Related Experiment Video
Updated: Sep 4, 2026

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method
Published on: September 10, 2017
p53 status and the efficacy of cancer therapy in vivo
S W Lowe1, S Bodis, A McClatchey
1Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.
Abstract:
The therapeutic responsiveness of genetically defined tumors expressing or devoid of the p53 tumor suppressor gene was compared in immunocompromised mice. Tumors expressing the p53 gene contained a high proportion of apoptotic cells and typically regressed after treatment with gamma radiation or adriamycin. In contrast, p53-deficient tumors treated with the same regimens continued to enlarge and contained few apoptotic cells. Acquired mutations in p53 were associated with both treatment resistance and relapse in p53-expressing tumors. These results establish that defects in apoptosis, here caused by the inactivation of p53, can produce treatment-resistant tumors and suggest that p53 status may be an important determinant of tumor response to therapy.
Insights
The p53 tumor suppressor gene is crucial for cancer treatment response. Tumors lacking p53 are resistant to therapies like radiation and adriamycin, highlighting p53
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- The p53 tumor suppressor gene plays a critical role in cellular responses to DNA damage.
- Understanding the role of p53 in therapeutic resistance is essential for developing effective cancer treatments.
Purpose of the Study:
- To investigate the impact of p53 gene status on tumor responsiveness to genotoxic therapies.
- To determine if p53 deficiency leads to acquired resistance and relapse.
Main Methods:
- Comparison of therapeutic responsiveness in genetically defined mouse tumor models (p53-expressing vs. p53-deficient).
- Treatment with gamma radiation and adriamycin.
- Assessment of apoptosis and tumor growth.
- Analysis of acquired p53 mutations.
Main Results:
- p53-expressing tumors showed high apoptosis and regression after treatment.
- p53-deficient tumors exhibited resistance, continued enlargement, and low apoptosis.
- Acquired p53 mutations correlated with treatment resistance and relapse in initially p53-expressing tumors.
Conclusions:
- Inactivation of the p53 gene leads to apoptosis defects, resulting in treatment-resistant tumors.
- p53 status is a significant determinant of tumor response to radiation and adriamycin therapy.
- Targeting p53 pathways may overcome therapeutic resistance.
Related Concept Videos
Negative Regulator Molecules
DNA Damage can Stall the Cell Cycle
Abnormal Proliferation
The Intrinsic Apoptotic Pathway
DNA Damage Can Stall the Cell Cycle

