Cancer Biology and Genetics Quiz

<p>Unordered mutations that bypass normal cellular checkpoints (C)</p> Signup and view all the answers

<p>By designing drugs that simultaneously target both the oncogene and tumor suppressor gene, enhancing cell death. (D)</p> Signup and view all the answers

<p>By leading to genetic instability and promoting rapid accumulation of mutations (B)</p> Signup and view all the answers

<p>Targeting and destroying abnormal cells before they proliferate. (D)</p> Signup and view all the answers

<p>A cell accumulates multiple mutations in a specific sequence: first in a DNA repair gene, then in a tumor suppressor gene, and finally in an oncogene. (B)</p> Signup and view all the answers

<p>Functioning as an E3 ubiquitin ligase to promote protein degradation and facilitate DNA repair. (D)</p> Signup and view all the answers

<p>It recruits and stabilizes RAD51 at DNA breaks to initiate homologous recombination. (D)</p> Signup and view all the answers

<p>Impaired homologous recombination (HR), leading to genomic instability. (A)</p> Signup and view all the answers

<p>70% (D)</p> Signup and view all the answers

<p>Autosomal dominant (B)</p> Signup and view all the answers

<p>By controlling the G1/S checkpoint (D)</p> Signup and view all the answers

<p>To phosphorylate and inhibit CDC25, preventing CDK1 activation and halting the cell cycle. (B)</p> Signup and view all the answers

<p>Two mutations (First Hit and Second Hit) in the RB1 gene; one germline/somatic and one somatic. (A)</p> Signup and view all the answers

<p>Hereditary retinoblastoma typically presents earlier in life and bilaterally. (D)</p> Signup and view all the answers

<p>By facilitating homologous recombination and repairing double-strand DNA breaks. (B)</p> Signup and view all the answers

<p>Up to 70% (C)</p> Signup and view all the answers

<p>Multiple pregnancies at a young age (B)</p> Signup and view all the answers

<p>It enforces G2/M arrest through CHK1 activation, providing time for DNA repair. (D)</p> Signup and view all the answers

<p>It is recruited to DNA damage sites by BRCA2 to facilitate DNA repair. (A)</p> Signup and view all the answers

<p>Homologous recombination repair pathways (C)</p> Signup and view all the answers

<p>Autosomal dominant (A)</p> Signup and view all the answers

<p>It partially or fully impairs the function of the entire p53 tetramer. (C)</p> Signup and view all the answers

<p>A mutation where p53 not only loses its tumor-suppressive role but actively promotes tumor progression. (A)</p> Signup and view all the answers

<p>Normal cellular metabolism (B)</p> Signup and view all the answers

<p>By regulating metabolism and autophagy. (B)</p> Signup and view all the answers

<p>High levels. (B)</p> Signup and view all the answers

<p>Cell cycle arrest genes. (A)</p> Signup and view all the answers

<p>The cell initiates DNA repair; if stress persists, it switches to apoptosis. (B)</p> Signup and view all the answers

<p>By acting as an E3 ubiquitin ligase that targets p53 for degradation. (A)</p> Signup and view all the answers

<p>By disrupting protein synthesis, leading to selective apoptosis in transduced tumor cells. (B)</p> Signup and view all the answers

<p>By increasing vector specificity and transduction efficiency through tumor-targeting ligands. (D)</p> Signup and view all the answers

<p>Restoration of growth regulation, leading to apoptosis and chemosensitization. (D)</p> Signup and view all the answers

<p>Tumor response, p53 restoration's impact on apoptosis, and cell cycle arrest. (A)</p> Signup and view all the answers

<p>It delivers functional p53 to tumor cells, restoring apoptosis and cell cycle regulation. (B)</p> Signup and view all the answers

<p>Intratumoral injection enhances transduction efficiency by directly targeting the tumor. (A)</p> Signup and view all the answers

<p>It prevents the virus from causing a systemic infection, enhancing safety. (D)</p> Signup and view all the answers

<p>Increased response rates when combined with chemotherapy and radiotherapy. (C)</p> Signup and view all the answers

<p>Poor infiltration into the tumor and immunosuppressive microenvironment. (A)</p> Signup and view all the answers

