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Oncogenes and clinical oncology
1Memorial Sloan-Kettering Cancer Center, New York, New York.
Abstract:
The past year has seen important advances in our understanding of the molecular biology of human cancer. We have learned more about how normal genes with critical functions in growth and development can induce cellular transformation and malignancy if mutated or overexpressed. The finding of such oncogenes in specific human cancers often portends a poor prognosis. We have learned more about tumor suppressor genes, whose loss by mutation, deletion, or translocation can lead to cancer. A series of defects involving both oncogenes and tumor suppressor genes has been shown to characterize the multistep development of a fully malignant colon cancer. We have new insights into the promotion of malignancy by the fused gene product resulting from the chromosomal abnormality diagnostic of one leukemia, chronic myelogenous leukemia. Recently, in acute promyelocytic leukemia, a characteristic chromosomal abnormality has been shown to result in a specific fusion of a nuclear receptor that activates transcription and a previously unknown gene. Most interestingly, a ligand for this rearranged receptor has been shown to be a novel effective treatment for the disease. This review summarizes many of these advances.
Insights
Recent advances reveal how oncogenes and tumor suppressor genes drive cancer development. Understanding these genetic changes offers new insights into cancer
Area of Science:
- Molecular biology of human cancer
- Cancer genetics
- Gene regulation in malignancy
Background:
- Normal genes can become oncogenes, promoting cancer when mutated or overexpressed.
- Tumor suppressor genes, when lost or inactivated, contribute to cancer development.
- Cancer arises from a multistep process involving defects in both oncogenes and tumor suppressor genes.
Purpose of the Study:
- To summarize recent advances in understanding the molecular biology of human cancer.
- To highlight the roles of oncogenes and tumor suppressor genes in cancer development.
- To discuss new insights into specific cancers like leukemia and colon cancer.
Main Methods:
- Review of recent scientific literature on human cancer molecular biology.
- Analysis of genetic alterations (mutations, overexpression, translocations) in cancer.
- Examination of specific gene fusions and their roles in leukemia.
Main Results:
- Oncogene activation and tumor suppressor gene inactivation are key to cancer.
- Multistep genetic defects characterize malignant progression, e.g., colon cancer.
- Specific chromosomal abnormalities create fusion genes in leukemia (CML, APL).
Conclusions:
- Understanding oncogenes and tumor suppressor genes is crucial for cancer prognosis.
- Fusion genes in leukemia, like in APL, offer therapeutic targets.
- Targeting specific molecular pathways provides novel treatment strategies for cancer.