[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 60 of about 60
1. Dearden CE, Matutes E, Cazin B, Tjønnfjord GE, Parreira A, Nomdedeu B, Leoni P, Clark FJ, Radia D, Rassam SM, Roques T, Ketterer N, Brito-Babapulle V, Dyer MJ, Catovsky D: High remission rate in T-cell prolymphocytic leukemia with CAMPATH-1H. Blood; 2001 Sep 15;98(6):1721-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High remission rate in T-cell prolymphocytic leukemia with CAMPATH-1H.
  • T-cell prolymphocytic leukemia (T-PLL) is a chemotherapy-resistant malignancy with a median survival of 7.5 months.
  • All but 2 patients had received prior therapy with a variety of agents, including 30 with pentostatin; none achieved complete remission (CR).
  • CAMPATH-1H (30 mg) was administered intravenously 3 times weekly until maximal response.
  • The overall response rate was 76% with 60% CR and 16% partial remission (PR).
  • These responses were durable with a median disease-free interval of 7 months (range, 4-45 months).
  • Survival was significantly prolonged in patients achieving CR compared to PR or no response (NR), including one patient who survived 54 months.
  • Nine patients remain alive up to 29 months after completing therapy.
  • Seven patients received high-dose therapy with autologous stem cell support, 3 of whom remain alive in CR 5, 7, and 15 months after autograft.
  • Stem cell harvests in these patients were uncontaminated with T-PLL cells as demonstrated by dual-color flow cytometry and polymerase chain reaction.
  • Four patients had allogeneic stem cell transplants, 3 from siblings and 1 from a matched unrelated donor.
  • Three are alive in CR up to 24 months after allograft.
  • The conclusion is that CAMPATH-1H is an effective therapy in T-PLL, producing remissions in more than two thirds of patients.
  • The use of stem cell transplantation to consolidate responses merits further study.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic, T-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Combined Modality Therapy. Cytogenetic Analysis. Female. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. Male. Middle Aged. Remission Induction. Survival Rate. Transplantation, Homologous

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11535503.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


2. Singhal M, Raina V, Gupta R, Das P: T cell-prolymphocytic leukemia detected in a patient of breast cancer at the time of recurrence: a case report. Cases J; 2010;3:4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T cell-prolymphocytic leukemia detected in a patient of breast cancer at the time of recurrence: a case report.
  • INTRODUCTION: Therapy related second malignancy of the hematological system is small but real risk after adjuvant chemotherapy for breast cancer.
  • It includes acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS); however T-cell prolymphocytic leukemia (T-PLL) has not been described earlier in relation to breast cancer and its therapy.
  • T-PLL is a rare chronic T-cell lymphoproliferative disease with a mature post-thymic T-cell immunophenotype and aggressive clinical course.
  • CASE PRESENTATION: A 45 year old Indian female of Nordic origin presented 5 years back with a lump in the right breast and the axilla.
  • Histophotomicrograph of the excised breast lesion showed a 2.1 cm duct carcinoma, positive for ER and PR with 1 out of 25 lymph nodes positive for metastasis.
  • She received 6 cycles of chemotherapy with cyclophosphamide, epirubicin, and 5-fluorouracil.
  • She was doing well on follow up until the completion of fifth year of her disease, when she presented with complaints of mild fever and weakness.
  • Examination revealed generalized lymph node enlargement along with hepatomegaly.
  • Peripheral blood examination revealed medium sized lymphoid cells, constituting almost 75% of total nucleated cell population.
  • Immunophenotying, established a diagnosis of post thymic T-cell prolymphocytic leukemia.
  • Contrast-enhanced computed tomography of the chest and abdomen was done which revealed an anterior mediastinal mass with destruction of sternum along with multiple small nodular shadows in bilateral lung fields suggestive of lung metastasis.
  • She was started on chemotherapy for T-PLL along with hormonal therapy with aromatase inhibitor.
  • Unfortunately, both her malignancies progressed after an initial stable disease of two months.
  • CONCLUSION: Our case describes the potential of breast chemotherapy to cause grave second hematological malignancies of the T-cell lymphoid lineage, not described earlier.
  • Such events highlight the importance to identify those patients of breast cancer in whom chemotherapy can safely be avoided.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):791-8 [19124806.001]
  • [Cites] BMC Cancer. 2007;7:152 [17683622.001]
  • [Cites] J Clin Oncol. 2007 Jan 20;25(3):292-300 [17159192.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4179-91 [15961765.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1721-6 [11535503.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2588-93 [7989933.001]
  • [Cites] N Engl J Med. 1992 Jun 25;326(26):1745-51 [1594016.001]
  • [Cites] J Clin Oncol. 1985 Dec;3(12):1640-58 [3906049.001]
  • [Cites] Clin Breast Cancer. 2003 Oct;4(4):273-9 [14651772.001]
  • [Cites] J Clin Oncol. 1996 Oct;14(10):2722-30 [8874333.001]
  • (PMID = 20076807.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2806858
  •  go-up   go-down


3. Fløisand Y, Brinch L, Gedde-Dahl T, Tjønnfjord GE: [Treatment of T-cell prolymphocytic leukemia with monoclonal anti- CD52 antibody (alemtuzumab]. Tidsskr Nor Laegeforen; 2004 Mar 18;124(6):768-70
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of T-cell prolymphocytic leukemia with monoclonal anti- CD52 antibody (alemtuzumab].
  • [Transliterated title] Behandling av T-prolymfocyttleukemi med monoklonalt anti-CD52-antistoff (alemtuzumab).
  • INTRODUCTION: T-cell prolymphocytic leukaemia (T-PLL) is a rare post-thymic T-cell malignancy with an aggressive clinical course.
  • It has generally been resistant to alkylating chemotherapy, but some effect has been observed with the purine analog 2-deoxycoformicin with documented partial or complete response rates in up to 45% of patients.
  • Treatment with monoclonal antibodies against CD 52 has been shown to be highly effective in T-PLL with response rates of up to 76%.
  • This may allow for further consolidating treatment with high-dose chemotherapy with autologous stem cell support or allogeneic stem cell transplantation.
  • One patient underwent allogeneic stem cell transplantation with an HLA-identical sibling, but died on day 21 as a result of transplantation complications.
  • The treatment is generally well tolerated; the principal management problem is immunosuppression, as shown in one patient who developed a varicella-zoster meningoencephalomyelitis as a consequence of not receiving antiviral prophylaxis.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Humanized. Diagnosis, Differential. Humans. Male. Middle Aged. Prognosis

