Molecular Biology of Cancer Quiz

Viral genes that can cause cancer by triggering uncontrolled cell growth.

A type of oncogene that produces a mutant form of a growth factor, leading to continuous cell proliferation.

A gene that codes for the platelet-derived growth factor (PDGF), a protein that promotes cell division.

A type of oncogene that produces an altered version of an EGF receptor, lacking the EGF binding site but retaining tyrosine kinase activity.

A protein that binds to epidermal growth factor (EGF), triggering a signaling cascade and cell growth.

An oncogene that produces normal receptor proteins in excessive quantities, leading to excessive cell proliferation.

The process by which cells are triggered to grow and divide in a controlled manner.

A protein that helps transduce signals within cells, leading to activation of cellular processes like growth and division.

A type of oncogene that codes for a mutant form of the Raf kinase, frequently found in melanomas and other cancers.

These tyrosine kinases reside within the cell, unlike their receptor counterparts. They lack receptor sites and are involved in cell signaling.

An example of an intracellular tyrosine kinase that plays a role in cell growth and signaling. It is frequently mutated in various cancers.

These oncogenes produce altered versions of transcription factors, often leading to excessive cell proliferation.

A protein involved in cell proliferation and survival. Its gene is frequently amplified in various cancers.

The BCL2 gene produces a protein that inhibits apoptosis, leading to an accumulation of cancer cells.

A common chromosomal translocation in non-Hodgkin's lymphomas that causes the BCL2 gene to produce excessive Bcl2 protein, leading to uncontrolled cell growth.

This gene produces a protein (Mdm2) that inhibits apoptosis, allowing cancer cells to survive longer.

A type of G protein that is activated by GTP and inactivated by GDP. It is a key signaling molecule in many cellular processes, including cell growth.

An enzyme that helps Ras exchange GDP for GTP, activating Ras.

An enzyme that helps Ras convert GTP to GDP, deactivating Ras.

A mutated form of the Ras protein found in approximately 30% of all human cancers.

A kinase that transfers phosphate groups primarily to serine and threonine residues in target proteins, regulating their activity.

A kinase that transfers phosphate groups to tyrosine residues in target proteins, modifying their function.

A molecular switch that is controlled by the binding of GTP or GDP, which determines its active or inactive state.

A type of gene that is typically involved in regulating cell growth and division. When mutated, they can promote uncontrolled cell proliferation and lead to cancer.

Genes that normally suppress cell growth and division. When mutated, they can lose their ability to control cell proliferation, contributing to cancer development.

A phenomenon where a cell loses one copy of a gene, often a tumor suppressor gene, leaving just the mutated copy. This can lead to uncontrolled cell growth.

Tumor suppressor genes that directly control cell proliferation and survival, acting like 'gatekeepers' that prevent uncontrolled growth.

Tumor suppressor genes that are involved in maintaining the integrity of the genome, acting as 'caretakers' that prevent mutations.

A transcription factor that plays a crucial role in regulating cell cycle progression. It is often regulated by the Rb protein and other tumor suppressors.

The process of adding phosphate groups to a protein, often changing its activity. This can be a crucial step in regulating cell cycle progression.

A gene that encodes for two proteins, p16 and ARF, which act independently on the Rb and p53 pathways respectively.

This gene codes for two independent proteins, both acting as tumor suppressors by regulating cell cycle progression.

The CDKN2A gene can have mutations that lead to a lack of either p16 or ARF proteins.

The inactivation of the TGF-Smad signaling pathway is commonly observed in various types of cancer.

The TGF-Smad pathway is crucial for regulating epithelial cell proliferation, and its inactivation can contribute to the development of carcinomas.

Mutations in genes like BRCA1 and BRCA2 can lead to a lack of proper DNA repair, causing increased chromosomal instabilities which lead to cancer.

BRCA1 and BRCA2 genes are involved in the process of homologous recombination, a critical DNA repair pathway.

BRCA1 and BRCA2 genes are essential for maintaining genomic stability and preventing uncontrolled cell growth.

ATM, a protein kinase, activates BRCA1 in response to DNA damage, suggesting that BRCA1 plays a crucial role in the early stages of DNA double-strand break repair.

Cells lacking either BRCA1 or BRCA2 exhibit extreme sensitivity to carcinogens that induce double-strand DNA breaks, highlighting these genes' critical role in maintaining genomic stability.

At metaphase, all chromosomes must be properly attached to the mitotic spindle before anaphase can begin. This ensures equal distribution of chromosomes to daughter cells.

Unattached chromosomes send a 'wait' signal, mediated by Mad and Bub proteins, which inhibit the anaphase-promoting complex, preventing premature separation of chromosomes.

The Mad and Bub proteins, when bound to unattached chromosomes, form a complex that blocks the activation of the anaphase-promoting complex by inhibiting Cdc20.

Once all chromosomes are attached, the Mad/Bub complex disassembles, allowing the anaphase-promoting complex to activate separase, triggering the separation of sister chromatids.

Mutations in Mad or Bub genes disrupt the spindle checkpoint mechanism, resulting in chromosomal instability. This can lead to aneuploidy, a condition where cells have an abnormal number of chromosomes.

The anaphase-promoting complex activates separase, an enzyme that degrades cohesin proteins, which hold sister chromatids together. This allows the duplicated chromosomes to separate and move to opposite poles.