Dural arteriovenous fistulas in cerebral venous thrombosis: Data from the International Cerebral Venous Thrombosis Consortium: Data from the International Cerebral Venous Thrombosis Consortium.

BACKGROUND AND PURPOSE: To explore the prevalence, risk factors, time correlation, characteristics and clinical outcome of dural arteriovenous fistulas (dAVFs) in a cerebral venous thrombosis (CVT) population. METHODS: We included patients from the International CVT Consortium registries. Diagnosis of dAVF was confirmed centrally. We assessed the prevalence and risk factors for dAVF among consecutive CVT patients and investigated its impact on clinical outcome using logistic regression analysis. We defined poor outcome as modified Rankin Scale score 3-6 at last follow-up. RESULTS: dAVF was confirmed in 29/1218 (2.4%) consecutive CVT patients. The median (interquartile range [IQR]) follow-up time was 8 (5-23) months. Patients with dAVF were older (median [IQR] 53 [44-61] vs. 41 [29-53] years; p < 0.001), more frequently male (69% vs. 33%; p < 0.001), more often had chronic clinical CVT onset (>30 days: 39% vs. 7%; p < 0.001) and sigmoid sinus thrombosis (86% vs. 51%; p < 0.001), and less frequently had parenchymal lesions (31% vs. 55%; p = 0.013) at baseline imaging. Clinical outcome at last follow-up did not differ between patients with and without dAVF. Additionally, five patients were confirmed with dAVF from non-consecutive CVT cohorts. Among all patients with CVT and dAVF, 17/34 (50%) had multiple fistulas and 23/34 (68%) had cortical venous drainage. Of 34 patients with dAVF with 36 separate CVT events, 3/36 fistulas (8%) were diagnosed prior to, 20/36 (56%) simultaneously and 13/36 after (36%, median 115 [IQR 38-337] days) diagnosis of CVT. CONCLUSIONS: Dural arteriovenous fistulas occur in at least 2% of CVT patients and are associated with chronic CVT onset, older age and male sex. Most CVT-related dAVFs are detected simultaneously or subsequently to diagnosis of CVT.

Facing up to stereotypes: surgeons and physicians are no different in their emotional expressiveness.

Of all the differences between surgeons and physicians that are discussed in the medical profession and in the community at large, one distinction stands out for its frequency of use: surgeons are less emotional than physicians, particularly in their relationships with patients. Here we tested this stereotype by analysing the portraits that 5914 surgeons and physicians had provided for patients to view when selecting a doctor. There is an asymmetry in the degree to which emotional information is conveyed by the face, with the right side being less expressive than the left. Hence, if the stereotype were true, surgeons would be more likely than physicians to show their right cheek in the photographs. While the results for doctors confirmed previous reports of a difference due to sex in which female doctors were more likely to show the left cheek than male doctors, we found that the doctors' specialization did not predict the way they turned in their portraits. Hence, the notion that surgeons face their patients less emotionally than physicians is not supported by the data.

Incidence of colorectal cancer in West Virginia from 1993-1999: an update by gender, age, subsite and stage.

The sensitivities of different screening methods for pre-cancerous adenomas may affect the apparent anatomical distribution of colorectal cancers. Our objective was to describe changes in the distribution of left and right-sided colon cancers by time while adjusting for age, gender, stage and year of diagnosis. We studied the 7,895 cases of colorectal cancer reported to the West Virginia Cancer Registry between 1993 and 1999 and termed cancers proximal to, but not including the sigmoid colon as "right-sided," and the remaining tumors as "left-sided." Multivariate analyses were used to differentiate the effects of age and gender on changes in tumor location over time. The impact of screening was shown by the increase in the percentage of localized disease from 30.5% among cancers in the proximal colon to 37.6% in the distal colorectum. In contrast, the percentage of regional disease decreased from 50% among cancers in the proximal colon to the distal colorectum. The male to female ratios also increased from the proximal colon to the distal colorectum. Incidence rates, regardless of time, increased with advancing age for cancers located in all anatomical subsite groups, but more substantially for proximal colon cancer than for descending and distal colorectal cancers. For males ages > 85 and for females who are > 75 years of age, the cancer rates arising in the proximal colon exceeded observed in groups but more substantially for proximal colon cancer than for descending and distal colorectal cancers. For males age > 85 and females > 75, the cancer rates arising in the proximal colon exceeded those arising in the distal colorectum. This shift occurred at a younger age among females than males. The apparent shift of colorectal cancers to more proximal locations with advancing age has important implications for screening strategies. A further decrease in the relative incidence of left-sided colon cancers may require modifying current practices to include more frequent use of screening colonoscopy, particularly in women ages 75 years or older.

