mechlorethamine

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mechlorethamine

 [mek″lor-eth´ah-mēn]
an alkylating agent that produces interstrand and intrastrand cross-linkages in DNA with resultant miscoding, breakage, and failure of replication. Used primarily for the treatment of disseminated hodgkin's disease, especially in the MOPP treatment regimen, and for other lymphomas, including mycosis fungoides; administered intravenously as the hydrochloride salt. Called also nitrogen mustard.

mechlorethamine

/mech·lor·eth·amine/ (mek″lor-eth´ah-mēn) one of the nitrogen mustards, used in the form of the hydrochloride salt as an antineoplastic, particularly in disseminated Hodgkin's disease.

mechlorethamine

A nitrogen mustard derivative which binds to DNA, crosslinking both strands to prevent its replication.

Global village
Mechlorethamine was first developed as a chemical weapon.

Oncology
A nitrogen mustard alkylating agent used for managing lymphomas; part of MOPP.
 
Adverse effects
Nausea, vomiting, marrow suppression, skin vesiculation at injection site.

mechlorethamine

Oncology An alkylating nitrogen mustard chemotherapeutic used for lymphomas Adverse effects GI Sx, BM suppression, skin vesiculation at injection site. See MOPP regimen.

ni·tro·gen mus·tards

(HN) (nī'trŏ-jĕn mŭs'tărdz)
A group of toxic chemicals developed for use as chemical-warfare agents.

mechlorethamine

References in periodicals archive ?
Additional studies were conducted to determine if the increased sensitivity of neurons to MAM and HN2 was due to their genotoxic (i.
0 [micro]M HN2 for 24 hr and examined total RNA for gene expression changes using high-density microarrays.
Even though the majority of genes influenced by sublethal concentrations of MAM or HN2 were of unknown function (63 and 77%, respectively), analysis of the known genes perturbed by MAM (225 genes) or HN2 (141 genes) revealed prominent changes in several different categories (Figure 3C,D), indicating that the molecular networks targeted by these two genotoxicants are quite distinct.
Even though MAM and HN2 both alkylated neuronal DNA, the genes specifically targeted by HN2 were quite distinct from those targeted by MAM.
Although MAM and HN2 targeted distinct neuronal genes, there were a number of genes that were common targets for both genotoxicants (Table 3).
2003) to identify the biologically relevant transcription factor binding sites within the regulatory regions of the genes targeted by HN2 and MAM.
2004), it is conceivable that the DNA lesions formed by MAM or HN2 profoundly influenced the expression of developmentally regulated neuronal genes.
One key finding of the present studies is that the molecular pathways controlling neuronal migration and maturation were predominantly targeted by MAM but not by the related genotoxicant HN2.