Genetics of Oncogenes 🧬

Question 1

Protooncogene vs. Oncogene

Answer 1

Protooncogenes are normal genes that promote cell growth, while oncogenes are mutated forms of protooncogenes that drive excessive cell growth and division.

Question 2

Activation of Protooncogene to Oncogene

Answer 2

Mutations like point mutation, nonsense mutation, chromosomal translocation, and gene amplification can convert a protooncogene to an oncogene, leading to uncontrolled cell growth.

Question 3

Tumor Suppressor Genes

Answer 3

Genes that inhibit cell cycle and prevent proliferation, loss of function mutations require both alleles to be affected for malignant transformation.

Question 4

Major Cellular Proliferative Pathway

Answer 4

A pathway involving growth factor binding, receptor autophosphorylation, and a phosphorylation cascade promoting cell survival and proliferation under normal conditions.

Question 5

Constitutively Active Growth Factor Receptor

Answer 5

Point mutations in growth factor receptors can render them constitutively active, promoting continuous cell signaling and proliferation.

Question 6

Chromosomal Translocation in CML

Answer 6

Chromosomal translocation in CML leads to the fusion gene BCR-ABL, encoding a constitutively active tyrosine kinase.

Question 7

Chromosomal Translocation in Burkitt’s Lymphoma

Answer 7

Burkitt’s Lymphoma results from an 8:14 translocation leading to increased C-MYC expression.

Question 8

Classes of Proteins in Cellular Proliferative Pathway

Answer 8

Includes growth factors (hormones), growth factor receptors, signal transduction proteins, and DNA binding transcription factors, which can all be mutated to cause cancer.

Question 9

Oncogenes

Answer 9

Genes that promote cell growth and proliferation, can become constitutively active due to mutations in proto-oncogenes.

Question 10

DNA Repair Genes

Answer 10

Genes that help cells recognize and repair genetic damage, mutations impair this ability and can lead to genomic instability.

Question 11

Oncogene Amplification

Answer 11

Occurs through double minutes or homogenously staining regions, leading to aberrant production of oncoproteins and unregulated cell division.

Question 12

Imatinib Therapy in CML

Answer 12

Imatinib mesylate is a BCR-ABL tyrosine kinase inhibitor used in targeted molecular therapy for CML.

Question 13

Tumor Suppressor Genes, DNA Repair Genes, and Oncogenes

Answer 13

Tumor suppressor genes regulate cell growth and division, DNA repair genes fix mutations in DNA, and oncogenes drive excessive cell growth and division, leading to cancer.

Question 14

Major Types of Mutations in Chronic Myeloid Leukemia and Burkitt Lymphoma

Answer 14

Certain chromosomal translocations in these cancers affect specific genes, resulting in abnormal cell proliferation. Chromosomal abnormalities can be detected through cytogenetic tests.

Question 15

Apoptosis-Regulating Genes

Answer 15

Genes that can have gain of function (anti-apoptotic) or loss of function (pro-apoptotic) mutations affecting apoptosis.

Question 16

Growth Factor Receptor Activation

Answer 16

Growth factors bind to receptors, activating them transiently and leading to downstream signaling cascades for cell growth.

Question 17

Philadelphia Chromosome Translocation

Answer 17

The Philadelphia chromosome translocation t(9;22)(q34;q11) is associated with CML.

Question 18

Ras Proto-oncogene Activation

Answer 18

Ras is a GTPase that activates cellular proliferation through phosphorylation cascade in the MAP-Kinase pathway.