Advances in Malignant Mesothelioma

Robinson, B. W.; Lake, Richard

doi:10.1056/nejmra050152

Cited by 971 publications

(843 citation statements)

References 70 publications

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“…Asbestos-induced mesothelioma is still an annoying social problem in many countries (4,7). Considering the long incubation period of 30 to 40 years, there is a possibility to conduct certain preventive interventions especially for the high-risk population after asbestos exposure.…”

Section: Discussionmentioning

confidence: 99%

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Deferasirox Induces Mesenchymal–Epithelial Transition in Crocidolite-Induced Mesothelial Carcinogenesis in Rats

Nagai

Okazaki

Chew

et al. 2013

Cancer Prevention Research

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Asbestos was used worldwide in huge quantities in the past century. However, because of the unexpected carcinogenicity to mesothelial cells with an extremely long incubation period, many countries face this long-lasting social problem. Mesothelioma is often diagnosed in an advanced stage, for which no effective therapeutic protocols are yet established. We previously reported on the basis of animal experiments that the major pathology in asbestos-induced mesothelial carcinogenesis is local iron overload. Here, we undertook to find an effective strategy to prevent, delay, or lower the malignant potential of mesothelioma during asbestos-induced carcinogenesis. We used intraperitoneal injections of crocidolite to rats. We carried out a 16-week study to seek the maximal-tolerated intervention for iron reduction via oral deferasirox administration or intensive phlebotomy. Splenic iron deposition was significantly decreased with either method, and we found that Perls' iron staining in spleen is a good indicator for iron reduction. We injected a total of 10 mg crocidolite at the age of six weeks, and the preventive measures were via repeated oral administration of 25 to 50 mg/kg/d deferasirox or weekly to bimonthly phlebotomy of 4 to 10 mL/kg/d. The animals were observed until 110 weeks. Deferasirox administration significantly increased the fraction of less malignant epithelioid subtype. Although we found a slightly prolonged survival in deferasirox-treated female rats, larger sample size and refinement of the current protocol are necessary to deduce the cancer-preventive effects of deferasirox. Still, our results suggest deferasirox serves as a potential preventive strategy in people already exposed to asbestos via iron reduction. Cancer Prev Res; 6(11); 1222-30. Ó2013 AACR.

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Section: Discussionmentioning

confidence: 99%

“…Because of the long latency period (30-40 years) after asbestos exposure, the number of patients with mesothelioma is estimated to increase in most of the countries. In Japan, the number of the patients will peak in 2025 and 100,000 new patients are expected in the coming 40 years (7).…”

Section: Introductionmentioning

confidence: 99%

Deferasirox Induces Mesenchymal–Epithelial Transition in Crocidolite-Induced Mesothelial Carcinogenesis in Rats

Nagai

Okazaki

Chew

et al. 2013

Cancer Prevention Research

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“…21 Considering the long latency period of mesothelioma, the incidence is expected to increase further in the coming decades. 36 …”

Section: Asbestos Fibersmentioning

confidence: 99%

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

Okada

2007

Intl Journal of Cancer

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Foreign-body-induced carcinogenesis is a traditional, maybe old, way of understanding cancer development. A number of novel approaches are available today to elucidate cancer development. However, there are things we learn from the old, and thus I bring out some examples of various clinical cases and experimental models of foreign-body-induced tumorigenesis. What is notable is that the foreign bodies themselves are unrelated to each other, whereas commonly underlying in them is to induce inflammatory reaction, especially stromal proliferation, where those exogenous materials are incorporated and undigested. Such foreign-body-induced carcinogenesis is also recognized in the step of tumor progression, the final step of carcinogenesis that tumor cells acquire malignant phenotypes including metastatic properties. And the phenomenon is universally observed in several cell lines of different origins. In this review I would like to show the evidence that tumor development and progression are accelerated inevitably by inflammation caused from foreign bodies, and that reactive oxygen species derived from inflammatory cells are one of the most important genotoxic mediators to accelerate the process. ' 2007 Wiley-Liss, Inc.

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“…Approximately 80% of pleural MM cases are attributed to asbestos exposure, and the latency after exposure could be 20–60 years 2. Asbestos exposure, genetics, and other factors likely contribute to the etiology of pleural MM 3. Chrysotile, the major type of asbestos, was widely used for commercial purposes during the 20th century, which suggests that the number of mesothelioma cases will increase in the upcoming decades.…”

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confidence: 99%

miR‐30d is related to asbestos exposure and inhibits migration and invasion in NCI‐H2452 cells

Yin

et al. 2017

FEBS Open Bio

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Pleural malignant mesothelioma (MM) is a highly aggressive tumor that is typically related to asbestos exposure and has a latency of 20–60 years. Several microRNA contribute to MM initiation and progression, but the mechanisms are not clear. Here, we found that miR‐30d is downregulated in the pleural MM cell line NCI‐H2452, in the plasma of asbestos‐exposed individuals, and in asbestos‐exposed mesothelial cells. Furthermore, we investigated the influence of the overexpression of miR‐30d in pleural MM cells. We demonstrated that miR‐30d overexpression could suppress pleural MM cell proliferation, migration, and invasion in vitro and could promote cell apoptosis but could not significantly influence cell cycle. The mRNA and protein expression of vimentin and TWIST1 decreased, and the mRNA expression of CDH1 increased in NCI‐H2452 cells that overexpressed miR‐30d. We therefore conclude that miR‐30d is related to asbestos exposure and inhibits cell migration and invasion by regulating the epithelial–mesenchymal transition in NCI‐H2452 cells.

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Advances in Malignant Mesothelioma

Cited by 971 publications

References 70 publications

Deferasirox Induces Mesenchymal–Epithelial Transition in Crocidolite-Induced Mesothelial Carcinogenesis in Rats

Deferasirox Induces Mesenchymal–Epithelial Transition in Crocidolite-Induced Mesothelial Carcinogenesis in Rats

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

miR‐30d is related to asbestos exposure and inhibits migration and invasion in NCI‐H2452 cells

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