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|Title:||Sensitivity of human Cord Blood Cells to Tetrachloroethylene: Cellular and Molecular Endpoints|
|Authors:||DIODOVICH Cristina; FERRARIO DANIELE; CASATI BARBARA; MALERBA Ilaria; MARAFANTE ERMINIO; PARENT-MASSIN Dominique; GRIBALDO LAURA|
|Citation:||ARCHIVES OF TOXICOLOGY vol. 79 p. 508-514|
|Type:||Articles in periodicals and books|
|Abstract:||The International Agency for Research on Cancer (IARC) currently lists tetrachloroethylene [perchloroethylene (PCE)] as being carcinogenic in animals. PCE is listed as possibly carcinogenic to humans upon occupational exposure. Human exposure to PCE can produce oesophageal cancer, cervical cancer, non- Hodgkin’s lymphoma, urinary bladder cancer and leukemia. This work shows that PCE modulates the expression of some genes implicated in cancer induction, cell diﬀerentiation, cell-cycle progression, and the survival and clonogenic potential of human cord blood cells. After exposure to the compound, the modulated genes were involved in inﬂammatory responses as with the mitogen-activated protein kinase 14 (MPK 14), or in tumor and metastasis progression as with the matrix metalloproteinase 17 (MMP 17), in cell proliferation as with c-jun and c-fos, and moreover in the apoptotic process as with interferon alpha-inducible protein (IFI), BAX and BCL-2. Analysis of cord blood cells via ﬂow cytometry showed that PCE treatment induced a statistically signiﬁcant increase in necrosis after 24 h, while the clonogenicity of Human Colony-Forming Unit- Granulocyte/Macrophage (CFU-GM) and Burst- Forming Unit-Erythrocyte (BFU-E) progenitors did not change. In conclusion, our data showed that PCE affected various pathways involved in cancer induction, but its action on cell proliferation and diﬀerentiation is not yet clearly understood.|
|JRC Institute:||Institute for Health and Consumer Protection Historical Collection|
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