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15039804.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


Advertisement
4. Meeuse JJ, Sprenger HG, van Assen S, Leduc D, Daenen SM, Arends JP, van der Werf TS: Rhodococcus equi infection after alemtuzumab therapy for T-cell prolymphocytic leukemia. Emerg Infect Dis; 2007 Dec;13(12):1942-3
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rhodococcus equi infection after alemtuzumab therapy for T-cell prolymphocytic leukemia.
  • We report a patient in whom Rhodococcus equi infection developed after alemtuzumab therapy.
  • [MeSH-major] Actinomycetales Infections / etiology. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / adverse effects. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Leukemia, Prolymphocytic, T-Cell / drug therapy. Rhodococcus equi
  • [MeSH-minor] Aged. Anti-Bacterial Agents / therapeutic use. Antibodies, Monoclonal, Humanized. Humans. Immunocompromised Host. Lung Abscess / drug therapy. Lung Abscess / microbiology. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Sep 15;98(6):1721-6 [11535503.001]
  • [Cites] Clin Infect Dis. 2002 May 15;34(10):1379-85 [11981734.001]
  • [Cites] Semin Oncol. 2003 Aug;30(4):424-33 [12939711.001]
  • [Cites] Clin Infect Dis. 2006 Jul 1;43(1):16-24 [16758413.001]
  • [Cites] Emerg Infect Dis. 1997 Apr-Jun;3(2):145-53 [9204295.001]
  • [Cites] Vet Microbiol. 1997 Jun 16;56(3-4):167-76 [9226831.001]
  • [Cites] Clin Microbiol Rev. 1991 Jan;4(1):20-34 [2004346.001]
  • (PMID = 18258054.001).
  • [ISSN] 1080-6040
  • [Journal-full-title] Emerging infectious diseases
  • [ISO-abbreviation] Emerging Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ PMC2876741
  •  go-up   go-down


5. Birhiray RE, Shaw G, Guldan S, Rudolf D, Delmastro D, Santabarbara P, Brettman L: Phenotypic transformation of CD52(pos) to CD52(neg) leukemic T cells as a mechanism for resistance to CAMPATH-1H. Leukemia; 2002 May;16(5):861-4
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Immunotherapy utilizing CAMPATH-1H for patients with chemotherapy-refractory chronic lymphocytic leukemia has yielded encouraging results with many reports of complete remission.
  • Here we report the outcome of two patients with CD4-positive T cell prolymphocytic leukemia treated with CAMPATH-1H.
  • Both patients responded rapidly to treatment and subsequently developed CD4 lymphopenia.
  • One patient remained in complete remission after 14 weeks of treatment.
  • Serial peripheral blood flow cytometry revealed that the CD52 antigen was present throughout treatment.
  • The other patient who was initially CD52-positive, became CD52-negative after 6 weeks of treatment, and developed progressive symptoms of T cell prolymphocytic leukemia.
  • Immunotherapy was stopped, chemotherapy proved futile, and the patient died.
  • This change in phenotype from CD52-positive to -negative during CAMPATH-1H therapy points out a need to develop strategies for maintaining antigenic expression during monoclonal antibody therapy.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antibodies, Neoplasm / pharmacology. Antigens, CD / analysis. Antigens, Neoplasm. Drug Resistance, Neoplasm. Glycoproteins / analysis. Leukemia, Prolymphocytic / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. CD4-Positive T-Lymphocytes / drug effects. CD4-Positive T-Lymphocytes / pathology. Fatal Outcome. Female. Humans. Immunophenotyping. Leukemia, Prolymphocytic, T-Cell / drug therapy. Leukemia, Prolymphocytic, T-Cell / genetics. Leukemia, Prolymphocytic, T-Cell / pathology. Lymphocyte Activation / genetics. Male. Middle Aged. Phenotype. Remission Induction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11986948.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  •  go-up   go-down


6. Ferrajoli A, O'Brien SM, Cortes JE, Giles FJ, Thomas DA, Faderl S, Kurzrock R, Lerner S, Kontoyiannis DP, Keating MJ: Phase II study of alemtuzumab in chronic lymphoproliferative disorders. Cancer; 2003 Aug 15;98(4):773-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of alemtuzumab in chronic lymphoproliferative disorders.
  • The authors conducted a Phase II trial to evaluate the efficacy and safety of alemtuzumab in advanced or refractory chronic lymphoproliferative disorders.
  • The most common diagnoses were chronic lymphocytic leukemia (n = 42 patients) and T-cell prolymphocytic leukemia (n = 18 patients).
  • Before entering the study, the patients had received multiple therapies (median, three therapies) and the median time from diagnosis was 7 years.
  • Alemtuzumab was given intravenously at doses of 3 mg, 10 mg, and 30 mg on 3 consecutive days, after which 30 mg was administered 3 times a week.
  • Patients were treated for 4-12 weeks depending on disease response.
  • RESULTS: The overall response rate was 35%, the complete response (CR) rate was 13%, and the partial response (PR) rate was 22%.
  • The median duration of response was 18 months for patients achieving a CR and 7 months for patients achieving a PR.
  • These were most common during the first week of therapy.
  • CONCLUSIONS: Alemtuzumab has a high response rate in patients with chronic lymphoproliferative disorders.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Humans. Immunocompromised Host. Infection / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Prolymphocytic / drug therapy. Middle Aged. Survival Rate

