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Monday, July 28, 2008

Fwd: Association between plasma cholesterol and prostate cancer in the PSA era.



---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Thu, Jul 24, 2008 at 7:29 AM
Subject: Association between plasma cholesterol and prostate cancer in the PSA era.
To: mesothelioma77@gmail.com


[1]Int J Cancer. 2008 Jul 21;
Platz EA, Clinton SK, Giovannucci E

We previously found that statin users had a lower risk of advanced and possibly high-grade prostate cancer compared with nonusers. We hypothesize that statins' effects on cholesterol synthesis may explain those findings because prostate cancer cells exhibit cholesterol dysregulation. Thus, we investigated whether low plasma cholesterol is associated with prostate cancer overall and by stage and grade. Participants were drawn from the 18,018 members of the Health Professionals Follow-Up Study who provided blood in 1993-1995. We ascertained 698 incident cases through January 2000. Controls were 698 men who had a PSA test and were matched to cases. Plasma cholesterol was measured enzymatically. Conditional logistic regression was used to estimate multivariable ORs and 95% CIs of total, clinically organ-confined (n = 518), advanced (T3b or worse; n = 61), low-grade (Gleason sum /= 7, n = 247) disease. Low cholesterol (/=25th percentile) was not associated with total (OR = 0.93, 95% CI: 0.72-1.20), organ-confined (OR = 0.87, 95% CI: 0.64-1.18) or low-grade (OR = 1.06, 95% CI: 0.75-1.51) disease. However, men with low cholesterol had a lower risk of high-grade disease (OR = 0.61, 95% CI: 0.39-0.98), especially if organ-confined (OR = 0.54, 95% CI: 0.29-0.99). The association for advanced disease appeared inverse, but number of cases was small (OR = 0.42, 95% CI: 0.13-1.36). Associations remained after excluding cholesterol-lowering drug users. These results coupled with prior statin findings suggest that mechanistic studies on cholesterol metabolism should be pursued to understand a possible target for preventing poorly differentiated prostate cancers. (c) 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18646186
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Fwd: Oral maxillofacial neoplasms in an East African population a 10 year retrospective study of 1863 cases using histopathological reports.



---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Fri, Jul 25, 2008 at 11:44 PM
Subject: Oral maxillofacial neoplasms in an East African population a 10 year retrospective study of 1863 cases using histopathological reports.
To: mesothelioma77@gmail.com


[1]BMC Oral Health. 2008 Jul 23; 8(1): 19
Kamulegeya A, Kalyanyama B

ABSTRACT: Introduction and objective Neoplasms of the oral maxillofacial area are an interesting entity characterized by differences in nomenclature and classification at different centers. We report neoplastic diagnoses seen at the departments of oral maxillofacial surgery of Muhimbili and Mulago referral hospitals in Tanzania and Uganda respectively over a 10 year period. METHODS: We retrieved histopathological reports archived at the departments of oral maxillofacial surgery of Muhimbili and Mulago referral hospitals in Tanzania and Uganda respectively over a 10 year period from June 1989-July 1999. RESULTS: In the period between June 1989 and July 1999, 565 and 1298 neoplastic oro-facial cases were retrieved of which 284 (50.53%) and 967 (74.54%) were malignant neoplasms at Muhimbili and Mulago hospitals respectively. Overall 67.28% of the diagnoses recorded were malignant with Kaposi's sarcoma (21.98%), Burkiits lymphoma (20.45%), and squamous cell carcinoma (15.22%) dominating that group while ameloblastoma (9.23%), fibromas (7.3%) and pleomorphic adenoma (4.95%) dominated the benign group. The high frequency of malignancies could be due to inclusion criteria and the clinical practice of selective histopathology investigation. However, it may also be due to higher chances of referrals in case of malignancies. CONCLUSION: There is need to reexamine the slides in these two centers in order to bring them in line with the most recent WHO classification so as to allow for comparison with reports from else where.



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Source: http://www.hubmed.org/display.cgi?uids=18651958
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Fwd: Body mass index and cancer risk in Korean men and women.



