A two-step toward personalized therapies for prostate cancer.
Level V
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- Record sourced from PubMed, PMID 21368221.
- Also identified by DOI 10.1126/scitranslmed.3002169 and PMC identifier 3089975.
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Abstract
Identifying the dominant genetic alterations that drive tumorigenesis is essential for developing targeted cancer therapies. Recent work has demonstrated that prostate tumors can be stratified by dominant genetic alterations, such as chromosomal rearrangements involving ETS (Erythroblastosis virus E26 transformation-specific) family transcription factors or overexpression of SPINK1, a gene that encodes a secreted serine protease inhibitor. In this issue of Science Translational Medicine, Ateeq et al. provide evidence to support a rationale for targeting the SPINK1 protein in the SPINK1+/ETS⁻ subset of prostate tumors and also describe a potential interaction of SPINK1 with epidermal growth factor receptor that could be an additional target for therapeutic intervention.
Medical subject headings
- Carrier Proteins
- Gene Targeting
- Precision Medicine
- Prostatic Neoplasms