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 American Cancer Society.DOI 10.1002/cncr.11551
  • (PMID = 12910522.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


7. Dearden CE: T-cell prolymphocytic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S239-43
Hazardous Substances Data Bank. PENTOSTATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia is a rare postthymic malignancy with distinctive clinical, morphologic, immunophenotypic, and cytogenetic features.
  • The clinical course is typically aggressive with poor response to conventional chemotherapy and short survival.
  • Treatment with purine analogues and alemtuzumab has resulted in significantly higher response rates and improved survival.
  • Nevertheless, responses are relatively short, and the only potential curative treatment is allogeneic stem cell transplantation.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia, Prolymphocytic, T-Cell / therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Female. Gene Expression Regulation, Leukemic. Humans. Immunophenotyping. Male. Medical Oncology / methods. Middle Aged. Pentostatin / therapeutic use. Stem Cell Transplantation / methods. Transplantation, Homologous / methods. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19778847.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab
  • [Number-of-references] 38
  •  go-up   go-down


8. Khot A, Dearden C: T-cell prolymphocytic leukemia. Expert Rev Anticancer Ther; 2009 Mar;9(3):365-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia is a rare post-thymic lymphoid disorder, which has distinctive clinical, morphologic, immunophenotypic and cytogenetic features.
  • It has previously been associated with an aggressive course, poor response to conventional chemotherapy and a short median survival.
  • Treatment with purine analogs and the monoclonal antibody alemtuzumab has resulted in significantly higher response rates and increased survival.
  • However, responses are transient and allogeneic hematopoietic progenitor-cell transplantation remains the only potential curative option.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / therapy
  • [MeSH-minor] Antibodies, Monoclonal / genetics. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / genetics. Antibodies, Neoplasm / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diagnosis, Differential. Drug Administration Schedule. Hematopoietic Stem Cell Transplantation. Humans. Prognosis. Stem Cell Transplantation. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19275513.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Number-of-references] 46
  •  go-up   go-down


9. Michallet AS, Lesca G, Radford-Weiss I, Delarue R, Varet B, Buzyn A: T-cell prolymphocytic leukemia with autoimmune manifestations in Nijmegen breakage syndrome. Ann Hematol; 2003 Aug;82(8):515-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia with autoimmune manifestations in Nijmegen breakage syndrome.
  • Nijmegen breakage syndrome (NBS) is characterized by growth retardation, microcephaly, mental retardation, immunodeficiency, and predisposition to malignancies, especially B-cell lymphomas.
  • In contrast, leukemia is rare.
  • The diagnosis of T-cell prolymphocytic leukemia (T-PLL) was confirmed by cytological and immunological assays (TdT(-), CD2(+), CD5(+), CD3m, and CD7(+)).
  • Since T-PLL is refractory to conventional therapies with a poor prognosis, an intensive chemotherapy such as 2'-deoxycoformycin with anti-CDw52 monoclonal antibodies is usually favored.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / etiology. Growth Disorders / complications. Immunologic Deficiency Syndromes / complications. Intellectual Disability / complications. Leukemia, Prolymphocytic / etiology. Leukemia, T-Cell / etiology. Microcephaly / complications
  • [MeSH-minor] Adolescent. Antibiotics, Antineoplastic / therapeutic use. Cytogenetic Analysis. Factor V Deficiency / etiology. Genes, Recessive. Glucocorticoids / therapeutic use. Humans. Infant, Newborn. Male. Methylprednisolone / therapeutic use. Pentostatin / therapeutic use. Syndrome

  • Genetic Alliance. consumer health - Nijmegen breakage syndrome.
  • MedlinePlus Health Information. consumer health - Growth Disorders.
  • Hazardous Substances Data Bank. PENTOSTATIN .
  • Hazardous Substances Data Bank. METHYLPREDNISOLONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12845481.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Glucocorticoids; 395575MZO7 / Pentostatin; X4W7ZR7023 / Methylprednisolone
  •  go-up   go-down


10. Toyota S, Nakamura N, Dan K: T-cell prolymphocytic leukemia with hemorrhagic gastrointestinal involvement and a new chromosomal abnormality. Int J Hematol; 2002 Apr;75(3):314-7
MedlinePlus Health Information. consumer health - Gastrointestinal Bleeding.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia with hemorrhagic gastrointestinal involvement and a new chromosomal abnormality.
  • We report a case of T-cell prolymphocytic leukemia in a 56-year-old woman who exhibited hemorrhaging with gastric involvement as the first manifestation.
  • This patient's condition was diagnosed as T-cell prolymphocytic leukemia based on the findings of lymphocytosis, abnormal immunophenotype, hepatosplenomegaly, lymphadenopathy, and cutaneous involvement.
  • Cytogenetic analysis revealed chromosomal abnormalities, 46,XX,der(1), add(1)(p36), that have not previously been described in T-cell prolymphocytic leukemia.
  • In spite of a transient response to chemotherapy, the patient died 15 months after onset of the disease.
  • [MeSH-major] Chromosome Aberrations. Gastrointestinal Hemorrhage / complications. Leukemia, Prolymphocytic / genetics. Leukemia, T-Cell / genetics. T-Lymphocytes / immunology. X Chromosome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11999363.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, CD
  •  go-up   go-down


