Kamis, 13 November 2014

Mesothelioma From Metastatic Adenocarcinoma

Another interesting study is known as, Worth of the Mesothelium-Connected Antibodies Thrombomodulin, Cytokeratin 5/6, Calretinin, and CD44H in Distinguishing Epithelioid Pleural Mesothelioma cancer from Adenocarcinoma Metastatic towards the Pleura by P M Cury M.D., D N Butchers, C Fisher M.D., B Corrin M.D. along with a G Nicholson D.M. - Mod Pathol 200013(2):107112. Here's an excerpt: Abstract - Until lately, the conventional approach on most labs in distinguishing epithelioid pleural mesothelioma cancer from metastatic adenocarcinoma continues to be an adverse derive from a panel of adeno-carcinoma-connected antibodies. However, several "mesothelium-connected" antibodies happen to be suggested as helpful in cases like this, and that we have applied four of those putative mesothelioma cancer markersthrombomodulin, cytokeratin 5/6, calretinin, and CD44Hto a number of 61 epithelioid pleural mesotheliomas and 63 metastatic adenocarcinomas with known primary sites (lung = 19 breast = 21 ovary = 6 colon = 10 kidney = 4 uterus, epididymis, pancreas = 1 situation each). From the mesotheliomas, 55 of 61 (90%) stained for thrombomodulin, 56 of 61 (92%) for cytokeratin 5/6, 47 of 51 cases (92%) were positive for calretinin, and 39 of 43 (91%) were positive for CD44H. From the metastatic adenocarcinomas, 12 of 63 (19%) cases were positive for thrombomodulin, 9 of 63 (14%) were positive for CK5/6, and 27 of 60 (45%) were positive for CD44H. With calretinin, only one situation of 59 (2%) demonstrated positive nuclear discoloration. All antibodies stained reactive mesothelium thrombomodulin also stained endothelium and CD44H variably stained lymphocytes, macrophages, and fibroblasts. We conclude that four antibodies show high sensitivity for epithelioid mesothelioma cancer, only calretinin (98%), cytokeratin 5/6 (86%), and thrombomodulin (81%) show sufficient specificity for practical use in cases like this.

Another interesting study is known as, Surgical procedure of pleural Mesothelioma cancer by PM McCormack, F Nagasaki, Baloney Hilaris and N Martini - The Journal of Thoracic and Cardiovascular Surgery, Vol 84, 834-842. Here's an excerpt: From 1939 through 1981, 170 patients were seen and treated for pleural mesothelioma cancer. Twenty-one growths were benign, 47 were fibrosarcomatous, and 102 were epithelioma. Resection was the primary mode of treatment in benign and fibrosarcomatous mesothelioma cancer. Management of diffuse epithelial mesothelioma cancer presented the finest challenge. Surgical therapy, radiotherapy, and chemotherapy were utilized in combination during these patients. Review in our patients treated just before 1972 had proven no take advantage of including lung resection within the surgical procedure of those growths. Since that time, all patients with diffuse mesothelioma cancer were treated by pleurectomy without lung resection. Both internal and exterior radiotherapy were also accustomed to enhance local control. Forty-nine percent of patients with epithelial mesothelioma cancer resided 12 months. The median survival in patients whose disease was controlled by these techniques was 21 several weeks. Regardless of the poor prognosis in malignant mesothelioma cancer, better controlled by these techniques was 21 several weeks. .

Another interesting study is known as, RB protein status and clinical correlation from 171 cell lines representing cancer of the lung, extrapulmonary small cell carcinoma, and mesothelioma cancer. By Shimizu E, Coxon A, Otterson GA, Steinberg SM, Kratzke RA, Kim YW, Fedorko J, Oie H, Manley BE, Mulshine JL, et al. - National Cancer Institute-Navy Oncology Branch, National Cancer Institute, Bethesda, Maryland 20889. - Oncogene. 1994 Sep9(9):2441-8. Here's an excerpt: Abstract - We've analyzed RB protein expression in 171 cell lines produced from patients with small cell cancer of the lung (SCLC), non-small cell cancer of the lung (NSCLC), lung carcinoid, mesothelioma cancer, and extrapulmonary small cell cancer (EPSC) and also have correlated this data with clinical outcome. We detected absent or aberrant RB protein expression in 66/75 SCLC, 12/80 NSCLC, 1/6 carcinoid, /5 mesothelioma cancer, and 4/5 EPSC samples. Additionally, we observed integration of human papilloma virus (Warts) DNA within the single EPSC cell line that maintained wildtype RB protein. We didn't identify integration of Warts, SV40 or adenoviral DNA in other tumor samples with wildtype RB status. We noted a reliable, hypophosphorylated mutant RB in 12 SCLC and three NSCLC samples which may have been wrongly construed as wildtype by current immunohistochemical techniques. Research into the matched up clinical data demonstrated no associations between RB status and age, sex, extent of disease, performance status, smoking history, and former treatment. Additionally, retrospective analyses demonstrated no consistent correlation of RB protein expression with either best clinical response, overall survival, or perhaps in vitro chemotherapeutic drug sensitivity. The stable expression of RB after gene transfection into RB(-) SCLC cells, however, led to a trend toward elevated in vitro potential to deal with etoposide, cisplatin and doxorubicin.

All of us owe a personal debt of gratitude to those fine scientists. Should you found these excerpts interesting, please browse the studies within their whole.

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