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Fw: Canadian cancer statistics at a glance: mesothelioma.

Mesothelioma Diagnosis...

Mesothelioma diagnosis in this disease, malignant cells develop in the mesothelium, a protective lining that covers transcendently of the spread's internal organs. Greatest malignant mesothelioma set up complex karyotypes, with extensive aneuploidy and rearrangement of tons chromosomes.

Symptoms of mesothelioma may not appear until 20 to 50 years after exposure to asbestos. Mesothelioma diagnosis is often difficult, because the symptoms are similar to those of a number of other conditions. A history of exposure to asbestos may increase clinical suspicion for mesothelioma. A physical examination is performed, followed by chest X-ray and often lung function tests. The X-ray may reveal pleural thickening commonly seen after asbestos exposure if mesothelioma diagnosis is done.

If the cancer has length beyond the mesothelium to other parts of the size, symptoms may include pain, trouble swallowing, or swelling of the neck or engage.

Symptoms of peritoneal mesothelioma include weight loss and cachexia, abdominal swelling and suffering due to ascites (a buildup of fluid in the abdominal cavity). Exposure to airborne asbestos particles increases one's risk of developing malignant mesothelioma.

Mesothelioma diagnosis of malignant mesothelioma has a peak incidence 35-45 years after asbestos exposure. Malignant mesothelioma is a rare type of cancer in which malignant cells are found in the sac lining the chest or abdomen. Most people with malignant mesothelioma have on worked on jobs where they breathed asbestos.

It can also occur in children; however, these cases are not thought to be associated with asbestos exposure.

----- Forwarded Message ----
From: HubMed - mesothelioma <rssfwd@rssfwd.com>
To: shell8377@yahoo.com
Sent: Thursday, March 13, 2008 11:06:01 AM
Subject: Canadian cancer statistics at a glance: mesothelioma.

[1]CMAJ. 2008 Mar 11; 178(6): 677-8
Marrett LD, Ellison LF, Dryer D

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Source: http://www.hubmed.org/display.cgi?uids=18332380
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Fw: Expression of cell adhesion molecule 1 in malignant pleural mesothelioma as a cause of efficient adhesion and growth on mesothelium.

----- Forwarded Message ----
From: HubMed - mesothelioma <rssfwd@rssfwd.com>
To: shell8377@yahoo.com
Sent: Thursday, March 13, 2008 11:06:01 AM
Subject: Expression of cell adhesion molecule 1 in malignant pleural mesothelioma as a cause of efficient adhesion and growth on mesothelium.

[1]Lab Invest. 2008 Mar 10;
Ito A, Hagiyama M, Mimura T, Matsumoto M, Wakayama T, Iseki S, Yokozaki H, Okada M

Cell adhesion molecule 1 (CADM1), formerly referred to as SgIGSF, TSLC1, or Necl-2, has been characterized as a mast-cell adhesion molecule that mediates efficient interactions with mesothelial cells. Here, we examined whether CADM1 might be involved in the diffuse tumor growth over the pleural surface that characterizes malignant pleural mesothelioma (MPM). Immunohistochemical and western blot analyses revealed that 14 (25%) of 57 MPMs expressed the full-length form of CADM1 on the cell membrane, but non-neoplastic mesothelial cells did not express it at all. The majority of available MPM cell lines also expressed the full-length form of CADM1. We compared CADM1-positive and -negative MPM cells in culture within soft agar and in coculture on mesothelial or fibroblastic monolayers. Within soft agar, CADM1-negative MPM cells were capable of forming colonies, whereas CADM1-positive cells were not, suggesting that CADM1 is a potential tumor suppressor of MPM, consistent with the past characterization of this molecule in other types of tumors. However, in coculture on mesothelial cell monolayers lacking full-length CADM1, CADM1-positive MPM cells spread more widely and grew more quickly, whereas the CADM1-negative cells piled up. Transfection of the CADM1-negative cells with CADM1 cDNA caused them to behave like the CADM1-positive cells, with faster, more widespread growth. These phenotypic differences were not detectable in cocultures on lung fibroblastic monolayers, in which all MPM cells grew much more slowly than on mesothelial cells, irrespective of CADM1 positivity. CADM1 thus appears to mediate efficient adhesion and growth of MPM cells specifically on mesothelial cells, probably via trans-heterophilic binding, and thus may be involved in the manifestation of a considerable subset of MPMs as diffusely growing tumors disseminated over the pleural surface.Laboratory Investigation advance online publication, 10 March 2008; doi:10.1038/labinvest.2008.15.

