Microscopic analysis of the chromium content in the chromium-induced malignant and premalignant bronchial lesions of the rat

Takahashi, Yûji; Kondo, Kazuya; Ishikawa, Sumiyo; Uchihara, Hiroshi; Fujino, Haruhiko; Sawada, Naruhiko; Miyoshi, Takanori; Shoji, Shuichi; Izumi, Kiyotaka; Monden, Yasumasa

doi:10.1016/j.envres.2004.10.001

Cited by 17 publications

(7 citation statements)

References 12 publications

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“…Here too, a potential involvement of PCP in tumour genesis cannot be ruled out because 58.3% of all subjects with adenocarcinoma with primary woodworking occupation were in contact with wood preservatives. The same applies to chromates that have been used for a long time in pickling solutions and are likewise classed as carcinogenic, also in connection with tumours of the nasal cavity and paranasal sinuses (Hernberg et al 1983;Levy et al 1986;Takahashi et al 2005). In fact, half of all participants with adenocarcinoma and primary woodworking occupation were in contact with pickling solutions.…”

Section: Discussionmentioning

confidence: 85%

Characterization of initial clinical symptoms and risk factors for sinonasal adenocarcinomas: results of a case–control study

Mayr

Hafizovic

Waldfahrer

et al. 2009

Int Arch Occup Environ Health

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Section: Discussionmentioning

confidence: 85%

Characterization of initial clinical symptoms and risk factors for sinonasal adenocarcinomas: results of a case–control study

Mayr

Hafizovic

Waldfahrer

et al. 2009

Int Arch Occup Environ Health

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“…Hexavalent chromium [Cr 6+ ] is widely accepted as a carcinogen and is associated with lung inflammation, kidney damage and nasal ulcers. 154 , 155 , 156 Recent studies have shown that Cr 6+ can induce EMT and cell invasion to promote oncogenic transformation in lung epithelial cells. This effect is closely linked with ROS accumulation induced by Cr 6+ .…”

Section: Targeting Redox-regulated Emt For Cancer Therapymentioning

confidence: 99%

Redox regulation in tumor cell epithelial–mesenchymal transition: molecular basis and therapeutic strategy

Jiang

Wang

Chen

et al. 2017

Sig Transduct Target Ther

160

133

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Epithelial–mesenchymal transition (EMT) is recognized as a driving force of cancer cell metastasis and drug resistance, two leading causes of cancer recurrence and cancer-related death. It is, therefore, logical in cancer therapy to target the EMT switch to prevent such cancer metastasis and recurrence. Previous reports have indicated that growth factors (such as epidermal growth factor and fibroblast growth factor) and cytokines (such as the transforming growth factor beta (TGF-β) family) are major stimulators of EMT. However, the mechanisms underlying EMT initiation and progression remain unclear. Recently, emerging evidence has suggested that reactive oxygen species (ROS), important cellular secondary messengers involved in diverse biological events in cancer cells, play essential roles in the EMT process in cancer cells by regulating extracellular matrix (ECM) remodeling, cytoskeleton remodeling, cell–cell junctions, and cell mobility. Thus, targeting EMT by manipulating the intracellular redox status may hold promise for cancer therapy. Herein, we will address recent advances in redox biology involved in the EMT process in cancer cells, which will contribute to the development of novel therapeutic strategies by targeting redox-regulated EMT for cancer treatment.

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“…These deposited particles dissolve slowly over time resulting in a chronic exposure of lung cells to Cr(VI) and an accumulation of Cr in tissues [1]. Cr-induced tumors are typically found at these bifurcations and are associated with higher tissue burdens of Cr [2,3]. Thus, reoccurring exposure to Cr(VI) is key to its toxic effects.…”

Section: Introductionmentioning

confidence: 99%

Hexavalent Chromium–Induced Chromosome Instability Drives Permanent and Heritable Numerical and Structural Changes and a DNA Repair–Deficient Phenotype

et al. 2018

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A key hypothesis for how hexavalent chromium [Cr(VI)] causes cancer is that it drives chromosome instability (CIN), which leads to neoplastic transformation. Studies show chronic Cr(VI) can affect DNA repair and induce centrosome amplification, which can lead to structural and numerical CIN. However, no studies have considered whether these outcomes are transient or permanent. In this study, we exposed human lung cells to particulate Cr(VI) for three sequential 24-hour periods, each separated by about a month. After each treatment, cells were seeded at colony-forming density, cloned, expanded, and retreated, creating three generations of clonal cell lines. Each generation of clones was tested for chromium sensitivity, chromosome complement, DNA repair capacity, centrosome amplification, and the ability to grow in soft agar. After the first treatment, Cr(VI)-treated clones exhibited a normal chromosome complement, but some clones showed a repair-deficient phenotype and amplified centrosomes. After the second exposure, more than half of the treated clones acquired an abnormal karyotype including numerical and structural alterations, with many exhibiting deficient DNA double-strand break repair and amplified centrosomes. The third treatment produced new abnormal clones, with previously abnormal clones acquiring additional abnormalities and most clones exhibiting repair deficiency. CIN, repair deficiency, and amplified centrosomes were all permanent and heritable phenotypes of repeated Cr(VI) exposure. These outcomes support the hypothesis that CIN is a key mechanism of Cr(VI)-induced carcinogenesis. Chromium, a major public health concern and human lung carcinogen, causes fundamental changes in chromosomes and DNA repair in human lung cells. .

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Microscopic analysis of the chromium content in the chromium-induced malignant and premalignant bronchial lesions of the rat

Cited by 17 publications

References 12 publications

Characterization of initial clinical symptoms and risk factors for sinonasal adenocarcinomas: results of a case–control study

Characterization of initial clinical symptoms and risk factors for sinonasal adenocarcinomas: results of a case–control study

Redox regulation in tumor cell epithelial–mesenchymal transition: molecular basis and therapeutic strategy

Hexavalent Chromium–Induced Chromosome Instability Drives Permanent and Heritable Numerical and Structural Changes and a DNA Repair–Deficient Phenotype

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