Archive for the ‘Cystic Mesothelioma’ Category

Asbsestos Related Diseases Non-Gynaecological Cancers and Some Benign Diseases

Asbsestos Related Diseases Non-Gynaecological Cancers and Some Benign Diseases

Tumor Biology – Vol. 17, No. 1, 1996  by Assoc. Prof. Halis Simsek, MD, Section of Gastroenterology, Hacettepe University Medical School, Resat Nuri sokak No: 21/13, Yukariayranci, Ankara, 06100 (Turkey).  Here is an excerpt: “Abstract – Elevated levels of CA 125 have been shown to be present in the serum of patients with ovarian carcinoma, non-gynaecological cancers and some benign diseases. However, the value of CA 125 in malignant peritoneal mesothelioma has not been studied in detail. Therefore, 7 patients with diffuse malignant mesothelioma were included in this study. Median age was 52.4 (range 16-73), and 6 of them were women. The mean serum CA 125 level was 308kU/l (range 8-1,300 kU/1). Serum CA 125 concentrations were found to be elevated in all 6 female patients. In 3 patients, serum CA 125 levels were followed prospectively and showed a very close correlation with the response to chemotherapy. In 2 responder patients, initially elevated CA 125 levels returned to normal during remission after chemotherapy. In 1 non-responder patient, the serum CA 125 level continued to rise. In conclusion, the serum CA 125 level might be helpful in the diagnosis and follow-up of malignant peritoneal mesothelioma.”

Another interesting study is called, “High-performance capillary electrophoretic analysis of hyaluronan in effusions from human malignant Mesothelioma” – Journal of Chromatography B: Biomedical Sciences and Applications – Volume 697, Issues 1-2, 12 September 1997, Pages 277-281 by Nikos K. Karamanosa and Anders Hjerpeb – Here is an excerpt: “Abstract – A procedure to quantify hyaluronan in effusions from human malignant mesothelioma using a highly sensitive and reproducible high-performance capillary electrophoresis (HPCE) method is presented. Following ethanol precipitation, hyaluronan and galactosaminoglycans were degraded to Δ4.5-dissacharides with a mixture of chondroitinases ABC and AC. Heparan sulphate and proteins/glycoproteins were separated by ultrafiltration on a Centricon 3 membrane, and hyaluronan-derived disaccharides were analysed by direct injection of the filtrate into a HPCE system. Determination of hyaluronan in effusions from five healthy individuals and three patients with mesothelioma gave values comparable to those found using the HPLC method. One of the advantages of the HPCE method as compared to HPLC is the low solvent consumption. The much lower detection limit (attomole level) of the HPCE method may also allow the analysis of hyaluronan content in serum. The contribution of HPCE in diagnosis of a neoplasm, such as human malignant mesothelioma, illustrates the great potential of this technique in the field of life sciences.”

Another interesting study is called, “Protein expression of the RB-related gene family and SV40 large T antigen in mesothelioma and lung cancer” – Nature Publishing Group, Basingstoke, ROYAUME-UNI  (1987) (Revue).  Here is an excerpt: “Abstract – Mutational inactivation of the RB-related gene RBL2/ p130 has been reported as a common and important prognostic factor in human lung cancer. To examine the role of the RB-related gene family in lung cancer we analysed the protein expression of the RB gene in cell lines obtained from 83 patients with small cell lung cancer (SCLC) and 114 patients with non-SCLC that included 21 novel lung tumor samples. While we detected five new SCLC with mutant RB [removed]RB inactivation in 75/83; 90.4%), we did not detect any RB mutations in the new non-SCLC cell lines (RB inactivation in 13/114 non-SCLC and mesothelioma; 11.4%). In addition, we detected expression of a full-length RBL1/p107 and RBL2/p130 species in every sample tested (RBL1 or RBL2 inactivation in 0/69) and confirmed that both RB-related gene products retain functional binding activity to the E1A viral oncoprotein. Since expression of SV40 Large T antigen (Tag) has been reported in a subset of human lung tumors where it may inactivate RBL1 and RBL2, we also examined mesothelioma and non-mesothelioma lung tumors for Tag expression. Although we detected a faint 85 kDa protein species using specific anti-Tag antibodies, this signal migrated slightly faster than Tag extracted from Cos7 cells and did not exhibit binding activity to the RB or RBL1 proteins. Finally, we subjected 11 lung cancer cell lines to nucleotide sequencing and did not detect mutations within the C-terminal RBL2 exons 19-22 as recently reported. While the RB/p16 tumor suppressor pathway is targeted for mutations in 100% of lung cancers, mutational inactivation of the related RBL1 and RBL2 genes is a rare event.”

