Overexpression of the Myc genes promote cellular transformation. Max protein exerts a pivotal function with the Myc family, and Mxil/Mad proteins play a positive and negative activity, respectively, on transcription. The function of Mxil suggests that it might be a tumor suppressor protein. The Mxil gene map to 1Op24‐25 and deletions of this locus are frequently observed in prostate cancers. The N‐terminal helical motif, helix‐loop‐helix (HLH) and leucine zipper (ZIP) regions of the Mxil gene are functionally important. We analyzed most of the coding region of the Mxil gene, including these three important regions in 32 prostate cancers and three cell lines by PCR‐single strand conformational polymorphism (SSCP). To enrich neoplastic cells, the microdissection was performed on clinical samples. We detected a silent mutation in the HLH region, but no point mutations reflecting the functional change of Mxil were found in human prostate cancers. Point mutations of the Mxil gene, if they occur, must be minor events in primary prostate cancers. © 1996 Wiley‐Liss, Inc.
to evaluate patterns of chemotherapy use. Median, 1-year and 2-year OS were calculated for patients that received chemotherapy using Kaplan Meier method. Results: Among the 86,200 patients that met the eligibility criteria, 40,147 (46.6%) patients received chemotherapy, which included single agent (n¼3,912; 9.7%) multiagent (n¼32,737; 81.5%) and number of agents unknown (n¼3,498; 8.7%). A total of 46,053 (53.43%) patients did not receive chemotherapy due to chemotherapy not recommended (n¼5,397; 11.7%), patient refusal (n¼6,119; 13.3%) and other/unknown reasons (n¼34,537; 75%). Patients receiving multi-agent chemotherapy were younger than those receiving single agent chemotherapy (65.6 vs 71.5 years). Chemotherapy use declined with increase in comorbidity score (50.4% for score of 0, 44% for score of 1 and 36.2% for score of 2). The median, 1-year and 2-year OS for patients receiving chemotherapy were 7.5 months, 30.6% and 11.8% respectively (Table). Conclusion: Most patients with metastatic SCC do not receive chemotherapy. The OS for patients with metastatic SCC remains poor, especially in patients over the age of 70, in men and those with multiple comorbidities.
Controversy exists as to whether Kaposi's sarcoma–associated herpesvirus (KSHV) is more widespread than originally reported. Recently, Monini et al reported that KSHV is ubiquitous in urogenital and prostate tissues and sperm of healthy Italian adults using nested polymerase chain reaction (PCR). We have examined for the presence of KSHV in 10 normal prostates from Italian men and 10 from men from the United States, as well as 32 prostatic, 30 vulvar, 24 ovarian, 20 cervical, and 30 testicular cancer specimens from patients from the United States. None of the patients had a history of human immunodeficiency virus infection. The samples were tested by nested PCR. The sensitivity of this assay was determined by a dilution study performed by diluting KSHV DNA from the KS-1 cells (a primary effusion lymphoma cell line which is estimated to have 16 copies of KSHV per cell) in DNA from a K562 myeloid cell line. The nested PCR that we used can detect 2.4 copies of KSHV sequences on a background of K562 DNA. All the samples were negative for KSHV sequences. Therefore, we cannot confirm the finding that KSHV sequences are ubiquitous in urogenital and prostate tissues. Furthermore, because our samples were from both the United States and Italy, the discrepancy between results is unlikely to be explained by either ethnic or environmental factors. False-positive results easily occur using nested primer PCR because of contamination. Our data argue that KSHV is not widely disseminated in urogenital tissues from nonimmunosuppressed individuals.
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