PubMed · 8131663
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B J Kennedy. A lady and chronobiology.. https://pubmed.ncbi.nlm.nih.gov/8131663/
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Results of the evaluation of transrectal ultrasound (TRUS) guided needle biopsy of voxels identified as suspicious of malignancy on magnetic resonance spectroscopic imaging (MRSI) in a large cohort of men (n = 83) with abnormal digital rectal examination (DRE) [prostate specific antigen (PSA) 0-4 ng/ml] or PSA less than 10 ng/ml, are reported. Three-dimensional (1)H MRSI was carried out at 1.5 T using a pelvic-phased array coil in combination with an endorectal surface coil. Voxels were classified as suspicious of malignancy based on Cit/(Cho + Cr) metabolite ratio. TRUS-guided biopsy of suspicious voxels was performed using the z- and x-coordinates obtained from MR images and two to three cores were taken from the suspected site. A systematic sextant biopsy was also carried out. MRSI showed voxels suspicious of malignancy in 44 patients while biopsy revealed cancer in 11 patients (25%). Patients who were negative for malignancy on MRSI were also negative on biopsy. An overall sensitivity of 100%, specificity of 54%, negative predictive value of 100% and accuracy of 60% were obtained. The site of biopsy was confirmed (n = 20) as a hypo-intense area on repeat MRI while repeat MRSI revealed high choline and low citrate. The overall success rate of MRI-directed TRUS-guided biopsy of 25% was higher compared with a 9% success rate achieved without MR guidance in another group of 120 patients. Our results indicate that TRUS-guided biopsy of suspicious area identified as malignant from MRSI can be performed using the coordinates of the voxel derived from MR images. This increases the detection rate of prostate cancer in men with PSA level <10 ng/ml or abnormal DRE and also demonstrates the potential of MR in routine clinical practice.
It has recently been hypothesized that the general shift in use from suspenders to belts among men might be a factor that could promote reflux, particularly among overweight men, and thereby contribute to the alarmingly increasing incidence of esophageal and cardia adenocarcinoma. We addressed this hypothesis in a nationwide Swedish population-based case-control study, conducted in 1995-1997. Included were 189 patients with esophageal adenocarcinoma and 262 patients with cardia adenocarcinoma, who were compared with 167 patients with esophageal squamous cell carcinoma and 820 population-based control participants. Data were collected at structured face-to-face interviews with all study participants. Tumor classification was uniform and thorough. Odds ratios (OR) with 95% confidence intervals (CI), adjusted for potential confounders, were estimated in multivariable logistic regression models. Daily use of tight belts 20 years earlier did not entail an increased risk of adenocarcinoma of the esophagus (OR 1.1, 95% CI 0.7-1.8) or cardia (OR 0.8, 95% CI 0.5-1.3) compared to never use. Adjustment for reflux symptoms, body mass and other potentially relevant covariates did not influence the results. Similarly, in analyses restricted to overweight men, no associations were identified. No association with esophageal squamous cell carcinoma was found. In conclusion, this study provided no support for the hypothesis that use of tight belts is associated with an increased risk of developing esophageal or cardia adenocarcinoma.
Tumors arise initially as avascular masses in which central hypoxia induces expression of vascular endothelial growth factor-A (VEGF-A) and subsequently tumor vascularization. However, VEGF-A can also be constitutively expressed as a result of genetic events. VEGF-A is alternatively spliced to yield at least 6 different isoforms. Of these, VEGF-A(121) is freely diffusible whereas basically charged domains in the larger isoforms confer affinity for cell surface or extracellular matrix components. We previously reported that in a mouse brain metastasis model of human melanoma, VEGF-A(121) induced a qualitatively different tumor vascular phenotype than VEGF-A(165) and VEGF-A(189): in contrast to the latter ones, and VEGF-A(121) did not induce a neovascular bed but rather led to leakage and dilatation of preexistent brain vessels. Here, we correlate vascular phenotypes with spatial VEGF-A expression profiles in clinical brain tumors (low grade gliomas; n = 6, melanoma metastases; n = 4, adenocarcinoma metastases; n = 4, glioblastoma multiforme; n = 3, sarcoma metastasis; n = 1, renal cell carcinoma metastasis; n = 1). We show that tumors that constitutively express VEGF-A present with different vascular beds than tumors in which VEGF-A is expressed as a response to central hypoxia. This phenotypic difference is consistent with a model where in tumors with constitutive VEGF-A expression, all isoforms exert their effects on vasculature, resulting in a classical angiogenic phenotype. In tumors where only central parts express hypoxia-induced VEGF-A, the larger angiogenic isoforms are retained by extracellular matrix, leaving only freely diffusible VEGF-A(121) to exert its dilatation effects on distant vessels.