Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression

Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute myeloid leukemia, myelodysplastic syndrome...
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Gespeichert in:

Autor*in:	Giovanna Spatari [verfasserIn] Alessandro Allegra [verfasserIn] Mariella Carrieri [verfasserIn] Giovanni Pioggia [verfasserIn] Sebastiano Gangemi [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	benzene epigenetic leukemia lymphoma hematological malignancies gene expression

Übergeordnetes Werk:	In: Cancers - MDPI AG, 2010, 13(2021), 10, p 2392
Übergeordnetes Werk:	volume:13 ; year:2021 ; number:10, p 2392

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/cancers13102392

Katalog-ID:	DOAJ011602910

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language	English
source	In Cancers 13(2021), 10, p 2392 volume:13 year:2021 number:10, p 2392
sourceStr	In Cancers 13(2021), 10, p 2392 volume:13 year:2021 number:10, p 2392
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	benzene epigenetic leukemia lymphoma hematological malignancies gene expression Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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container_title	Cancers
authorswithroles_txt_mv	Giovanna Spatari @@aut@@ Alessandro Allegra @@aut@@ Mariella Carrieri @@aut@@ Giovanni Pioggia @@aut@@ Sebastiano Gangemi @@aut@@
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callnumber-first	R - Medicine
author	Giovanna Spatari
spellingShingle	Giovanna Spatari misc RC254-282 misc benzene misc epigenetic misc leukemia misc lymphoma misc hematological malignancies misc gene expression misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression
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topic_title	RC254-282 Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression benzene epigenetic leukemia lymphoma hematological malignancies gene expression
topic	misc RC254-282 misc benzene misc epigenetic misc leukemia misc lymphoma misc hematological malignancies misc gene expression misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc benzene misc epigenetic misc leukemia misc lymphoma misc hematological malignancies misc gene expression misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc benzene misc epigenetic misc leukemia misc lymphoma misc hematological malignancies misc gene expression misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression
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title_sort	epigenetic effects of benzene in hematologic neoplasms: the altered gene expression
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title_auth	Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression
abstract	Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute myeloid leukemia, myelodysplastic syndromes, aplastic anemia, and lymphomas. Possible mechanisms of benzene initiation of hematological tumors have been identified, as a genotoxic effect, an action on oxidative stress and inflammation and the provocation of immunosuppression. However, it is becoming evident that genetic alterations and the other causes are insufficient to fully justify several phenomena that influence the onset of hematologic malignancies. Acquired epigenetic alterations may participate with benzene leukemogenesis, as benzene may affect nuclear receptors, and provoke post-translational alterations at the protein level, thereby touching the function of regulatory proteins, comprising oncoproteins and tumor suppressor proteins. DNA hypomethylation correlates with stimulation of oncogenes, while the hypermethylation of CpG islands in promoter regions of specific tumor suppressor genes inhibits their transcription and stimulates the onset of tumors. The discovery of the systems of epigenetic induction of benzene-caused hematological tumors has allowed the possibility to operate with pharmacological interventions able of stopping or overturning the negative effects of benzene.
abstractGer	Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute myeloid leukemia, myelodysplastic syndromes, aplastic anemia, and lymphomas. Possible mechanisms of benzene initiation of hematological tumors have been identified, as a genotoxic effect, an action on oxidative stress and inflammation and the provocation of immunosuppression. However, it is becoming evident that genetic alterations and the other causes are insufficient to fully justify several phenomena that influence the onset of hematologic malignancies. Acquired epigenetic alterations may participate with benzene leukemogenesis, as benzene may affect nuclear receptors, and provoke post-translational alterations at the protein level, thereby touching the function of regulatory proteins, comprising oncoproteins and tumor suppressor proteins. DNA hypomethylation correlates with stimulation of oncogenes, while the hypermethylation of CpG islands in promoter regions of specific tumor suppressor genes inhibits their transcription and stimulates the onset of tumors. The discovery of the systems of epigenetic induction of benzene-caused hematological tumors has allowed the possibility to operate with pharmacological interventions able of stopping or overturning the negative effects of benzene.
abstract_unstemmed	Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute myeloid leukemia, myelodysplastic syndromes, aplastic anemia, and lymphomas. Possible mechanisms of benzene initiation of hematological tumors have been identified, as a genotoxic effect, an action on oxidative stress and inflammation and the provocation of immunosuppression. However, it is becoming evident that genetic alterations and the other causes are insufficient to fully justify several phenomena that influence the onset of hematologic malignancies. Acquired epigenetic alterations may participate with benzene leukemogenesis, as benzene may affect nuclear receptors, and provoke post-translational alterations at the protein level, thereby touching the function of regulatory proteins, comprising oncoproteins and tumor suppressor proteins. DNA hypomethylation correlates with stimulation of oncogenes, while the hypermethylation of CpG islands in promoter regions of specific tumor suppressor genes inhibits their transcription and stimulates the onset of tumors. The discovery of the systems of epigenetic induction of benzene-caused hematological tumors has allowed the possibility to operate with pharmacological interventions able of stopping or overturning the negative effects of benzene.
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title_short	Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression
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