A 55-Year-Old Man with Stage IV Squamous Cell Carcinoma of the Right Groin after External Beam Radiation for Testicular Cancer.

Treating testicular cancer with adjuvant radiation has been associated with a number of second malignancies affecting the genitourinary tract and retroperitoneal structures; however, there have been few reported cases of cutaneous second malignancies. We report the case of a man who developed stage IV squamous cell carcinoma (SCC) of a condyloma after orchiectomy and adjuvant radiation for testicular cancer. We also review relevant literature available to date. A 55-year-old Caucasian man presented to the hospital with a large growth at the right groin which had grown into his right thigh preventing ambulation. His past medical history was significant for right testicular cancer of unknown pathology treated with orchiectomy and adjuvant radiation twenty years ago. Punch biopsy of the lesion revealed superficially invasive squamous cell carcinoma. He underwent excision of the growth with subsequent Cisplatin, radiation boost, and Paclitaxel regimens. Despite an aggressive treatment regimen and an initial good response, the patient's cancer progressed requiring palliative care. It is unclear whether or not therapeutic radiation in this case promoted the conversion of the patient's condyloma to a malignant lesion. Further studies are required at this time to clarify the clinical implications of these findings.

Postmenopausal obesity promotes tumor angiogenesis and breast cancer progression in mice.

Obese postmenopausal women have a 50% higher risk of breast cancer than non-obese women. There is not an animal model that mimics postmenopausal obesity related to breast cancer progression. Using age-relevant C57BL/6 mice, this study determined whether postmenopausal obesity increases VEGF expression, tumor angiogenesis, and breast tumor growth. Ovariectomy (OVX) was performed in 12 sixty week-old female mice, then followed by a low-fat (5%, LF, n=6) or a high-fat (60%, HF, n=6) diet for 12 weeks. In the eighth week of the dietary program, 10(6) E0771 (mouse breast cancer) cells were injected in the left fourth mammary gland. Tumor size was monitored for 4 weeks. Body weights were monitored weekly. At the end of the experiment, blood samples, visceral fat and tumors were collected for measuring VEGF expression using ELISA and intratumoral microvessel density (IMD) using CD31 immunochemistry. Body weight was significantly increased in OVX/HF mice, compared to OVX/LF group (55.3±1.7 vs. 41.5±1.5 g; p < 0.01). There was a two-fold increase in the ratio of visceral fat/BW in OVX/HF mice, compared to those in OVX/LF group (0.062±0.005 vs. 0.032±0.003; p < 0.01). Postmenopausal obesity significantly increased breast tumor weight over the control (4.62±0.63 vs. 1.98±0.27 g; p < 0.01) and IMD (173±3.7 vs. 139±4.3 IM#/mm^2; p < 0.01). Tumor VEGF levels were higher in OVX/HF mice, compared to OVX/LF group (73.3±3.8 vs. 49.5±4.3 pg/mg protein; p < 0.01). Plasma VEGF levels (69±7.1 vs. 48±3.5 pg/ml) and visceral fat VEGF levels (424.4±39.5 vs. 208.5±22.4 pg/mg protein) were significantly increased in OVX/HF mice, compared to OVX/LF group, respectively (n=6; p < 0.01). Interestingly, adipose tissue primary culture showed that subcutaneous fat released more VEGF, compared to visceral fat (6.77±1.14 vs. 0.94±0.16 pg/mg tissue; n=6; p < 0.01). These findings support the hypothesis that postmenopausal obesity promotes tumor angiogenesis and breast cancer progression, possibly through increased adipose tissue mass and adipokines such as VEGF that could systemically and locally affect breast cancer progression.