Another interesting study is called, “Benign cystic mesothelioma involving the female genital tract: report of four cases” by Schneider V, Partridge JR, Gutierrez F, Hurt WG, Maizels MS, Demay RM. – Am J Obstet Gynecol. 1983 Feb 1;145(3):355-9.  Here is an excerpt: “Abstract – Four cases of benign cystic mesothelioma are described. The disease affects young white women (mean age, 30 years), and they present with chronic pelvic pain. At laparoscopy or laparotomy, multiple cysts ranging in size from 0.5 to 4 cm in diameter and containing clear fluid are seen. The disease commonly affects the pelvic organs and/or omentum. With the electron microscope, the cell of origin of this proliferative process is shown to be the mesothelial cell. The disease has been previously described under a variety of terms. There seems to be a tendency for recurrence, but no malignant potential is apparent. Treatment may be conservative with preservation of pelvic organs. Benign cystic mesothelioma should be considered in the differential diagnosis of cystic lesions of the female genital tract.”

Another interesting study is called, “Monoclonal antibody Ber-EP4: Its use in the differential diagnosis of malignant mesothelioma and carcinoma in cell blocks of malignant effusions and FNA specimens” by Dr. Brigid Maguire M.B.B.S., Darrel Whitaker Ph.D., C.F.I.A.C., F.I.M.L.S., A.A.I.M.S., Salvatore Carrello B.App.Sc., Dominic Spagnolo M.B.B.S., F.R.C.P.A. – Diagnostic Cytopathology – Volume 10, Issue 2, pages 130–134, March 1994.  Here is an excerpt: “Abstract – Formal sublimate-fixed cell blocks derived from 129 malignant pleural (and some peritoneal) effusions, 8 benign effusions with reactive mesothelial cells, and 23 FNA specimens, were immunostained with monoclonal antibody Ber-EP4 to assess its ability to distinguish malignant mesothelioma (MM) from carcinoma.

Only 2 of 44 (4%) well-characterized MM were Ber-EP4+, while none of 8 benign mesothelial proliferations reacted with the antibody. Fifty-seven percent of 23 pulmonary adenocarcinomas (AC) and 60% of 43 pulmonary carcinomas of all other histological types were Ber-EP4+. Of 40 metastatic AC originating from breast, gastrointestinal tract, ovary, endometrium, and kidney, 80% were Ber-EP4+. The predictive value of positive Ber-EP4 staining in distinguishing AC from MM was 96%. The predictive value of a negative Ber-EP4 in excluding MM was 70%, when the differential diagnosis was adenocarcinoma. These results suggest that Ber-EP4 is helpful in differentiating MM and AC if used together with other discriminating antibodies.”

We all owe a debt of gratitude to these fine researchers.  If you found any of these excerpts interesting, please read the studies in their entirety.

Monty Wrobleski is the author of this article.  For more information please click on the following links

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Asbestos and Inactive Mesothelioma Cells

