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Updated: Jun 27, 2026
A Time-lapse, Label-free, Quantitative Phase Imaging Study of Dormant and Active Human Cancer Cells
Published on: February 16, 2018
Reversing cancer from inside and out: oncogene addiction, cellular senescence, and the angiogenic switch
1Division of Oncology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. dfelsher@stanford.edu
Abstract:
Cancer is largely caused by genetic events that result in the mutation of oncogenes or tumor suppressor genes, leading to cell autonomous proliferation and growth. The repair of these mutant gene products may be expected to subvert this neoplastic behavior. Indeed, oncogene inactivation can result in the elimination of all or almost all tumor cells by various mechanisms through the phenomena described as oncogene addiction. Recently, we have shown that oncogene addiction occurs through at least two broad classes of mechanisms: tumor cell intrinsic mechanisms of cellular senescence and apoptosis; and tumor cell extrinsic host-dependent mechanisms that include the shut-down of angiogenesis. We have argued that the abatement of oncogenic activity within a cancer cell not only leads to the demise of a tumor from within but also through the instruction of the restoration of the microenvironment.
Insights
Inactivating cancer-driving oncogenes can eliminate tumors through cell death and by restoring the tumor microenvironment. This oncogene addiction phenomenon offers new therapeutic strategies for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cancer arises from genetic mutations in oncogenes and tumor suppressor genes.
- Uncontrolled cell proliferation is a hallmark of neoplastic growth.
- Targeting these genetic drivers offers a potential therapeutic avenue.
Purpose of the Study:
- To investigate the mechanisms underlying oncogene addiction in cancer.
- To explore both intrinsic and extrinsic pathways involved in tumor regression upon oncogene inactivation.
Main Methods:
- Analysis of oncogene inactivation effects on cancer cells.
- Examination of cellular senescence and apoptosis induction.
- Assessment of host-dependent mechanisms, including anti-angiogenesis.
Main Results:
- Oncogene inactivation triggers tumor cell elimination via intrinsic (senescence, apoptosis) and extrinsic (anti-angiogenesis) mechanisms.
- Tumor microenvironment restoration is observed following oncogenic activity abatement.
- Oncogene addiction involves both direct cell killing and indirect host-mediated responses.
Conclusions:
- Oncogene addiction is a critical vulnerability in cancer.
- Therapeutic strategies targeting oncogenes can induce tumor regression through multiple pathways.
- Restoration of the tumor microenvironment is a key outcome of successful oncogene inactivation.
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