SU11248, a selective tyrosine kinases inhibitor suppresses breast tumor angiogenesis and growth via targeting both tumor vasculature and breast cancer cells.

SU11248 is a selective inhibitor of certain protein kinases including VEGFR types 1-3 that are expressed in human breast cancer. The present study determines whether the anti-tumor activity of SU11248 results from the inhibition of angiogenesis, as well as direct anti-proliferation and anti-migration effects on breast tumors. Eight-wk old female mice (C57BL/6) were given SU11248 at 20-40 mg/kg/d in drinking (distilled) water for 4 wks. Control mice received drinking water only. In the 2nd wk, 10(6) E0771 (mouse breast cancer) cells were injected in the left fourth mammary gland. Tumor size was monitored using dial calipers. At the end, tumors were isolated for measuring tumor size and intratumoral microvessel density (IMD) using CD31 immunohistochemistry. SU11248 significantly reduced tumor weight over the control (1.22 ± 0.28 vs. 3.28 ± 0.31 g; n = 8; p < 0.01) and IMD (111 ± 10 vs. 155 ± 6 IM#/mm2; p < 0.01). RT-PCR indicated that VEGFR1 and R2 were expressed in cultured E0771 cells. VEGF (10 ng/ml) caused a 42% increase in proliferation of E0771 cells, compared to the control (p < 0.01; n = 8), and there was a significant decrease in proliferation of E0771 cells treated with VEGF plus SU11248 (10 µmol/L) vs. the control (65%, p < 0.01). VEGF caused a 2-fold increase in the proliferation of HUVEC vs. the control (p < 0.01; n = 8), but its action was completely eradicated by SU11248. Neither VEGF nor SU11248 had any effect on the proliferation of cultured HAS MC. Migration assay showed that SU11248 (10 µmol/L) significantly inhibited the migration of cultured E0771 cells. SU11248 significantly inhibited the proliferation of MCF-7 and MDAMB-231 cells in a dose-related manner. These findings support the hypothesis that the antitumor activity of SU11248 on breast cancer is possibly mediated by targeting the paracrine and autocrine effects of VEGF on breast cancer to suppress tumor angiogenesis, proliferation and migration.

Race as an independent risk factor for breast cancer survival: breast cancer outcomes from the medical college of georgia tumor registry.

BACKGROUND: Causes of racial disparities in breast cancer survival remain unclear. This study assesses overall survival (OS) after diagnosis between black and white women and examines factors that might correlate with this disparity. PATIENTS AND METHODS: Data were obtained from the Medical College of Georgia Tumor Registry. Cases included those diagnosed between 1990 and 2005. We analyzed race, stage, age of diagnosis, and treatment received: chemotherapy, radiation, surgery, and hormonal therapy. A Cox proportional hazards model was used to determine differences in OS. RESULTS: Compared with 670 white women, 489 black women were more likely to be younger, have later-stage disease at diagnosis, and were less likely to have received hormonal therapy. Both groups received similar rates of radiation, surgery, and chemotherapy. Black women had significantly poorer OS (adjusted hazard ratio, 1.35; 95% CI, 1.12-1.63). White women had a 5-year OS of 54% compared with 45% in black women (P = .0031). Having received radiation, surgery, or chemotherapy was not associated with OS. White women were more likely to have received hormonal therapy, which had a significant protective effect. However, a stratified analysis (between those who received hormonal therapy and those who did not) showed similar results, whereas black women experienced poorer OS in both strata. CONCLUSION: Black women with breast cancer had a significantly poorer OS compared with white women. White women received more hormonal therapy, which had a protective effect. There were no differences in treatment received regarding radiation, surgery, or chemotherapy, and these treatments were not associated with OS. The reasons for racial disparities in breast cancer OS remain complex.