Skip to content
Login Register

#cancer

27 public questions tagged with this topic.

Gene Therapy

Cancer gene therapy often uses strategy of:

Cancer gene therapy predominantly adopts tumoricidal strategy rather than restoration tumor suppressor because cancer genome carries multiple gain-of-function oncogenes KRAS MYC aneuploidy heterogeneity complicating simple addition. Methods eliminate malignant clone through introduction genes triggering death or immune recruitment. Oncolytic adenoviruses engineered deletion E1B 55 kDa protein normally inactivating p53 replicate selectively p53-deficient cancers lysing cells via viral burst releasing PAMPs tumor antigens danger signals ATP calreticulin HMGB1 driving immunogenic cell death. Suicide enzyme systems HSV TK ganciclovir produce toxic dGTP analog inducing apoptosis. Cytokine transgenes GM-CSF IL-12 IFN-alpha secreted transduced tumor cells recruit dendritic cells cytotoxic T lymphocytes cross-presenting released antigens epitope spreading generating systemic immunity targeting distant metastases abscopal effect. CAR-T gene editing deleting TRAC preventing graft-versus-host PDCD1 enhancing persistence exemplifies combined transfer editing enhancing tumoricidal efficacy overcoming resistance inherent monogenic correction approaches limited single gene restoration. This mechanistic insight guides vector optimization, dosing strategies, and clinical safety monitoring essential for translational development and regulatory evaluation.

Ref: Nature Reviews Cancer Gene Therapy Oncolytic Mechanisms 2021; NCI Cancer Gene Therapy Targeted Killing; Molecular Therapy Oncolytic Viruses 2021.

View Details
Membrane Transportation

Which ABC transporter is associated with multidrug resistance in cancer?

Cancer multidrug efflux is dominated not by CFTR or P-type ATPases but by ABC transporters that expel amphipathic chemotherapeutics from cytoplasm. ABCB1 P-glycoprotein MDR1 is best studied, overexpressed in colonic, renal, adrenocortical carcinomas and after chemotherapy induction in leukemia, lymphoma and breast cancer. Its polyspecific hydrophobic binding chamber accommodates doxorubicin, daunorubicin, vinblastine, vincristine, paclitaxel and etoposide causing cross-resistance. ABCC1 MRP1 exports glutathione conjugates of drugs, ABCG2 BCRP expels mitoxantrone and topotecan. Expression correlates with poor response, reduced disease-free interval, and altered pharmacokinetics influencing oral bioavailability and blood-brain barrier penetration. Mechanistically transporter uses ATP hydrolysis at two NBDs to switch from inward-high affinity to outward-low affinity releasing drug. Inhibitors verapamil, cyclosporine, tariquidar attempted clinically to reverse resistance, but toxicity and redundant export pathways limit success, prompting development of nanoparticle formulations to bypass efflux and selective modulators. Such detailed mechanistic insight is frequently examined in competitive tests including NEET, CUET, CSIR-NET and GATE where transporter classification, energetics and disease linkage are integrated into problem-solving questions.

Ref: Gottesman et al., Annu Rev Med 2002, MDR in cancer; Szakacs et al., Nat Rev Drug Discov 2006.

View Details
Cancer

Multidrug resistance in cancer commonly involves overexpression of

Over-expression of ATP-binding cassette transporters such as P-glycoprotein (encoded by MDR1) actively effluxes a wide range of hydrophobic drugs from the cytoplasm, reducing their intracellular concentration below the therapeutic threshold. This mechanism is a major cause of multidrug resistance in cancer chemotherapy. Inhibition of these pumps is therefore an active area of pharmacological research aimed at restoring drug sensitivity.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

View Details
Cancer

Viral oncoproteins contribute to cancer mainly by

Neutralizing tumor suppressor proteins, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

View Details
Cancer

Combined action of HPV E6 and E7 results in

High-risk human papillomavirus oncoproteins E6 and E7 cooperate to drive cervical carcinogenesis. E7 binds and inactivates Rb, releasing E2F and promoting cell-cycle progression. E6 recruits the ubiquitin ligase E6AP to target p53 for degradation, thereby disabling the apoptotic and checkpoint responses that would otherwise eliminate the proliferating infected cell. The combined action removes both major tumor-suppressor barriers.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

View Details
Cancer

HPV E6 oncoprotein promotes cancer by

High-risk human papillomavirus oncoproteins E6 and E7 cooperate to drive cervical carcinogenesis. E7 binds and inactivates Rb, releasing E2F and promoting cell-cycle progression. E6 recruits the ubiquitin ligase E6AP to target p53 for degradation, thereby disabling the apoptotic and checkpoint responses that would otherwise eliminate the proliferating infected cell. The combined action removes both major tumor-suppressor barriers.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

View Details
Cancer

HPV E7 oncoprotein promotes cancer by

High-risk human papillomavirus oncoproteins E6 and E7 cooperate to drive cervical carcinogenesis. E7 binds and inactivates Rb, releasing E2F and promoting cell-cycle progression. E6 recruits the ubiquitin ligase E6AP to target p53 for degradation, thereby disabling the apoptotic and checkpoint responses that would otherwise eliminate the proliferating infected cell. The combined action removes both major tumor-suppressor barriers.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

View Details
Cancer

Hyperphosphorylation of Rb leads to

Hypophosphorylated Rb binds and represses E2F transcription factors, preventing expression of genes required for S-phase entry. Mitogenic signaling activates cyclin-D–CDK4/6 and cyclin-E–CDK2 complexes that progressively phosphorylate Rb. Hyperphosphorylated Rb releases E2F, allowing S-phase progression. Loss of Rb function therefore removes a critical G1 checkpoint and contributes to uncontrolled proliferation. Careful

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

View Details