11. Maeda A, Iwai K, Ishibashi T: [Successful treatment of T-cell prolymphocytic leukemia (T-PLL) with fludarabine monophosphate]. Rinsho Ketsueki; 2009 Aug;50(8):658-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful treatment of T-cell prolymphocytic leukemia (T-PLL) with fludarabine monophosphate].
  • We report a 79-year-old woman with T-cell prolymphocytic leukemia (T-PLL) who was successfully treated with fludarabine monophosphate.
  • Therapy with oral cyclophosphamide (50 mg/day) was started, but was discontinued because of agranulocytosis.
  • The reticulocyte count increased gradually, and she became free from red cell transfusions.
  • Unfortunately, she finally died from massive gastro intestinal hemorrhage, but T-PLL was well controlled at the time of death.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Leukemia, Prolymphocytic, T-Cell / drug therapy. Vidarabine Phosphate / analogs & derivatives
  • [MeSH-minor] Aged. Drug Administration Schedule. Fatal Outcome. Female. Gastrointestinal Hemorrhage. Humans. Infusions, Intravenous. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19915381.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 106XV160TZ / Vidarabine Phosphate; 1X9VK9O1SC / fludarabine phosphate
  •  go-up   go-down


12. Miyata A, Yoshino T, Kojima K, Fujii S, Kikuchi T: [T-cell prolymphocytic leukemia complicated by diffuse large B-cell lymphoma of the stomach]. Rinsho Ketsueki; 2001 Jan;42(1):47-50
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [T-cell prolymphocytic leukemia complicated by diffuse large B-cell lymphoma of the stomach].
  • We describe a case of T-cell prolymphocytic leukemia (T-PLL) in a 76-year-old man, who developed diffuse large B-cell lymphoma (DLBL) of the stomach, a previously unreported occurrence.
  • He was diagnosed as having T-PLL on the basis of the characteristic cell morphology and immunophenotype (CD2+, CD3+, CD4+, CD5+, CD7+, CD8-, CD25-, TCR alpha/beta+), but cytogenetic analysis showed no abnormalities.
  • Fifteen months later, he developed a gastric tumor.
  • Chemotherapy eradicated the tumor, whereas the T-PLL was resistant to the therapy.
  • The disease showed an indolent course for about 2 years thereafter.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Stomach Neoplasms / pathology

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • Genetic Alliance. consumer health - B Cell Prolymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11235134.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


13. Dearden CE: T-cell prolymphocytic leukemia. Med Oncol; 2006;23(1):17-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive post-thymic malignancy with poor response to conventional treatment and short survival.
  • It can readily be distinguished from other T-cell leukemias on the basis of the distinctive morphology, immunophenotype, and cytogenetics.
  • Consistent chromosomal translocations involving the T-cell receptor gene and one of two protooncogenes (TCL-1 and MTCP-1) are seen in the majority of cases and are likely to be involved in the pathogenesis of the disorder.
  • The CD52 antigen is expressed at high density on the malignant T-cells and therapy with alemtuzumab, a humanized IgG1 antibody that targets this antigen, has produced promising results.
  • However, relapse is inevitable and strategies using both autologous and allogeneic stem cell transplantation are currently being explored.
  • Additional clinical trials are investigating the use of alemtuzumabin combinations with chemotherapy, either concurrent or sequential.
  • In the future we hope to have a betterunderstanding of how best to integrate these therapeutic approaches to further prolong survival for patients with T-PLL.
  • [MeSH-major] Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Dev. 1996 Oct 1;10(19):2411-22 [8843194.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1721-6 [11535503.001]
  • [Cites] Leuk Lymphoma. 2002 Dec;43(12):2331-4 [12613520.001]
  • [Cites] Mol Cell. 2000 Aug;6(2):395-407 [10983986.001]
  • [Cites] Ann Hematol. 2001 Dec;80(12):749-51 [11797117.001]
  • [Cites] Br J Haematol. 1997 Mar;96(4):724-32 [9074412.001]
  • [Cites] Br J Haematol. 1998 Nov;103(2):488-94 [9827924.001]
  • [Cites] J Clin Oncol. 1997 Jul;15(7):2667-72 [9215839.001]
  • [Cites] Nat Med. 1997 Oct;3(10):1155-9 [9334731.001]
  • [Cites] Science. 1985 Mar 1;227(4690):1044-7 [3919442.001]
  • [Cites] Br J Haematol. 1986 Sep;64(1):111-24 [3489482.001]
  • [Cites] Blood. 1996 Mar 1;87(5):1923-7 [8634440.001]
  • [Cites] Leukemia. 1997 Aug;11(8):1305-11 [9264385.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Jul;31(3):248-54 [11391795.001]
  • [Cites] Blood. 1991 Dec 15;78(12):3269-74 [1742486.001]
  • [Cites] Cancer Res. 1997 Dec 15;57(24):5452-6 [9407948.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Apr;30(4):336-41 [11241786.001]
  • [Cites] Oncogene. 1993 Sep;8(9):2475-83 [8361760.001]
  • [Cites] Blood. 1998 May 15;91(10):3920-6 [9573030.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2588-93 [7989933.001]
  • [Cites] Br J Haematol. 1996 Jun;93(4):921-7 [8703826.001]
  • [Cites] Leuk Res. 1998 Feb;22(2):185-91 [9593475.001]
  • [Cites] J Clin Oncol. 2002 Jan 1;20(1):205-13 [11773171.001]
  • [Cites] Lancet. 1973 Aug 4;2(7823):232-4 [4124423.001]
  • (PMID = 16645226.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 28
  •  go-up   go-down


