And the action of sulfur mustard on tumors in laboratory animals was investigated for the first time.After the U.S. entry into the Second World War the nitrogen mustards were candidate chemical warfare agents and research on them was initiated by the Office of Scientific Research and Development (OSRD). The OSRD let contracts to study them to two universities—Yale University and the University of Chicago. Inspired perhaps by the preliminary research in 1935, independently both groups thought to test whether a medically useful differential toxicity between animals and animal tumors existed. The Yale pharmacologists Louis Goodman and Alfred Gilman were the first to conduct a clinical trial, on 27 August 1942, using the agent HN3 (tris(2-chloroethyl)amine) on a patient known as J.D.The next year the Chicago group, led by Leon O. Jacobson, conducted trials with HN2 (chlormethine) which was the only agent in this group to see eventual clinical use. Wartime secrecy prevented any of this ground-breaking work on chemotherapy from being published, but papers were released once wartime secrecy ended, in 1946.Further clinical trials after the war, led by Cornelius P. Rhoads at Memorial Sloan-Kettering, helped establish the medical utility of the drug for Hodgkins disease and several other lymphomas and leukemia. Chemistry
Chlormethine is combustible and becomes explosive under extreme conditions. It can react with metals to form gaseous hydrogen. See also
Nitrogen mustards
HN1
HN3

References
External links
British Columbia Cancer Agency profile
"Chlormethine". Drug Information Portal. U.S. National Library of Medicine.
The inheritance probabilities per birth are as follows:
If both parents are carriers:
25% (1 in 4) children will have the disease
50% (2 in 4) children will be carriers, but unaffected
25% (1 in 4) children will be free of MLD – unaffected child that is not a carrier
If one parent is affected and one is free of MLD:
0% (0) children will have the disorder – only one parent is affected, other parent always gives normal gene
100% (4 in 4) children will be carriers (but unaffected)
If one parent is a carrier and the other is free of MLD:
50% (2 in 4) children will be carriers (but unaffected)
50% (2 in 4) children will be free of MLD – unaffected child that is not a carrierIn addition to these frequencies there is a pseudo-deficiency that affects 7–15% of the population. People with the pseudo deficiency do not have any MLD problems unless they also have affected status. With the current diagnostic tests, Pseudo-deficiency reports as low enzyme levels but sulfatide is processed normally so MLD symptoms do not exist. This phenomenon wreaks havoc with traditional approaches to Newborn Screening so new screening methods are being developed. Diagnosis
Clinical examination and MRI are often the first steps in an MLD diagnosis. MRI can be indicative of MLD but is not adequate as a confirming test. An ARSA-A enzyme level blood test with a confirming urinary sulfatide test is the best biochemical test for MLD. The confirming urinary sulfatide is important to distinguish between MLD and pseudo-MLD blood results.