{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:36:29Z","timestamp":1791329789959,"version":"4.3.1"},"reference-count":159,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,12,1]],"date-time":"2004-12-01T00:00:00Z","timestamp":1101859200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2005,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Richter's transformation denotes the development of high\u2010grade non\u2010Hodgkin lymphoma, prolymphocytic leukemia, Hodgkin disease, or acute leukemia in patients with chronic lymphocytic leukemia (CLL)\/small lymphocytic lymphoma. A search of published articles in Medline (PubMed) and abstracts from professional meetings was performed. An electronic database search of patients with CLL at The University of Texas M. D. Anderson Cancer Center (Houston, TX) determined the incidence of Richter syndrome (RS) in patients with CLL between 1992 and 2002. RS occurs in approximately 5% of patients with CLL. The large cells of RS may arise through transformation of the original CLL clone or represent a new neoplasm. RS may be triggered by viral infections, such as Epstein\u2013Barr virus. Trisomy 12 and chromosome 11 abnormalities are more frequent in patients with RS than in the overall population of patients with CLL. Multiple genetic defects, such as mutations of the\n                    <jats:italic>p53<\/jats:italic>\n                    tumor suppressor gene,\n                    <jats:italic>p16INK4A<\/jats:italic>\n                    , and\n                    <jats:italic>p21<\/jats:italic>\n                    , loss of\n                    <jats:italic>p27<\/jats:italic>\n                    expression, deletion of retinoblastoma, increased copy number of\n                    <jats:italic>C\u2010MYC<\/jats:italic>\n                    , and decreased expression of the\n                    <jats:italic>A\u2010MYB<\/jats:italic>\n                    gene, have been described. These abnormalities may cause CLL cells to proliferate and\u2014by facilitating the acquisition of new genetic abnormalities\u2014to transform into RS cells. Therapeutic strategies include intensive chemotherapy, monoclonal antibodies, and stem cell transplantation. The response rates range from 5% to 43% (complete response, 5\u201338%), and the median survival duration ranges from 5 months to 8 months. In conclusion, RS may be triggered by viral infections or by genetic defects. Current treatments are aggressive, but prognosis is poor. Novel curative treatment strategies are needed. Cancer 2005. \u00a9 2004 American Cancer Society.\n                  <\/jats:p>","DOI":"10.1002\/cncr.20773","type":"journal-article","created":{"date-parts":[[2004,12,1]],"date-time":"2004-12-01T12:50:02Z","timestamp":1101905402000},"page":"216-228","source":"Crossref","is-referenced-by-count":232,"title":["Richter syndrome"],"prefix":"10.1002","volume":"103","author":[{"given":"Apostolia\u2010Maria","family":"Tsimberidou","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Keating","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,1,5]]},"reference":[{"key":"e_1_2_10_2_2","first-page":"285","article-title":"Generalized reticular cell sarcoma of lymph nodes associated with lymphatic leukemia","volume":"4","author":"Richter MN","year":"1928","journal-title":"Am J 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