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.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

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.
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.

mechlorethamine

Oncology An alkylating nitrogen mustard chemotherapeutic used for lymphomas Adverse effects GI Sx, BM suppression, skin vesiculation at injection site. See MOPP regimen.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

ni·tro·gen mus·tards

(HN) (nī'trŏ-jĕn mŭs'tărdz)
A group of toxic chemicals developed for use as chemical-warfare agents.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012
References in periodicals archive ?
We isolated RNA from cerebellar neuronal cultures treated for 24 hr with 100 [micro]M MAM or 1.0 [micro]M HN2 using Tri-Reagent (Molecular Research Corp.) according to the manufacturer's protocol.
In the present study, our goal was to determine the relationship between the sensitivity of immature postmitotic neurons to MAM or HN2 and their ability to damage DNA.
Additional studies were conducted to determine if the increased sensitivity of neurons to MAM and HN2 was due to their genotoxic (i.e., DNA damaging) properties.
To identify the specific molecular networks targeted by MAM or HN2, we examined genotoxicant-treated neurons for genomewide expression using high-density mouse cDNA microarrays (Figure 3).
As shown in the heatmap (Figure 3A), we observed distinct clusters for MAM and HN2. The number of genes uniquely regulated by each genotoxicant and their overlap is shown in Figure 3B.
Functional classes targeted by MAM and HN2. 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.