ArticleThe American journal of pathology1998
Genetic alterations in hormone-refractory recurrent prostate carcinomas.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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77 citing papers in PubMed, 311 citations in OpenAlex.
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- Variability of Inverted Repeats in All Available Genomes of Bacteria.Microbiology spectrum · 2023Article
- Cancer Stem Cells and Prostate Cancer: A Narrative Review.International journal of molecular sciences · 2023Review
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- Racial disparity in prostate cancer in the African American population with actionable ideas and novel immunotherapies.Cancer reports (Hoboken, N.J.) · 2021Review
- Structural recognition of the MYC promoter G-quadruplex by a quinoline derivative: insights into molecular targeting of parallel G-quadruplexes.Nucleic acids research · 2021Article
- Olfactomedin 4 mediation of prostate stem/progenitor-like cell proliferation and differentiation via MYC.Scientific reports · 2020Article
- Roles of Farnesyl-Diphosphate Farnesyltransferase 1 in Tumour and Tumour Microenvironments.Cells · 2020Review
- Loss of USF2 promotes proliferation, migration and mitophagy in a redox-dependent manner.Redox biology · 2020Article
- A piece in prostate cancer puzzle: Future perspective of novel molecular signatures.Saudi journal of biological sciences · 2020Review
- Structures of 1:1 and 2:1 complexes of BMVC and MYC promoter G-quadruplex reveal a mechanism of ligand conformation adjustment for G4-recognition.Nucleic acids research · 2019Article
- Prognostic Significance of High Androgen Receptor Expression in Prostatic Acinar AdenocarcinomaAsian Pacific journal of cancer prevention : APJCP · 2019Article
- Concise Review: Prostate Cancer Stem Cells: Current Understanding.Stem cells (Dayton, Ohio) · 2018Review
- Eukaryotic translation initiation factor 3H suppression inhibits osteocarcinoma cell growth and tumorigenesis.Experimental and therapeutic medicine · 2018Article
- c-Myc regulates the CDK1/cyclin B1 dependent‑G2/M cell cycle progression by histone H4 acetylation in Raji cells.International journal of molecular medicine · 2018Article
- Telomeres and telomerase in prostate cancer development and therapy.Nature reviews. Urology · 2017Review
- Pathway-based expression profiling of benign prostatic hyperplasia and prostate cancer delineates an immunophilin molecule associated with cancer progression.Scientific reports · 2017Article
- Review
- HER2 gene amplification in patients with prostate cancer: Evaluating a CISH-based method.Oncology letters · 2016Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To study the genetic basis of tumor progression, we have screened 37 hormone-refractory prostate carcinomas for genetic changes by comparative genomic hybridization (CGH). All recurrent tumors showed genetic aberrations, with a mean total number of changes per tumor of 11.4 (range, 3 to 23). The most common genetic aberrations were losses of 8p (72.5%), 13q (50%), 1p (50%), 22 (45%), 19 (45%), 10q (42.5%), and 16q (42.5%) and gains of 8q (72.5%), 7q (40%), Xq (32.5%), and 18q (32.5%). The CGH results were further validated with fluorescence in situ hybridization (FISH) using probes for pericentromeric regions of chromosomes 7, 8, and 18 as well as probes for caveolin (7q31), c-myc (8q24), and bcl-2 (18q21.3). In addition, the samples had previously been analyzed for androgen receptor gene copy number. CGH and FISH results were concordant in 78% of cases. Seventeen of twenty-two tumors showed an increased copy number of c-myc by FISH. However, only 5 of 17 (29%) of the cases showed high-level (more than threefold) amplification. Both CGH and FISH findings suggested that in most of the cases 8q gain involves the whole q-arm of the chromosome. Four of seventeen (24%) cases showed increased copy number of bcl-2 by FISH; however, no high-level amplifications were found. To evaluate the clonal relationship of the primary and recurrent tumors, six primary-recurrent tumor pairs from the same patients were studied by CGH. In three of six cases (50%), the recurrent tumor had more than one-half of the aberrations found in the corresponding primary tumor, indicating a close clonal relationship. In the rest of the cases, such a linear clonal relationship was less evident. Altogether, these results suggest that recurrent prostate carcinomas are genetically unstable. The resulting heterogeneity may well underlie the poor responsiveness of hormone-refractory tumors to treatment.
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