General Concepts of Cancer and Cell Cycle

The earliest known documentation of cancer, dating back to ~3000 BC.

Uncontrolled growth of cells that form a mass and invade nearby tissues.

Factors that contribute to the development of cancer. These can include lifestyle choices, exposure to carcinogens, and viral infections.

The average age when people receive a cancer diagnosis.

A type of cancer-causing agent that includes things like asbestos and UV radiation.

A checkpoint that makes sure there are enough nutrients and that the DNA is intact before entering the S phase.

These complexes are activated during the G1 phase, triggered by growth factor signaling pathways (like PI3K/Akt/mTOR).

This transcription factor is released when Rb is phosphorylated, allowing cells to enter the S phase.

This complex plays a role in the initiation of DNA replication by recruiting helicase during the S phase.

The checkpoint that verifies that DNA replication is complete and free of errors before mitosis.

A highly accurate DNA repair pathway that relies on a complementary DNA strand as a template.

A protein that recognizes mismatched bases during DNA replication in the process of mismatch repair.

A DNA repair pathway considered error-prone because it doesn't always restore the original genetic sequence.

BRCA1 plays a role in stabilizing the repair complex for homologous recombination, ensuring accurate DNA repair.

Ku proteins are involved in Non-Homologous End Joining (NHEJ), a repair pathway that uses a quick and often error-prone approach.

A proto-oncogene, when mutated, becomes an oncogene that promotes uncontrolled cell growth, contributing to cancer.

Tumor suppressor genes, when mutated or inactivated, lose their ability to control cell growth, leading to cancer development.

An example of a tumor suppressor gene that plays a role in DNA repair, especially in homologous recombination.

BRCA1/2 mutations are inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to increase cancer risk.

Cells with defective BRCA1/2 experience genomic instability due to impaired DNA repair, increasing their likelihood of acquiring mutations and forming tumors.

PARP inhibitors work by blocking single-strand break repair, leading to cell death in cells that rely on a broken homologous recombination repair system.

The concept of exploiting specific vulnerabilities in cancer cells that are dependent on defective pathways to target them with treatment.

p53, a tumor suppressor gene, responds to DNA damage by initiating apoptosis (programmed cell death) or cell cycle arrest to prevent further mutations.

Myc, a key regulator of cell growth and proliferation, is often hyper-activated in cancer, leading to uncontrolled cell division.

At the metaphase-to-anaphase checkpoint, if chromosomes aren't properly attached to spindle fibers, Mad2 inhibits APC/C, halting cell division to ensure proper chromosome segregation.

The phase in the cell cycle where DNA synthesis and replication takes place, ensuring a copy of the genetic material for each daughter cell.

A complex called Cdk1/Cyclin B promotes chromatin condensation in mitosis, making sure chromosomes are organized for proper cell division.

Cyclin D activates Cdk4/6 in the G1 phase, allowing the cell to enter the S phase for DNA replication.

Ras, a signaling protein, activates the MAPK pathway in response to growth factors, promoting cell growth and proliferation.

Homologous recombination is the most effective repair pathway for double-strand breaks, using a complementary DNA strand as a template to restore the original sequence.