Asbestos and Inactive Mesothelioma Cells

One interesting study is called, “c-Jun N-terminal Kinase Contributes to Apoptotic Synergy Induced by Tumor Necrosis Factor-related Apoptosis-inducing Ligand plus DNA Damage in Chemoresistant, p53 Inactive Mesothelioma Cells” by Claire Vivo, Weihong Liu and V. Courtney Broaddus – July 11, 2003 The Journal of Biological Chemistry, 278, 25461-25467.  Here is an excerpt: “Abstract – Apoptotic resistance of cancer cells may be overcome by the combination of treatments that activate the two major apoptotic pathways: (i) the death receptor pathway activated by death ligands and (ii) the DNA damage pathway activated by chemotherapy. We have previously shown that mesothelioma cells, resistant to most treatments, are sensitive to the combination of the death ligand tumor necrosis factor-related apoptosis inducing ligand (TRAIL/Apo2L) plus chemotherapy. We investigated a possible role for c-Jun N-terminal kinase (JNK) in the synergistic effect, knowing that JNK can be activated separately by TRAIL and by DNA damage. We chose to study the M28 and REN human mesothelioma cell lines, which are p53-inactivated, to avoid an interaction between p53 and JNK. We showed that JNK was activated by TRAIL and by etoposide and that the activation was enhanced by the combination of the two treatments. We found this activation to be caspase-independent. To inhibit the JNK pathway, we used either dominant-negative constructs of JNK1 and JNK2 (compared with dominant-negative caspase 9) or a chemical inhibitor of the JNK pathway (SP600125). In cells treated with TRAIL plus etoposide, JNK inhibition increased cell survival and decreased apoptosis significantly. In transfected M28 cells, the effect of JNK inhibition was as great as that of the dominant-negative caspase 9 construct. We conclude that JNK contributes to the synergistic effect of TRAIL combined with DNA damage by mediating signals independent of p53 leading to apoptosis.

Previous SectionNext SectionDefects in normal apoptotic programs contribute to the formation of tumors (1) and interfere with the tumor response to conventional therapy (2, 3). Abnormal apoptotic responses may arise from defective apoptotic machinery, as by mutation in p53 or up-regulation of anti-apoptotic Bcl-2 (B-cell lymphoma-2), which provide both a survival advantage and resistance to therapy (4). Among strategies to bypass sites of apoptotic resistance are the use of death receptor ligands that can directly engage the apoptotic caspases of the cell. Indeed, one death receptor ligand, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L),1 appears to have selective activity toward transformed or malignant cells (,5). In some cases, the action of TRAIL and other death ligands can be enhanced significantly by concomitant DNA damage resulting in a synergistic apoptotic response. Although this synergistic apoptosis has been described in many tumor cells (6), the mechanism is not yet understood. Understanding the mechanism of synergy between two different apoptotic stimuli that effectively bypass sites of apoptotic resistance may provide insights into more effective anti-tumor approaches.”

Another interesting study is called, “Peritoneal cystic mesothelioma: A case series” –
Piensero Scientifico, Roma, ITALIE  (1911) (Revue) 2003, vol. 89, no1, pp. 31-35.  Here is an excerpt: “Abstract – Background: Cystic peritoneal mesothelioma is a rare disease associated with a favorable short-term prognosis. Longer follow-up documenting a persistence of symptoms and a high rate of recurrence after debulking surgery along with an uncertain natural history prompt a re-valuation of prior treatment recommendations. No prior long-term clinical study of these patients is available. Methods: The experience with five cases of cystic peritoneal mesothelioma, four females and one male, are reviewed. All of these patients were treated with cytoreductive surgery with peritonectomy procedures and heated Intraoperative intraperitoneal chemotherapy. CT, pathology and current status were investigated in order to learn more about the natural history of this disease. Results: All patients were symptomatic from abdominal distention and three of the four complained of severe pain. Female patients complained of long periods of recurrent abdominal and pelvic pain poorly managed by oral analgesics. In one patient prolonged conservative management over ten years resulted in transition to an invasive process with extensive lymph nodal metastases. Her prognosis for long-term survival Is guarded because of mesothelioma extension Into the chest. Disease control of both ascltes and pain In the abdomen and pelvis was achieved In all five patients treated with cytoreductive surgery plus intraperitoneal chemotherapy. Conclusions: Cystic peritoneal mesothelioma should no longer be referred to as “benign” cystic mesothelloma. An aggressive approach with complete disease eradication is the correct goal of treatment. From our experience, cytoreductive surgery to remove all visible tumor and intraperitoneal chemotherapy to control microscopic residual disease will help patients with peritoneal cystic mesothelioma to remain symptom- and disease-free over an extended time period with a single surgical intervention. Disease eradication may prevent the transition to an aggressive and fatal disease process.”

Monty Wrobleski is the author of this article.  For more information please click on the following links

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Malignant Mesothelioma


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