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B L Jenkins

Publications and source records attributed to B L Jenkins.

4 recordsLinked to original sources
PubMed2003

MEK5 overexpression is associated with metastatic prostate cancer, and stimulates proliferation, MMP-9 expression and invasion.

The novel mitogen/extracellular-signal-regulated kinase kinase 5/extracellular signal-regulated kinase-5 (MEK5/ERK5) pathway has been implicated in the regulation of cellular proliferation. MEK5 expression has been detected in prostate cancer cells, although the significance of the MEK5/ERK5 pathway in human prostate cancer has not been tested. We examined MEK5 expression in 127 cases of prostate cancer and 20 cases of benign prostatic hypertrophy (BPH) by immunohistochemistry and compared the results to clinical parameters. We demonstrated that MEK5 expression is increased in prostate cancer as compared to benign prostatic tissue. Strong MEK5 expression correlates with the presence of bony metastases and less favourable disease-specific survival. Furthermore, among the patients with high Gleason score of 8-10, MEK5 overexpression has an additional prognostic value in survival. MEK5 transfection experiments confirm its ability to induce proliferation (P < 0.0001), motility (P = 0.0001) and invasion in prostate cancer cells (P = 0.0001). MEK5 expression drastically increased MMP-9, but not MMP-2 mRNA expression. Luciferase report assays suggest that the -670/MMP-9 promoter is upregulated by MEK5 and electromobility shift assay further suggests the involvement of activator protein-I (AP-1), but not the NF-kappa B, binding site in the MMP-9 promoter. Using an AP-1 luciferase construct, activation of MEK5 was confirmed to enhance AP-1 activities up to twofold. Taken together, our results establish MEK5 as a key signalling molecule associated with prostate carcinogenesis. As the MEK5/ERK5 interaction is highly specific, it represents a potential target of therapy.

Adenocarcinoma↗
PubMedDate not supplied

Reproductive function in relation to duty assignments among military personnel.

As a follow-up to the pilot study of semen quality of soldiers with various military assignments a larger, more complete study was conducted. Soldiers were recruited at Fort Hood, Texas. Thirty-three men were exposed to radar as part of their duty assignment in the Signal Corps, 57 men were involved with firing the 155 mm howitzer (potential lead exposure), and 103 soldiers had neither lead nor radar exposure and served as the comparison control group. Both serum and urinary follicle-stimulating hormone and luteinizing hormone and serum, salivary, and urine testosterone levels were determined in all men. A complete semen analysis was conducted on each soldier. For statistical analysis, the primary study variables were: sperm concentration, sperm/ejaculate, semen volume, percent normal morphology, percent motile, percent viable (both vital stain and hypoosmotic swelling), curvilinear velocity, straight-line velocity, linearity, sperm head length, width, area, and perimeter. Variables were adjusted for significant confounders (e.g., abstinence, sample age, race). No statistical differences (P < 0.05) were observed in any measurement. While these results are in agreement with two previous studies assessing soldiers firing the 155-mm howitzer, they contradict our previous report indicating that radar exposure caused a significant decrease in sperm numbers. A possible explanation is that the radar exposure in this study was that used in Signal Corps operations while the men in the previous study were using different radar as part of military intelligence operations. The data presented here in men firing the 155-mm howitzer combined with the results from the previous studies confirms that there are no deficits in semen quality in these men. The contradiction between the results of the radar exposure studies indicates that more data are needed to evaluate the relationship of military radar and male reproductive health.

Adult↗