14. Dhar-Munshi S, Alton P, Ayliffe WH: Masquerade syndrome: T-cell prolymphocytic leukemia presenting as panuveitis. Am J Ophthalmol; 2001 Aug;132(2):275-7
Genetic Alliance. consumer health - Panuveitis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Masquerade syndrome: T-cell prolymphocytic leukemia presenting as panuveitis.
  • PURPOSE: To report a case of T-cell prolymphocytic leukemia with panuveitis as the primary presenting feature.
  • She was found to have signs of panuveitis with a central exudative retinal detachment.
  • Further investigations revealed that she was suffering from the rare T-cell prolymphocytic leukemia.
  • Both systemic and ocular manifestations of the disease resolved after chemotherapy with Campath-IH antigen and as she went into complete remission.
  • CONCLUSION: This case illustrates that leukemias can present with primarily ocular findings, and the sudden appearance of a serous retinal detachment with inflammatory signs in an otherwise healthy person warrants a thorough systemic screening for an underlying malignancy.
  • [MeSH-major] Antigens, Neoplasm. Leukemia, Prolymphocytic / diagnosis. Leukemia, T-Cell / diagnosis. Panuveitis / diagnosis. Retinal Neoplasms / diagnosis
  • [MeSH-minor] Antigens, CD. Diagnosis, Differential. Female. Fluorescein Angiography. Glycoproteins. Humans. Middle Aged. Retinal Detachment / diagnosis. Syndrome. Visual Acuity

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11476701.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins
  •  go-up   go-down


15. Madaris L: T-cell prolymphocytic leukemia: A rare disease in an elderly female. J Am Acad Nurse Pract; 2010 Dec;22(12):648-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia: A rare disease in an elderly female.
  • This report includes a review of the morphology of T-cell prolymphocytic leukemia (PLL), diagnosis, and the treatment options considered.
  • DATA SOURCES: T-cell PLL is a rare blood disorder that represents a very small number of all chronic leukemias.
  • An extensive review of scientific literature related to the cell morphology and pathology of this disease, as well as clinical trials of treatment options provided the background for this case report.
  • CONCLUSION: A diagnosis of T-cell PLL was made after a computed tomography scan of the abdomen confirmed splenomegaly and a bone marrow biopsy showed a hypercellular marrow infiltrated with numerous small lymphocytes, consistent with this disease.
  • Currently, there is no optimal treatment for T-cell PLL, but alemtuzumab has shown success with extending survival 1-3 years.
  • IMPLICATIONS FOR PRACTICE: This case presented several ethical and practical challenges for this patient and her family in making a decision for chemotherapy treatment.
  • This case underscores the need for the physicians and nurse practitioners to establish a collaborative relationship with patient, family, and other care providers when advocating for or against treatment.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia, Prolymphocytic, T-Cell / drug therapy
  • [MeSH-minor] Abdominal Pain / etiology. Aged, 80 and over. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / adverse effects. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Bone Marrow Examination. Dementia / complications. Fatal Outcome. Female. Humans. Nurse Practitioners. Patient Selection. Rare Diseases. Tomography, X-Ray Computed

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 The Author Journal compilation ©2010 American Academy of Nurse Practitioners.
  • (PMID = 21129072.001).
  • [ISSN] 1745-7599
  • [Journal-full-title] Journal of the American Academy of Nurse Practitioners
  • [ISO-abbreviation] J Am Acad Nurse Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


16. Rao RA, Chin K, Pilichowska M, Foss F: Outcomes in peripheral T-cell lymphoma: Prognosis based on IPI staging. J Clin Oncol; 2004 Jul 15;22(14_suppl):6706

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes in peripheral T-cell lymphoma: Prognosis based on IPI staging.
  • : 6706 Background: The T cell non-Hodgkin's lymphomas comprise a heterogeneous group of diseases which, with the exception of anaplastic large cell lymphoma, are associated with short response durations and survival after conventional cytotoxic chemotherapy .
  • METHODS: We performed a retrospective analysis of 35 patients (m=20, f=15) with non-cutaneous T-cell lymphoma treated at a single institution to determine whether clinical features or IPI classification were predictive of outcome.
  • The histopathologic subtypes included: AILD (5), NK-T cell lymphoma (2), PTCLu (14), HTLV-1 associated ATL (3), T-CLL (6), T-ALL (5).
  • The majority of patients had advanced disease (31 stage IV, 3 Stage III) at presentation.
  • Extranodal disease was found in 16 of 35, with bone marrow involvement in 8, visceral infiltration in 9, and skin in 6.
  • The majority of patients (68%) were treated with anthracycline based multi-agent chemotherapy.
  • Further multi-institutional studies are warranted to further explore the predictors of outcome in underrepresented histologic subtypes of T-cell NHL.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28014609.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


17. Sugimoto T, Imoto S, Matsuo Y, Kojima K, Yasukawa M, Murayama T, Kohfuku J, Mizuno I, Yakushijin K, Sada A, Nishimura R, Koizumi T: T-cell receptor gammadelta T-cell leukemia with the morphology of T-cell prolymphocytic leukemia and a postthymic immunophenotype. Ann Hematol; 2001 Dec;80(12):749-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell receptor gammadelta T-cell leukemia with the morphology of T-cell prolymphocytic leukemia and a postthymic immunophenotype.
  • T-cell prolymphocytic leukemia (T-PLL) is a postthymic T-cell neoplasm with a characteristic morphology and heterogeneous immunophenotype.
  • Most cases of T-PLL express membrane T-cell receptors (TCRs) of the alphabeta phenotype.
  • We experienced a 30-year-old man suffering from TCRgammadelta T-cell leukemia with morphology compatible to T-PLL with a postthymic phenotype.
  • Peripheral blood and bone marrow were occupied with medium-sized lymphocytes, which had moderately condensed chromatin with a single nucleolus and sparse, nongranular basophilic cytoplasm.
  • He was diagnosed as having T-PLL and was treated with combination chemotherapy.
  • Six months later the leukemic cell became chemoresistant.
  • Although the patient showed transient improvement in response to pentostatin, he died 13 months after the diagnosis.
  • To our knowledge, this is the first case of T-PLL with a TCRgammadelta phenotype.
  • [MeSH-major] Immunophenotyping. Leukemia, Prolymphocytic / immunology. Leukemia, Prolymphocytic / pathology. Leukemia, T-Cell / immunology. Leukemia, T-Cell / pathology. Receptors, Antigen, T-Cell, gamma-delta / analysis
  • [MeSH-minor] Adult. Anemia. Antigens, CD / analysis. Bone Marrow / pathology. Cell Membrane / immunology. Cytogenetic Analysis. Erythema. Flow Cytometry. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. HLA-DR Antigens / analysis. Humans. Leukocyte Count. Lymphatic Diseases. Lymphocyte Count. Male. Microscopy, Electron. Thymus Gland / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11797117.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / HLA-DR Antigens; 0 / Receptors, Antigen, T-Cell, gamma-delta
  •  go-up   go-down