---------- Forwarded message ----------
From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Fri, Jul 25, 2008 at 11:44 PM
Subject: Body mass index and cancer risk in Korean men and women.
To: mesothelioma77@gmail.com


[1]Int J Cancer. 2008 Jul 23;
Jee SH, Yun JE, Park EJ, Cho ER, Park IS, Sull JW, Ohrr H, Samet JM

Obesity is associated with diverse health risks, but the role of body weight (BMI) as a risk factor for all and site-specific cancers remains controversial and risks for cancer associated with obesity have not been well-characterized in Asians. Body weight and risk for cancer were examined in a 14-year prospective cohort study of 1,213,829 Koreans aged 30-95 years insured by the National Health Insurance Corporation who had a biennial medical evaluation in 1992-1995. Incidence rates for all cancers and site-specific cancers were examined in relation to BMI. Age- and smoking-status adjusted hazard ratios (HR) with 95% confidence intervals (CI) were examined using the Cox proportional hazards model. For both sexes, the average baseline BMI was 23.2 kg/m(2), and the association of risk for all-cancers with BMI was positive. Obese men (BMI >/= 30 kg/m(2)) were at increased risk for developing the following cancers: stomach (1.31, 1.05-1.64), colon (1.42, 1.02-1.98), liver (1.63, 1.27-2.10) and gallbladder (1.65, 1.11-2.44). Obese women (BMI >/= 30 kg/m(2)) were at increased risk for developing liver cancer (1.39, 1.00-1.94), pancreatic cancer (1.80, 1.14-2.86) and breast cancer among women aged >/=50 years old (1.38, 1.00-1.90). The HRs were comparable in never and ever smokers for all cancers and all specific sites except for lung cancer. For all cancers common to both sexes, the association was significantly weaker (p

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Source: http://www.hubmed.org/display.cgi?uids=18651571
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Fwd: Molecular analysis of t(15;17) genomic breakpoints in secondary acute promyelocytic leukemia arising after treatment of multiple sclerosis.



---------- Forwarded message ----------
From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Fri, Jul 25, 2008 at 11:44 PM
Subject: Molecular analysis of t(15;17) genomic breakpoints in secondary acute promyelocytic leukemia arising after treatment of multiple sclerosis.
To: mesothelioma77@gmail.com


[1]Blood. 2008 Jul 23;
Hasan SK, Mays AN, Ottone T, Ledda A, La Nasa G, Cattaneo C, Borlenghi E, Melillo L, Montefusco E, Cervera J, Stephen C, Satchi G, Lennard A, Libura M, Byl JA, Osheroff N, Amadori S, Felix CA, Voso MT, Sperr WR, Esteve J, Sanz MA, Grimwade D, Lo-Coco F

Therapy-related acute promyelocytic leukemia (t-APL) with the t(15;17) translocation is a well-recognized complication of cancer treatment with agents targeting topoisomerase II. However, cases are emerging following mitoxantrone therapy for multiple sclerosis (MS). Analysis of 12 cases of mitoxantrone-related t-APL in MS patients revealed an altered distribution of chromosome 15 breakpoints compared to de novo APL, biased towards disruption within PML intron 6 (11/12, 92% vs 622/1022, 61%: p=0.035). Despite this intron spanning approximately 1kb, the breakpoint in five mitoxantrone-treated patients fell within an 8bp region (1482-9) corresponding to the "hotspot" previously reported in t-APL complicating mitoxantrone-containing breast cancer therapy. Another shared breakpoint was identified within the approximately 17kb RARA intron 2 involving two t-APL cases arising after mitoxantrone treatment for MS and breast cancer, respectively. Analysis of PML and RARA genomic breakpoints in functional assays in 4 cases, including the shared RARA intron 2 breakpoint at 14446-49, confirmed each to be preferential sites of topoisomerase IIalpha-mediated DNA cleavage in the presence of mitoxantrone. This study further supports the presence of preferential sites of DNA damage induced by mitoxantrone in PML and RARA genes that may underlie the propensity to develop this particular subtype of leukemia following exposure to this agent.



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Source: http://www.hubmed.org/display.cgi?uids=18650449
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Fwd: A case of plasmacytoma of the breast mimicking an inflammatory carcinoma.



---------- Forwarded message ----------
From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Fri, Jul 25, 2008 at 11:44 PM
Subject: A case of plasmacytoma of the breast mimicking an inflammatory carcinoma.
To: mesothelioma77@gmail.com


[1]Clin Lymphoma Myeloma. 2008 Jun; 8(3): 191-2
Gupta A, Kumar L, Aaron M

A 42-year-old woman presented to our institution with asymptomatic swelling of the left breast for the previous 6 months along with pathologic fractures in the right humerus and the left femur for the past 2 months. Radiology revealed multiple lytic lesions throughout the skeletal system. The breast swelling was approximately 6 cm x 6 cm. The swelling was cystic-to-firm in consistency, with ill-defined margins. The skin overlying the swelling was red and had a peau d'orange appearance. There was no nipple discharge or lymphadenopathy. A differential diagnosis of breast carcinoma with multiple bone secondaries, carcinoma of unknown primary origin with breast abscess, or breast secondary or a plasmacytoma with multiple myeloma was made. Fine-needle aspiration cytology revealed sheets of immature and mature plasma cells, suggesting that it was a plasmacytoma.



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Source: http://www.hubmed.org/display.cgi?uids=18650186
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