National Cancer Institute®
Last Modified: June 1, 2002
UI - 11994981
AU - Larsen CR; Hansen PB; Clausen NT
TI - Aggressive growth of epithelial carcinomas following treatment with nucleoside analogues.
SO - Am J Hematol 2002 May;70(1):48-50
AD - Department of Internal Medicine F, Section of Hematology and Oncology, Hillerod Hospital, Hillerod, Denmark. email@example.com
Two patients, one with B-cell chronic lymphocytic leukemia (CLL) and one with hairy-cell leukemia (HCL), were treated with immunosuppressive chemotherapy. The patient with CLL was a 54-year-old female, who had had a squamous cell carcinoma (SCC) excised from her forehead 5 months before receiving the first course of fludarabine. During the fludarabine treatment, the patient developed a local SCC relapse and metastases in the neck. The carcinoma was treated by excision and radiotherapy, and further fludarabine treatment was withheld. Nevertheless, the SCC metastasized aggressively and the patient died 3 months after the start of fludarabine treatment, primarily due to respiratory failure. The autopsy revealed heavy SCC infiltrations involving the lungs, pleura, mediastinum, pericardium, and liver. The patient with HCL was a 69-year-old male. At the time of diagnosis of HCL, the patient had two solid tumors in the liver containing poorly differentiated epithelial carcinoma cells of unknown origin. During treatment with 2-chlorodeoxyadenosine (2CdA), the tumors in the liver rapidly spread in multiple intrahepatic metastases, followed by liver failure and death within 1 month. Fludarabine and 2CdA cause a substantial suppression of all lymphocyte subsets, in particular the T-cell line. T-lymphocytes are believed to be responsible for the usually slow growth and the low metastatic rate of the SCC skin lesions. It is therefore assumed that fludarabine and 2CdA in these two cases triggered an exacerbation of both tumors due to the T-cell depletion. Copyright 2002 Wiley-Liss, Inc.
UI - 12034522
AU - Pajor L; Kereskai L; Tamaska P; Vass JA; Radvanyi G
TI - Coexistence of chronic myeloid leukemia and hairy cell leukemia of common clonal origin.
SO - Cancer Genet Cytogenet 2002 Apr 15;134(2):114-7
AD - Department of Pathology, Medical Faculty, University of Pecs, Pecs, Hungary. firstname.lastname@example.org
The history of a forty year old patient is presented who was admitted with a clinical picture of chronic myeloid leukemia (CML). Laboratory findings, bone marrow morphology and molecular investigations supported this diagnosis, including b3/a2 as well as b2/a2 chimeric mRNA expression in support of a Philadelphia chromosome positive chronic myeloproliferation. In a fraction of the bone marrow content, however, an infiltrate different from that of CML could be seen. In addition, the morphology, cytochemistry, immunophenotyping and molecular analysis indicated that the coexisting neoplasia is hairy cell leukemia (HCL). Cell lineage specific interphase cytogenetic analysis proved a clonal relationship between the two neoplasias in a way that the HCL arose from one of the B-cells which, based on two cytogenetic markers, belonged to the original CML clone.
UI - 11692413
AU - Nuno Mateo FJ; Noval Menendez J; Llorente de Jesus R; Menendez Calderon
TI - MJ [Pancytopenia and focal splenic lesions in an 80-year-old man. Hairy cell leukemia]
SO - Rev Clin Esp 2001 Sep;201(9):541-2
AD - Servicios de Medicina Interna, Hospital de Cabuenes, Gijon.
UI - 11982619
AU - Cesana C; Brando B; Boiani E; Chiodo F; Cairoli R; Intropido L; Morra E
TI - Effective treatment of autoimmune hemolytic anemia and hairy cell leukemia with interferon-alpha.
SO - Eur J Haematol 2002 Feb;68(2):120-1
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