18. Keating MJ, Cazin B, Coutré S, Birhiray R, Kovacsovics T, Langer W, Leber B, Maughan T, Rai K, Tjønnfjord G, Bekradda M, Itzhaki M, Hérait P: Campath-1H treatment of T-cell prolymphocytic leukemia in patients for whom at least one prior chemotherapy regimen has failed. J Clin Oncol; 2002 Jan 01;20(1):205-13
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Campath-1H treatment of T-cell prolymphocytic leukemia in patients for whom at least one prior chemotherapy regimen has failed.
  • PURPOSE: We conducted a retrospective analysis to evaluate the safety and efficacy of Campath-1H, an anti-CD52 humanized monoclonal antibody, in previously treated T-prolymphocytic leukemia (T-PLL) patients in a compassionate-use program.
  • PATIENTS AND METHODS: Seventy-six patients with T-PLL (including four chemotherapy-naive patients) received 3, 10, and 30 mg of Campath-1H on sequential days, followed by 30 mg three times weekly, as 2-hour intravenous infusions, for 4 to 12 weeks.
  • Spleen liver, lymph node, and skin involvement were present in 64%, 40%, 54%, and 18% of patients, respectively.
  • The objective response rate was 51% (95% confidence interval [CI], 40% to 63%), with a 39.5% complete response (CR) rate (95% CI, 28% to 51%).
  • The median duration of CR was 8.7 months (range, 0.13+ to 44.4), and median time to progression was 4.5 months (range, 0.1 to 45.4) compared with 2.3 months (range, 0.2 to 28.1) after first-line chemotherapy.
  • The median overall survival was 7.5 months (14.8 months for CR patients).
  • Fifteen infectious episodes occurred during treatment in 10 patients (13%), leading to treatment discontinuation in three.
  • Severe thrombocytopenia and/or neutropenia occurred in six patients (8%), leading to treatment discontinuation in four.
  • Two treatment-related deaths occurred.
  • CONCLUSION: Campath-1H is an active drug in T-PLL patients for whom first-line therapy has failed.
  • It has a favorable risk/benefit ratio and should be prospectively investigated in chemotherapy-naive patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, T-Cell / drug therapy. Salvage Therapy / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Consumer Product Safety. Female. Hematologic Diseases / chemically induced. Hematologic Diseases / epidemiology. Humans. Infusions, Intravenous. Male. Middle Aged. Opportunistic Infections / chemically induced. Opportunistic Infections / epidemiology. Retrospective Studies. Survival Rate. Time Factors

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11773171.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


19. Delgado J, Bustos JG, Jimenez MC, Quevedo E, Hernandez-Navarro F: Are activation markers (CD25, CD38 and CD103) predictive of sensitivity to purine analogues in patients with T-cell prolymphocytic leukemia and other lymphoproliferative disorders? Leuk Lymphoma; 2002 Dec;43(12):2331-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Are activation markers (CD25, CD38 and CD103) predictive of sensitivity to purine analogues in patients with T-cell prolymphocytic leukemia and other lymphoproliferative disorders?
  • T-cell prolymphocytic leukemia (T-PLL) is a rare lymphoproliferative disorder with distinctive clinical and laboratory features.
  • It is often resistant to conventional chemotherapy, but complete or partial responses have been documented with the use of purine analogues.
  • We report on two cases of T-PLL with a slightly different immunophenotype but a remarkably different response to pentostatin.
  • We discuss the possible therapeutic implications of this finding and establish a comparison between immunophenotype and sensitivity to purine analogues in patients with T-PLL and other chronic lymphoproliferative disorders.
  • [MeSH-major] Antigens, CD / analysis. Drug Resistance, Neoplasm. Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy. Lymphocyte Activation / drug effects. Purines / therapeutic use
  • [MeSH-minor] ADP-ribosyl Cyclase / analysis. Antigens, CD38. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers / analysis. Female. Humans. Immunophenotyping. Integrin alpha Chains / analysis. Lymphoproliferative Disorders / drug therapy. Male. Membrane Glycoproteins. Middle Aged. Predictive Value of Tests. Receptors, Interleukin-2 / analysis. Remission Induction / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12613520.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / Integrin alpha Chains; 0 / Membrane Glycoproteins; 0 / Purines; 0 / Receptors, Interleukin-2; 0 / alpha E integrins; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
  •  go-up   go-down


20. Dumont FJ: CAMPATH (alemtuzumab) for the treatment of chronic lymphocytic leukemia and beyond. Expert Rev Anticancer Ther; 2002 Feb;2(1):23-35
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CAMPATH (alemtuzumab) for the treatment of chronic lymphocytic leukemia and beyond.
  • CAMPATH (CAMPATH-1H, alemtuzumab, MabCAMPATH), is a lymphocyte-depleting humanized monoclonal antibody that was recently approved in the USA and Europe for the treatment of chronic lymphocytic leukemia (CLL).
  • It targets CD52--a small glycosylphosphatidylinositol-anchored glycoprotein that is highly expressed on normal T- and B-lymphocytes and on a large proportion of lymphoid cell malignancies--but not on hematopoietic progenitor cells.
  • CAMPATH was shown to be effective against CLL refractory to chemotherapy with an acceptable toxicity profile.
  • CAMPATH is also active against T-cell prolymphocytic leukemia and has been extensively used to prevent graft-versus-host disease associated with bone marrow transplantation.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Clinical Trials as Topic. Drug Approval. Hematopoietic Stem Cell Transplantation. Humans. Safety