<p>By disrupting the tumor microenvironment and promoting T-cell infiltration. (C)</p> Signup and view all the answers

<p>They recruit T-cells to the tumor by binding to CD3 and tumor antigens, inducing cytotoxicity. (A)</p> Signup and view all the answers

<p>Autosis is a unique cell death pathway driven by autophagy dysfunction, which MYXV can induce in apoptosis-resistant cells. (C)</p> Signup and view all the answers

<p>Combining oncolytic viruses with immune checkpoint inhibitors and CAR T-cells to enhance immune responses. (A)</p> Signup and view all the answers

<p>Acute lymphoblastic leukemia (ALL) (C)</p> Signup and view all the answers

<p>It provides a pathway to target cancers that evade apoptosis. (C)</p> Signup and view all the answers

<p>BiTEs offer high precision by directly activating T-cells against tumor cells. (D)</p> Signup and view all the answers

Cancer is primarily a disease of aging, with higher risks after age 60.

Men have a 43.5% and women a 38.5% lifetime risk of cancer.

DNA repair declines with age, increasing mutation risks.

Tumor formation occurs through successive genetic alterations.

The immune system identifies and destroys abnormal cells.

Mutations accumulate due to frequent cell division over a lifetime.

Programmed cell death that removes cells with oncogenic mutations.

Abnormal number of chromosomes, leading to genetic instability.

Kinases that phosphorylate CDC25, halting cell cycle at G2/M checkpoint.

Phosphatase inhibited by CHK1/CHK2 to prevent CDK1 activation.

Tumor suppressor genes critical for DNA repair via homologous recombination.

BRCA1 mutations confer up to a 70% risk of breast cancer by age 80.

Loss of BRCA function leads to mutations and cancer proliferation.

Includes family history, reproductive factors, and lifestyle choices.

Essential for DNA repair, checkpoint regulation, and transcriptional control.

Preventative actions, such as mastectomy, for BRCA1/2 mutation carriers.

A mutation that impairs the function of the entire protein complex, even with one mutant allele.

Mutant p53 proteins lose tumor suppression and promote tumor progression.

A protein like p53 that helps prevent tumor formation.

Factors such as DNA damage, hypoxia, and oncogene activation that activate p53.

Different levels of p53 lead to cell cycle arrest, senescence, or apoptosis.

E3 ubiquitin ligase that degrades p53, regulating its levels in the cell.

Binding sites that promote transcription of cell cycle arrest genes.

Areas where p53 activates pro-apoptotic genes like BAX and NOXA.

Cancers affecting B-cells, like leukemia and lymphoma.

Difficulties in effectively treating solid tumors due to poor T-cell infiltration.

A severe inflammatory response to CAR T-cell therapy.

Viruses that selectively infect and lyse tumor cells.

Engineered proteins that activate T-cells against tumor antigens.

A unique form of cell death resulting from autophagy dysfunction.

A poxvirus that infects tumor cells without harming normal tissues.

Using combined approaches like OVs with CAR T cells to improve treatment.

Toxins disrupt protein synthesis, causing selective apoptosis in tumor cells.

Promoters control toxin expression specifically in tumor cells, reducing toxicity.

Combining viral proteins with ligands enhances adenoviral vector targeting and efficiency.

Vectors often deliver tumor suppressor genes like p53 to restore cell growth regulation.

Evaluate response to p53 therapy, its apoptosis impact, and combination treatments.

First approved gene therapy for cancer, using a replication-defective adenovirus to deliver p53.

Includes intratumoral injection for solid tumors and intravenous delivery for metastatic cases.

Improves response in head and neck cancer when combined with chemotherapy.

Acts as an E3 ubiquitin ligase, tagging proteins for degradation to aid DNA repair.

Recruits and stabilizes RAD51 at DNA breaks to initiate homologous recombination.

Process by which BRCA1 modifies histones for chromatin remodeling at damage sites.

Severe form of DNA damage that can result from BRCA1/2 dysfunction.

Up to 70% lifetime risk of breast cancer and 40-50% risk of ovarian cancer.

Carries 45-65% risk for breast cancer and 10-20% risk for ovarian cancer.

Explains retinoblastoma development through two mutations in the RB1 gene.

Tumor suppressor that regulates the cell cycle at the G1/S checkpoint.