Another interesting study is known as, Induction of mesothelioma cancer in p53 mouse by intraperitoneal use of multi-wall carbon nanotube by Atsuya Takagi, Akihiko Hirose, Tetsuji Nishimura, Nobutaka Fukumori, Akio Ogata, Norio Ohashi, Satoshi Kitajima and Jun Kanno - The Journal of Toxicological Sciences Vol. 33 (2008) , No. 1 Feb 105-116. Here's an excerpt: ABSTRACT- Nanomaterials of carbon origin have a tendency to form various shapes of contaminants in micrometer dimensions. Included in this, multi-wall carbon nanotubes (MWCNT) form " floating " fibrous or fishing rod-formed contaminants of length around 10-20 micrometers by having an aspect ratio in excess of three. " floating " fibrous contaminants of the dimension including asbestos plus some guy-made materials are considered to be cancer causing, typically inducing mesothelioma cancer. Ideas are convinced that MWCNT induces mesothelioma cancer together with an optimistic control, crocidolite (blue asbestos), when given intraperitoneally to p53 heterozygous rodents which have been considered to be responsive to asbestos. Our results explain the chance that carbon-made " floating " fibrous or fishing rod-formed micrometer contaminants may share the cancer causing systems postulated for asbestos. To keep seem activity of industrialization of nanomaterials, it might be prudent to apply methods to help keep good charge of contact with " floating " fibrous or fishing rod-formed carbon materials in the place of work and later on market before the biological/ cancer causing qualities, especially of the lengthy-term biodurability, are fully evaluated.
One interesting study is known as, Inactivation of p16INK4a expression in malignant mesothelioma cancer by methylation. By Wong L, Zhou J, Anderson D, Kratzke RA. - Research Service, Ontario Veterans administration Clinic, Ontario, MN, USA - Cancer Of The Lung. 2002 Nov38(2):131-6. Here's an excerpt: Abstract - The molecular systems of oncogenesis in mesothelioma cancer involve losing negative government bodies of cell growth including p16(INK4a). Lack of expression from the p16(INK4a) gene method is showed in almost all mesothelioma cancer growths and cell lines examined up to now. Lack of p16(INK4a) expression has additionally been frequently noticed in more prevalent neoplasms for example cancer of the lung too. In a multitude of these malignancies, including cancer of the lung, p16(INK4a) expression is proven to be inactivated by hypermethylation from the first exon. Inside a survey of ten mesothelioma cancer cell lines, one cell line (NCI-H2596) was recognized as having lack of p16(INK4a) gene product following gene methylation. This methylation during these mesothelioma cancer cells might be corrected, leading to re-expression of p16(INK4a) protein, following treating cells with cytidine analogs, that are known inhibitors of DNA methylation. In the past clinical tests in mesothelioma cancer, the cytidine analog dihydro-5-azacytidine (DHAC) has been discovered to induce clinical reactions in roughly 17% of patients with mesothelioma cancer given this drug, including prolonged complete reactions. Additionally, we recognized evidence for methylation of p16(INK4a) in three of 11 resected mesothelioma cancer tumor samples. When both cell lines and growths are combined, inactivation of p16(INK4a) gene product expression following DNA hypermethylation was discovered in four of 21 samples (19%). We're further going through the clinical value of inhibition of methylation in mesothelioma cancer by cytidine analogs. This might give a potential treatment target in certain mesothelioma cancer growths by inhibition of methylation.
One interesting study is known as, Immunohistochemistry within the among malignant mesothelioma cancer and lung adenocarcinoma: a vital evaluation of recent antibodies with a S Abutaily, B J Addis, W R Roche - J Clin Pathol 200255:662-668 Here's an excerpt: Abstract - Goal: The need for immunohistochemical discoloration in distinguishing between malignant mesothelioma cancer and lung adenocarcinoma was re-examined using recently available commercial antibodies, using the goal of growing the sensitivity and specificity of diagnosis, and simplifying the antibody panel needed.
Techniques: Forty one malignant mesotheliomas and 35 lung adenocarcinomas were analyzed. Commercial antibodies to calretinin, E-cadherin, N-cadherin, surfactant apoprotein A (SP-A), thyroid transcription factor 1 (TTF-1), thrombomodulin, and cytokeratin 5/6 were applied while using streptavidinbiotinperoxidase complex procedure on formalin fixed, paraffin wax embedded tissue. Results: E-cadherin was expressed in most adenocarcinomas as well as in 22% from the mesotheliomas. TTF-1 expression was detected in 69% from the adenocarcinomas and no mesotheliomas. Positive discoloration with polyclonal anticalretinin was detected in 80% from the mesotheliomas and 6% from the adenocarcinomas. N-cadherin was expressed in 78% of mesotheliomas and 26% of adenocarcinomas. Thrombomodulin was expressed in 6% from the adenocarcinomas as well as in 53% from the mesotheliomas. Cytokeratin 5/6 expression was detected in 6% from the adenocarcinomas and 63% from the mesotheliomas. The outcomes were in comparison using the standard laboratory panel for mesothelioma cancer diagnosis: anticarcinoembryonic antigen (anti-CEA), LeuM1, BerEP4, and HBME-1.
Conclusion: From the antibodies utilized in this research, E-cadherin was 100% sensitive for lung adenocarcinoma and TTF-1 was 100% specific for lung adenocarcinoma. The use of both of these antibodies alone was sufficient for detecting 69% of adenocarcinomas and 78% of mesotheliomas. Where TTF-1 is negative and E-cadherin is positive, another panel of antibodies, including BerEP4 and LeuM1 (CD15) and antibodies directed against CEA, calretinin, cytokeratin 5/6, thrombomodulin, and N-cadherin, is needed for differentiation between malignant mesothelioma cancer and lung adenocarcinoma.
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