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12113063.001).
  • [ISSN] 1473-7140
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 75
  •  go-up   go-down


21. Dearden C: The role of alemtuzumab in the management of T-cell malignancies. Semin Oncol; 2006 Apr;33(2 Suppl 5):S44-52
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of alemtuzumab in the management of T-cell malignancies.
  • T-cell malignancies are rare, making up 10% to 15% of all lymphoid neoplasms in adults.
  • They include many different types of disorders such as T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia, adult T-cell leukemia/lymphoma, cutaneous T-cell lymphoma, and peripheral T-cell lymphoma, which are themselves divided into multiple subcategories.
  • Most T-cell malignancies arise as a result of chromosomal abnormalities, including T-cell receptor rearrangement anomalies.
  • Viral infections are implicated in the development of adult T-cell leukemia/lymphoma and some cases of peripheral T-cell lymphoma have been linked to Epstein-Barr virus or human immunodeficiency virus infection.
  • With the possible exception of T-cell large granular lymphocytic leukemia, which often has an indolent course, T-cell malignancies have not responded well to conventional chemotherapeutic treatment.
  • The introduction of monoclonal antibodies for the treatment of cancer has changed the outlook for patients with T-cell malignancies.
  • Recent studies with single-agent alemtuzumab, an anti-CD52 monoclonal antibody, have shown improved response rates and survival in patients with T-cell prolymphocytic leukemia and cutaneous T-cell lymphoma.
  • Preliminary data also suggest that alemtuzumab may have activity in patients with heavily pretreated peripheral T-cell lymphoma who are refractory to conventional chemotherapy.
  • Preclinical studies with mice bearing human adult T-cell leukemia/lymphoma cells suggest that alemtuzumab may have a potential therapeutic role in this setting.
  • Treatment of T-cell hematologic malignancies with alemtuzumab appears promising.
  • Earlier treatment and combination with chemotherapeutic agents may improve treatment outcome for patients with these malignancies and allow for consolidation with stem cell transplant strategies in selected patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Neoadjuvant Therapy. Remission Induction. Stem Cell Transplantation. Survival Rate

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16720203.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 103
  •  go-up   go-down


22. Dearden C: Alemtuzumab in peripheral T-cell malignancies. Cancer Biother Radiopharm; 2004 Aug;19(4):391-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab in peripheral T-cell malignancies.
  • Over the past 5 years, a number of trials have demonstrated that alemtuzumab has clinical activity in mature T-cell diseases such as T-cell prolymphocytic leukemia (T-PLL) and cutaneous T-cell lymphoma (CTCL).
  • Alemtuzumab is particularly effective in clearing malignant lymphocytes from peripheral blood and bone marrow and may therefore facilitate stem-cell transplantation (SCT) in selected patients.
  • The toxicity profile for the antibody is acceptable; the major complications are infusional reactions, which generally subside after the first 1-2 weeks of therapy, and prolonged lymphopenia associated with reactivation of viruses.
  • These can be minimized by careful monitoring and the use of prophylactic therapy.
  • Future studies will be directed toward: alternative routes (subcutaneous) and schedules of administration; use as first-line therapy; combination strategies with conventional chemotherapy; and use of alemtuzumab to purge minimal residual bone-marrow disease prior to SCT.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy. Lymphoma, T-Cell, Cutaneous / drug therapy. Skin Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright Mary Ann Liebert, Inc.
  • (PMID = 15453953.001).
  • [ISSN] 1084-9785
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 34
  •  go-up   go-down


23. Absi A, Hsi E, Kalaycio M: Prolymphocytic leukemia. Curr Treat Options Oncol; 2005 May;6(3):197-208
Hazardous Substances Data Bank. PENTOSTATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolymphocytic leukemia.
  • Prolymphocytic leukemia is a rare chronic lymphoproliferative disorder that includes two subtypes, B cell and T cell, each with its own distinct clinical, laboratory and pathological features.
  • T-cell prolymphocytic leukemia has an aggressive course with short median survival and poor response to chemotherapy.
  • With the introduction of alemtuzumab, most patients who progressed despite treatment with pentostatin had a major response with a complete remission rate higher than that obtained with pentostatin when used as a first line.
  • We recommend alemtuzumab as initial therapy and offer stem cell transplant (SCT) to selected young, healthy patients who respond.
  • Although B-cell prolymphocytic leukemia is also a progressive disease, some patients can achieve a prolonged progression-free-survival with fludarabine.
  • Rituximab is a promising agent and further investigations are warranted to better define its role in treatment of this disorder.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, B-Cell / therapy. Leukemia, Prolymphocytic / therapy. Leukemia, T-Cell / therapy
  • [MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / administration & dosage. Female. Humans. Male. Pentostatin / administration & dosage. Rituximab. Stem Cell Transplantation

