Cell Cycle, Apoptosis, and Cancer Biology Study Questions

G1 phase

The cell grows, senses nutrients, and decides whether to divide.

S phase

DNA replication.

G2 phase

The cell prepares for mitosis by growing and checking DNA.

M phase

Mitosis and cytokinesis (cell division).

G0 phase

A quiescent, non-dividing state.

Cell cycle checkpoints

They ensure the cell only proceeds if conditions are favorable and DNA is intact.

Cyclins and cyclin-dependent kinases (CDKs)

Molecules that control progression through the cell cycle.

MPF

Maturation promoting factor = Cyclin + CDK; it triggers mitosis.

Wee1 kinase

It inhibits CDK by phosphorylation.

Cdc25 phosphatase

It removes inhibitory phosphates from CDKs, activating them.

CAK

It activates CDKs by phosphorylating Thr161.

Wee1 mutation

It causes early mitosis and small 'wee' cells.

CDKs and cyclins

CDKs phosphorylate targets; cyclins regulate CDK activity.

Caspases

They cleave proteins to dismantle the cell in an orderly fashion.

Apoptosome

A complex formed by cytochrome c and procaspase-9 that activates caspase cascade.

Apoptosis vs necrosis

Apoptosis is ordered and caspase-driven; necrosis is uncontrolled and causes inflammation.

Intrinsic apoptosis pathway

Triggered by internal signals like DNA damage and oxidative stress.

Extrinsic apoptosis pathway

Triggered by external ligands such as TNF binding to death receptors.

Necroptosis enzymes

RIPK3 and MLKL.

Apoptosis in development

It shapes structures like limbs during morphogenesis.

Steroid hormone signaling

Mediated via intracellular receptors that directly regulate gene expression.

Nitric oxide (NO)

A gaseous signaling molecule that activates guanylyl cyclase to increase cGMP.

Mixing Viagra and Nitroglycerin

They both increase cGMP, leading to dangerously low blood pressure.

Signaling convergence

Different signals activate a shared downstream pathway.

Signaling divergence

A single signal can activate multiple pathways.

Signaling crosstalk

One signaling pathway influences another (e.g., cAMP blocking MAPK).

What is cancer?

Uncontrolled cell division due to genetic mutations.

What causes most cancers?

Somatic DNA damage, not inherited mutations.

What are the hallmarks of cancer cells?

Invasion, evasion of apoptosis, metastasis, and unregulated growth.

What are carcinomas?

Cancers originating in skin or epithelial tissues.

What are sarcomas?

Cancers of connective tissue like bone or muscle.

What is the difference between benign and malignant tumors?

Benign tumors are localized and non-invasive; malignant tumors invade and spread.

Why is telomerase reactivation important in cancer?

It allows cancer cells to divide indefinitely by maintaining telomere length.

What is the function of tumor suppressor genes?

They inhibit growth, repair DNA, and promote apoptosis.

What happens when tumor suppressor genes are mutated?

They lose function, allowing uncontrolled cell division.

What is p53 and why is it important?

A tumor suppressor known as the 'guardian of the genome'; it induces cell cycle arrest or apoptosis in response to damage.

What is the role of Rb in the cell cycle?

Rb inhibits G1→S transition by binding E2F.

What is an oncogene?

A mutated proto-oncogene that promotes cell division even without growth signals.

What are examples of oncogenes?

Ras, Myc, HER2, CDK4.

How can proto-oncogenes become oncogenes?

By gene amplification, point mutation, translocation, or viral insertion.

What is the function of the Ras protein?

It is a GTPase that activates the MAPK pathway and promotes proliferation.

What is HER2 and why is it a drug target?

A growth factor receptor amplified in breast cancer; targeted by Herceptin.

What is metastasis?

The spread of cancer cells from the original site to distant organs.

What is aneuploidy and how is it linked to cancer?

Abnormal chromosome number; common in cancer and contributes to genomic instability.

What is the cancer progression model in colon cancer?

Stepwise mutations causing chromosomal instability, aneuploidy, and evasion of checkpoints.

What are cancer stem cells?

Cells in a tumor that self-renew and give rise to heterogeneous cancer cells.

What is Herceptin and how does it work?

An antibody that targets HER2, blocking growth signaling.

What are checkpoint inhibitors?

Drugs that block PD-1, PD-L1, or CTLA-4 to unleash T-cell responses against tumors.

What are some lifestyle-related cancer risk factors?

Smoking, alcohol, obesity, poor diet, and UV exposure.

What tools are used for early cancer detection?

Pap smear, PSA test, and mammogram.

What is precision medicine in cancer therapy?

Tailoring treatment based on genetic and molecular tumor profiles.

Q: What are stem cells?

Undifferentiated cells capable of self-renewal and differentiation into specialized cell types.

Q: What is the difference between totipotent, pluripotent, and multipotent stem cells?

Totipotent can form all cell types including placenta; pluripotent can form all body cells; multipotent can form a limited range of cells.

Q: Where do totipotent stem cells come from?

From the zygote (fertilized egg).

Q: Where are pluripotent stem cells found?

In the inner cell mass of the blastocyst (embryonic stem cells).

Q: What are multipotent stem cells and give an example?

Adult stem cells that differentiate into a specific family of cells; e.g., hematopoietic stem cells.

Q: What are iPSCs?

Induced pluripotent stem cells made by reprogramming somatic cells into a pluripotent state.

Q: Who pioneered iPSC technology?

Shinya Yamanaka and John Gurdon.

Q: What transcription factors are used to generate iPSCs?

Oct4, Sox2, Klf4, and c-Myc.

Q. What are organoids?

3D self-organizing mini-organs grown from stem cells for research or therapy.

Q: List applications of iPSCs.

Regenerative medicine, disease modeling, drug testing, and personalized medicine.

Q: How are iPSCs used in disease modeling?

By recreating patient-specific cells to study disease mechanisms.

Q: What makes iPSCs useful for personalized medicine?

They allow prediction of drug response using cells derived from individual patients.

Q: What is a real-world example of iPSC therapy?

A child with epidermolysis bullosa was treated with transgenic skin derived from iPSCs.

Q: What is the role of basal layer stem cells in the skin?

They regenerate the skin by differentiating into keratinocytes.

Q: Where are intestinal stem cells located?

In the crypts of the intestine.

Q: How are stem cells used in regenerative medicine?

To replace damaged tissues such as heart, neurons, and pancreas.

Q: What are common model organisms used in stem cell research?

E. coli, yeast, Arabidopsis, Drosophila, C. elegans, and mice.

Q: What is reprogramming in the context of stem cells?

Resetting a differentiated cell to a pluripotent state.

Q: What is epigenetics?

Study of gene expression changes without altering the DNA sequence.

Q: What advantages do organoids offer in research?

They mimic organ structure and function for realistic disease modeling and testing.