tumor activity. * Blocking the tumor directly may lead to tumor adaptation and the development of resistance mechanisms.

Answer 26

CML is a cancer of the white blood cells and accounts for 10-15% of all leukemia cases.

Answer 27

Results from: * ABL gene from the end of chromosome 9 *fused to* * BCR gene on the end of chromosome 22 Creating a BCR-ABL fusion gene - Philadelphia chromosome.

Answer 28

A constitutively active BCR-ABL fusion protein Which: * phosphorylates multiple signal transduction proteins * Is heavily involved with proliferation.

Answer 29

A selective small-molecule tyrosine kinase inhibitor

Answer 30

* Binds to the active site of the BCR-ABL kinase * inhibiting its enzyme activity * stabilizing the inactive non-ATP binding form. This prevents phosphorylation of substrates, resulting in the downregulation of signaling pathways required for leukemogenesis.

Answer 31

Cancer results from a series of genetic changes, and personalized medicine can select the best drugs that target certain mutations. Understanding the genome of a certain cancer can help understand it better and make better drugs, leading to further genetic research and development of more targeted therapeutics.