All flashcards
Flashcard 1: Identify the term for cancer cell growth without attachment to a surface or matrix.
Answer: Loss of anchorage dependence (anchorage-independent growth). Cancer cells evade anchorage requirements, allowing growth in suspension and metastasis.
Flashcard 2: What is the defining cellular characteristic of cancer related to cell cycle control?
Answer: Loss of normal cell cycle regulation causing uncontrolled proliferation. Cancer arises from dysregulation allowing cells to divide without normal checkpoints, leading to tumor formation.
Flashcard 3: What is an oncogene?
Answer: A gain-of-function mutated gene that promotes cell division. Oncogenes drive excessive cell growth by enhancing pathways that stimulate proliferation when mutated.
Flashcard 4: What is a proto-oncogene?
Answer: A normal gene that can become an oncogene after activating mutation. Proto-oncogenes regulate normal cell growth but can transform into oncogenes via mutations that increase their activity.
Flashcard 5: What is a tumor suppressor gene?
Answer: A gene that restrains proliferation; loss-of-function promotes cancer. Tumor suppressor genes inhibit cell division; their inactivation removes brakes on proliferation, facilitating cancer development.
Flashcard 6: Which mutation pattern is typical for oncogenes: dominant or recessive at the cellular level?
Answer: Dominant (one activating allele is sufficient). Oncogene mutations act dominantly because a single altered copy can overactivate proliferation signals.
Flashcard 7: Which mutation pattern is typical for tumor suppressor genes: dominant or recessive at the cellular level?
Answer: Recessive (both alleles usually must be inactivated). Tumor suppressor mutations are recessive as both copies must be lost to eliminate inhibitory function.
Flashcard 8: What is the two-hit hypothesis for tumor suppressor genes?
Answer: Both alleles must be inactivated to lose tumor suppressor function. The hypothesis explains that complete loss of tumor suppressor activity requires mutations in both gene copies.
Flashcard 9: What cell cycle checkpoint is primarily regulated by p53 in response to DNA damage?
Answer: The G1/S checkpoint. p53 halts progression at G1/S to allow DNA repair or apoptosis if damage is detected.
Flashcard 10: What is the main function of p53 in preventing cancer?
Answer: Induces p21, cell cycle arrest, DNA repair, or apoptosis after damage. p53 acts as a guardian by activating responses to prevent propagation of damaged DNA in cells.
Flashcard 11: What is the key role of p21 in cell cycle control?
Answer: Cyclin-dependent kinase inhibitor that enforces G1 arrest. p21 blocks cyclin-CDK activity to prevent progression from G1 to S phase during stress.
Flashcard 12: What is the primary role of Rb (retinoblastoma protein) at the G1/S transition?
Answer: Binds E2F to prevent S-phase gene transcription. Rb sequesters E2F transcription factors, inhibiting genes needed for DNA synthesis in S phase.
Flashcard 13: What is the immediate effect of a loss-of-function mutation in RB1 on the cell cycle?
Answer: Constitutive E2F activity and inappropriate S-phase entry. Mutated RB1 fails to repress E2F, allowing unchecked transcription and cell cycle progression.
Flashcard 14: What is apoptosis?
Answer: Programmed cell death with caspase activation and minimal inflammation. Apoptosis eliminates damaged cells orderly, preventing inflammation unlike necrosis.
Flashcard 15: What is the hallmark feature of caspases in apoptosis?
Answer: Cysteine proteases that cleave proteins after aspartate residues. Caspases dismantle cellular components specifically during apoptosis to ensure controlled demise.
Flashcard 16: What is the intrinsic (mitochondrial) apoptosis trigger?
Answer: Internal stress such as DNA damage causing cytochrome c release. Intrinsic pathway responds to cellular damage by mitochondrial release of pro-apoptotic factors.
Flashcard 17: What is the extrinsic apoptosis trigger?
Answer: Death receptor signaling (for example, Fas receptor activation). Extrinsic pathway initiates apoptosis via external signals binding death receptors on the cell surface.
Flashcard 18: Which BCL-2 family member is classically anti-apoptotic and often overexpressed in cancer?
Answer: BCL-2. BCL-2 inhibits apoptosis by preventing mitochondrial permeabilization, promoting cancer cell survival.
Flashcard 19: What is the effect of telomerase activation in cancer cells?
Answer: Maintains telomeres, enabling replicative immortality. Telomerase extends chromosome ends, countering shortening that limits divisions in normal cells.
Flashcard 20: What is contact inhibition?
Answer: Normal cells stop proliferating when they touch neighboring cells. Contact inhibition prevents overcrowding by signaling cells to stop dividing upon neighbor contact.
Flashcard 21: What is anchorage dependence?
Answer: Requirement for attachment to extracellular matrix to proliferate. Anchorage dependence ensures cells proliferate only when adhered, maintaining tissue architecture.
Flashcard 22: What is metastasis?
Answer: Spread of cancer cells to distant sites via blood or lymph. Metastasis allows cancer to colonize new sites, complicating treatment and worsening prognosis.
Flashcard 23: Which term describes a tumor that invades surrounding tissue and can spread to distant sites?
Answer: Malignant tumor. Malignant tumors exhibit invasive behavior, enabling distant spread and increased lethality.
Flashcard 24: Which term describes a tumor that remains localized and does not invade nearby tissue?
Answer: Benign tumor. Benign tumors grow locally without invading or spreading, posing less risk than malignant ones.
Flashcard 25: Identify what phosphorylation of Rb by cyclin-CDK complexes causes.
Answer: Releases E2F, enabling S-phase entry. Cyclin-CDK phosphorylation inactivates Rb, freeing E2F to transcribe S-phase promoting genes.