Editing David Baltimore (section)

===Whitehead Institute for Biomedical Research===
In 1982, with a charitable donation by businessman and philanthropist Edwin C. "Jack" Whitehead, Baltimore was asked to help establish a self-governed research institute dedicated to basic biomedical research.<ref name=WI1>{{cite web|title=Whitehead Institute Introduction|url=http://www.wi.mit.edu/about/history}}</ref> Baltimore persuaded Whitehead that MIT would be the ideal home for the new institute, convinced that it would be superior at hiring the best researchers in biology at the time, thus ensuring quality.<ref name=":0" /> Persuading MIT faculty to support the idea was far more difficult. MIT as an institution had never housed another before, and concerns were raised that the wealth of the institute might skew the biology department in directions faculty did not wish to take, and that Baltimore himself would gain undue influence over hiring within the department.<ref name=":0" /><ref name=":1" /><ref>{{Cite news| vauthors = Teltsch K |date=1992-02-04|title=Edwin C. Whitehead, 72, Dies; Financed Biomedical Research|language=en-US|work=The New York Times|url=https://www.nytimes.com/1992/02/04/nyregion/edwin-c-whitehead-72-dies-financed-biomedical-research.html|access-date=2021-04-14|issn=0362-4331}}</ref> The controversy was made worse by an article published by the Boston Globe framing the institute as corporate takeover of MIT.<ref name=":0" /><ref name=":1" /> After a year of intensive discussions and planning, faculty finally voted in favor of the institute.<ref name=":0" /> Whitehead, Baltimore, and the rest of the planning team devised a unique structure of an independent research institute composed of "members" with a close relationship with the department of biology of MIT. This structure continues to this day to attract an elite interactive group of faculty to the Department of Biology at MIT and has served as a model for other distinguished institutes such as the [[Broad Institute]].

[[Whitehead Institute|The Whitehead Institute for Biomedical Research]] (WIBR) was launched with $35 million to construct and equip a new building located across the street from the MIT cancer center at 9 Cambridge Center in Cambridge Massachusetts. The institute also received $5 million per year in guaranteed income and a substantial endowment in his will (for a total gift of $135 million). Under Baltimore's leadership, a distinguished group of founding members including [[Gerald Fink]], [[Rudolf Jaenisch]], [[Harvey Lodish]], and [[Robert Weinberg (biologist)|Robert Weinberg]] was assembled and eventually grew to 20 members in disciplines ranging from immunology, genetics, and oncology to fundamental developmental studies in mice and fruit flies.<ref name="WI2">{{cite web|title=Whitehead Institute Founding Faculty|url=http://www.wi.mit.edu/about/history/founders}}</ref> Whitehead Institute's contributions to bioscience have long been consistently outstanding. Less than a decade after its founding with continued leadership by Baltimore, the Whitehead Institute was named the top research institution in the world in molecular biology and genetics, and over a recent 10-year period, papers published by Whitehead scientists, including many from Baltimore's own lab, were the most cited papers of any biological research institute. The Whitehead Institute was an important partner in the [[Human Genome Project]].<ref name="genome">{{cite web| vauthors = Kumar S |date=July 12, 2000|title=Whitehead scientists enjoy genome sequence milestone|url=http://web.mit.edu/newsoffice/2000/whitehead-0712.html|publisher=Whitehead Institute}}</ref>

Baltimore served as director of the WIBR and expanded the faculty and research areas into key areas of research including mouse and drosophila genetics. During this time, Baltimore's own research program thrived in the new Institute. Important breakthroughs from Baltimore's lab include the discovery of the key transcription factor [[NF-κB]] by Dr. Ranjan Sen and David Baltimore in 1986.<ref name="pmid3091258">{{cite journal | vauthors = Sen R, Baltimore D | title = Multiple nuclear factors interact with the immunoglobulin enhancer sequences | journal = Cell | volume = 46 | issue = 5 | pages = 705–16 | date = August 1986 | pmid = 3091258 | doi = 10.1016/0092-8674(86)90346-6 | s2cid = 37832531 }}</ref> This was part of a broader investigation to identify nuclear factors required for lg gene expression in B lymphocytes. However, NF-κB turned out to have much broader importance in both innate and adaptive immunity and viral regulation. NF-κB is involved in regulating cellular responses and belongs to the category of "rapid-acting" primary transcription factors. Their discovery led to an "information explosion" involving "one of the most intensely studied signaling paradigms of the last two decades."<ref name=May2006>{{cite journal | vauthors = May MJ | title = A nuclear factor in B cells and beyond | journal = Journal of Immunology | volume = 177 | issue = 11 | pages = 7483–4 | date = December 2006 | pmid = 17114414 | doi = 10.4049/jimmunol.177.11.7483 | doi-access = free }}</ref>