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Source: http://www.hubmed.org/display.cgi?uids=18332875
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Fw: Diagnostic importance of 9p21 homozygous deletion in malignant mesotheliomas.

----- Forwarded Message ----
From: HubMed - mesothelioma <rssfwd@rssfwd.com>
To: shell8377@yahoo.com
Sent: Tuesday, March 11, 2008 10:08:52 PM
Subject: Diagnostic importance of 9p21 homozygous deletion in malignant mesotheliomas.

[1]Mod Pathol. 2008 Mar 7;
Chiosea S, Krasinskas A, Cagle PT, Mitchell KA, Zander DS, Dacic S

Definitive diagnosis of malignant mesothelioma in small specimens can be extremely difficult based on morphology alone. Homozygous deletion of 9p21, the locus harboring the p16 gene, has been reported as the most common genetic alteration in malignant mesotheliomas. Recent studies demonstrated that this alteration may be useful for differentiating benign from malignant mesothelial proliferations in cytology specimens. The aim of this study was to evaluate the diagnostic utility of homozygous deletion of 9p21 assessed by fluorescence in situ hybridization (FISH) in mesothelial proliferations involving serosal surfaces in paraffin-embedded tissue. p16 protein immunoexpression was also explored as a potential diagnostic aid. FISH analysis demonstrated homozygous deletion of the 9p21 locus in 35 of 52 cases (67%) of pleural mesothelioma and in 5 of 20 cases of peritoneal mesothelioma (25%) (P

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Source: http://www.hubmed.org/display.cgi?uids=18327208
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Fwd: Mutation spectrum in HNPCC in the Israeli population.

---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Apr 6, 2008 at 12:45 PM
Subject: Mutation spectrum in HNPCC in the Israeli population.
To: mesothelioma77@gmail.com

[1]Fam Cancer. 2008 Apr 4;
Goldberg Y, Porat RM, Kedar I, Shochat C, Sagi M, Eilat A, Mendelson S, Hamburger T, Nissan A, Hubert A, Kadouri L, Pikarski E, Lerer I, Abeliovich D, Bercovich D, Peretz T

Hereditary non-polyposis colon cancer is caused by mutations in DNA mismatch repair genes. The mutation spectrum in the Israeli population is poorly documented except for the c.1906G>C Ashkenazi founder mutation in the hMSH2 gene. To report our experience in HNPCC screening, the mutations detected and the clinical features among a cohort of Israeli patients. Diagnostic work-up was done in a multi-step process guided by clinical and ethnic information. Tumors of suspected patients were tested for microsatellite instability and immunohistochemistry. Based on tumor analyses, we proceeded to mutation screening by DHPLC followed by sequence analysis and multiplex ligase dependent probe amplification. Ashkenazi Jews were first tested for the c.1906G>C founder mutation. Of the 240 families, 24, including Arabs and Jews from different ethnic origins, were tested positive. All tumors that lost expression of mismatch repair proteins also showed microsatellite instability. There was evidence for involvement of hMSH2 (15) hMLH1 (6) and hMSH6 (3) genes. Mutations were identified in 17/24 (71%) patients: 6 Ashkenazi families harbored the c.1906G>C mutation. Eleven other mutations (2 nonsense, 3 splice site and 6 small deletions) were detected. Three of the mutations are novel. No gross deletions or insertions were detected. This is the first report that characterizes the profile of HNPCC in a cohort of patients in Israel. Tumor testing indicated that the 3 main MMR genes are involved, and that mutation spectrum is broad.

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Source: http://www.hubmed.org/display.cgi?uids=18389388
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Fwd: Cascade genetic testing for mismatch repair gene mutations.

---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Apr 6, 2008 at 12:45 PM
Subject: Cascade genetic testing for mismatch repair gene mutations.
To: mesothelioma77@gmail.com

[1]Fam Cancer. 2008 Apr 4;
Mitchell RJ, Ferguson RK, Macdonald A, Dunlop MG, Campbell H, Porteous ME

Mismatch repair gene mutation carriers have a high risk of developing colorectal cancer, and can benefit from appropriate surveillance. A combined population based ascertainment cascade genetic testing approach provides a systematic and potentially effective strategy for identifying such carriers. We have developed a Markov Chain computer model system which simulates various factors influencing cascade genetic testing; including demographics, uptake, genetic epidemiology and family size. This was used to evaluate cascade genetic testing for mismatch repair gene mutations in theory and practice. Simulations focussed on the population of Scotland by way of illustration, and were based on a 20-year programme in which index cases were ascertained from colorectal cancer cases aged

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Source: http://www.hubmed.org/display.cgi?uids=18389387
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