As early as 1984, Rudolf Grosschedl and David Weaver, postdoctoral fellows, in Baltimore's laboratory, were experimenting with the creation of [[Genetically modified mouse|transgenic mice]] as a model for the study of disease. They suggested that "control of lg gene rearrangement might be the only mechanism that determines the specificity of heavy chain gene expression within the lymphoid cell lineage."<ref name=Grosschedl1984>{{cite journal | vauthors = Grosschedl R, Weaver D, Baltimore D, Costantini F | title = Introduction of a mu immunoglobulin gene into the mouse germ line: specific expression in lymphoid cells and synthesis of functional antibody | journal = Cell | volume = 38 | issue = 3 | pages = 647–58 | date = October 1984 | pmid = 6091894 | doi = 10.1016/0092-8674(84)90259-9 | s2cid = 43466298 }}</ref> in 1987, they created transgenic mice with the fused gene that developed fatal leukemia.<ref>{{cite journal | vauthors = Herzenberg LA, Stall AM, Braun J, Weaver D, Baltimore D, Herzenberg LA, Grosschedl R | title = Depletion of the predominant B-cell population in immunoglobulin mu heavy-chain transgenic mice | journal = Nature | volume = 329 | issue = 6134 | pages = 71–73 | date = September 1987 | pmid = 3114639 | doi = 10.1038/329071a0 | s2cid = 4347294 }}</ref><ref>{{Cite web|title=Unraveling the Origins of Cancer|url=https://sphweb.bumc.bu.edu/otlt/MPH-Modules/PH/PH709_Cancer/PH709_Cancer3.html#:~:text=In%201987%20David%20Baltimore%27s%20lab,them%20with%20a%20phosphate%20group.|access-date=2021-02-28|website=sphweb.bumc.bu.edu}}</ref>

David G. Schatz and Marjorie Oettinger, as students in Baltimore's research group in 1988 and 1989, identified the protein pair that rearranges immunoglobulin genes, the [[recombination-activating gene]] RAG-1 and RAG-2.<ref name=Schatz>{{cite journal | vauthors = Schatz DG, Oettinger MA, Baltimore D | title = Pillars article: the V(D)J recombination activating gene, RAG-1. 1989 | journal = Journal of Immunology | volume = 180 | issue = 1 | pages = 5–18 | date = January 2008 | pmid = 18096996 | url = http://www.jimmunol.org/content/180/1/5.full.pdf+html | access-date = May 25, 2015 }}</ref> this was a key discovery in determining how the immune system can have specificity for a given molecule out of many possibilities,<ref name=Brandt>{{cite journal | vauthors = Brandt VL, Roth DB | title = G.O.D.'s Holy Grail: discovery of the RAG proteins | journal = Journal of Immunology | volume = 180 | issue = 1 | pages = 3–4 | date = January 2008 | pmid = 18096995 | doi = 10.4049/jimmunol.180.1.3 | doi-access = free }}</ref> and was considered by Baltimore as of 2005 to be "our most significant discovery in immunology".<ref name=NobelBio/>{{rp|Addendum, May 2005}}

In 1990, as a student in David Baltimore's laboratory at MIT, [[George Q. Daley]] demonstrated that a fusion protein called bcr-abl is sufficient to stimulate cell growth and cause chronic myelogenous leukemia (CML). This work helped to identify a class of proteins that become hyperactive in specific types of cancer cells. It helped to lay the groundwork for a new type of drug, attacking cancer at the genetic level: [[Brian Druker]]'s development of the anti-cancer drug [[Imatinib]] (Gleevec), which deactivates bcr-abl proteins. Gleevec has shown impressive results in treating [[chronic myelogenous leukemia]] and also promise in treating [[gastrointestinal stromal tumor]] (GIST).<ref name=Nathan>{{cite news| vauthors = Nathan DG |title=The Relevant Biomedical Research|url=http://harvardmagazine.com/2007/01/the-relevant-biomedical.html|access-date=May 25, 2015|work=Harvard Magazine|issue=January–February|date=2007}}</ref><ref name=Gleevec2001>{{cite news| vauthors = Wade N |title=Swift Approval For a New Kind Of Cancer Drug|url=https://www.nytimes.com/2001/05/11/us/swift-approval-for-a-new-kind-of-cancer-drug.html|access-date=May 25, 2015|work=The New York Times|date=May 11, 2001}}</ref><ref name=AMACON>{{cite book| vauthors = Smith G |title=The genomics age: how DNA technology is transforming the way we live and who we are|date=2005|publisher=AMACOM|location=New York|isbn=978-0814408438|page=[https://archive.org/details/genomicsagehowdn0000smit/page/140 140]|url=https://archive.org/details/genomicsagehowdn0000smit|url-access=registration|access-date=May 25, 2015}}</ref>