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):376-88 [11208829.001]
  • [Cites] Leuk Lymphoma. 1999 Mar;33(1-2):169-79 [10194135.001]
  • [Cites] Am J Hematol. 2003 Oct;74(2):145-7 [14508807.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1721-6 [11535503.001]
  • [Cites] Am J Hematol. 2000 Apr;63(4):230-1 [10706770.001]
  • [Cites] Eur J Haematol. 2001 Feb;66(2):137-9 [11168523.001]
  • [Cites] Leukemia. 1994 Oct;8(10):1640-5 [7523797.001]
  • [Cites] Blood. 1994 Jan 15;83(2):435-45 [7506951.001]
  • [Cites] Acta Haematol. 1999;102(2):94-8 [10529513.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):2949-51 [10077617.001]
  • [Cites] Am J Clin Pathol. 2001 Apr;115(4):571-81 [11293906.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3885-9 [9520462.001]
  • [Cites] Eur J Haematol. 1996 Apr;56(4):235-40 [8641392.001]
  • [Cites] Clin Lymphoma. 2004 Mar;4(4):220-7 [15072613.001]
  • [Cites] Br J Haematol. 1997 Mar;96(4):724-32 [9074412.001]
  • [Cites] Br J Haematol. 1998 Nov;103(2):488-94 [9827924.001]
  • [Cites] Cancer Genet Cytogenet. 1991 Aug;55(1):1-9 [1913594.001]
  • [Cites] J Clin Oncol. 1995 Mar;13(3):570-4 [7884417.001]
  • [Cites] J Clin Oncol. 1997 Jan;15(1):37-43 [8996122.001]
  • [Cites] J Clin Oncol. 1997 Jul;15(7):2667-72 [9215839.001]
  • [Cites] Nat Med. 1997 Oct;3(10):1155-9 [9334731.001]
  • [Cites] Blood. 2002 Aug 1;100(3):768-73 [12130484.001]
  • [Cites] Ann Hematol. 2004 May;83(5):319-21 [15060751.001]
  • [Cites] Am J Hematol. 1992 May;40(1):71-2 [1566752.001]
  • [Cites] Int J Clin Oncol. 2003 Dec;8(6):391-4 [14663643.001]
  • [Cites] Semin Oncol. 1990 Oct;17(5 Suppl 8):66-70 [1699285.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3555-61 [14506141.001]
  • [Cites] Eur J Haematol. 1997 Jan;58(1):46-50 [9020373.001]
  • [Cites] Bone Marrow Transplant. 1996 Mar;17(3):371-5 [8704689.001]
  • [Cites] Eur J Haematol. 1992 Jul;49(1):46-7 [1499697.001]
  • [Cites] Hematol Pathol. 1987;1(1):27-33 [3509770.001]
  • [Cites] Leukemia. 1997 Aug;11(8):1305-11 [9264385.001]
  • [Cites] J Clin Oncol. 1992 Nov;10(11):1821 [1357112.001]
  • [Cites] Blood. 1991 Dec 15;78(12):3269-74 [1742486.001]
  • [Cites] Anticancer Drugs. 2001 Jun;12 Suppl 2:S15-9 [11508932.001]
  • [Cites] Leuk Lymphoma. 2001 Sep-Oct;42(5):981-7 [11697653.001]
  • [Cites] J Biol Chem. 1995 Mar 17;270(11):6088-99 [7890742.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2588-93 [7989933.001]
  • [Cites] Br J Haematol. 1997 Mar;96(3):617-9 [9054672.001]
  • [Cites] J Clin Oncol. 1995 May;13(5):1284-5 [7738636.001]
  • [Cites] Br J Haematol. 1996 Sep;94(3):580 [8790162.001]
  • [Cites] Leuk Res. 1998 Feb;22(2):185-91 [9593475.001]
  • [Cites] J Clin Oncol. 2002 Jan 1;20(1):205-13 [11773171.001]
  • [Cites] J Clin Oncol. 1991 Jan;9(1):175-88 [1702143.001]
  • [Cites] Br J Haematol. 1996 Apr;93(1):157-9 [8611452.001]
  • [Cites] Leuk Lymphoma. 2002 Jan;43(1):149-51 [11908720.001]
  • [Cites] Jpn J Clin Oncol. 1998 Apr;28(4):267-9 [9657013.001]
  • [Cites] Ann Hematol. 1998 Feb;76(2):85-6 [9540763.001]
  • [Cites] Cancer Treat Res. 1993;64:105-19 [7680874.001]
  • [Cites] Clin Lymphoma. 2002 Sep;3(2):105-10 [12435283.001]
  • [Cites] Cancer. 2003 Jan 1;97(1):114-20 [12491512.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2825-33 [9704735.001]
  • (PMID = 15869731.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 54
  •  go-up   go-down


24. Osuji N, Del Giudice I, Matutes E, Morilla A, Owusu-Ankomah K, Morilla R, Dunlop A, Catovksy D: CD52 expression in T-cell large granular lymphocyte leukemia--implications for treatment with alemtuzumab. Leuk Lymphoma; 2005 May;46(5):723-7
MedlinePlus Health Information. consumer health - Chronic Lymphocytic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD52 expression in T-cell large granular lymphocyte leukemia--implications for treatment with alemtuzumab.
  • Few reports on the successful treatment of T-cell large granular lymphocyte (LGL) leukemia with the humanized anti-CD52 monoclonal antibody alemtuzumab are emerging in the literature.
  • Using semi-quantitative 2- and 3-color flow cytometry, we documented the expression of CD52 in 100% of abnormal cells in T-cell LGL leukemia (n = 11) and natural killer (NK) cell LGL leukemia (n = 2), and showed no significant difference in CD52 expression between T-cell prolymphocytic leukemia (PLL) and T-cell LGL leukemia.
  • Higher CD52 expression has been noted in responders to alemtuzumab in T-cell PLL and in chronic lymphocytic leukemia (CLL), a B-cell disorder.
  • The strong and consistent expression of CD52 shown here highlights the potential role of alemtuzumab in the treatment of refractory T-cell LGL leukemia and possibly aggressive NK cell leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / biosynthesis. Antigens, Neoplasm / biosynthesis. Antineoplastic Agents / therapeutic use. Glycoproteins / biosynthesis. Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / immunology. Leukemia, T-Cell / drug therapy

  • Genetic Alliance. consumer health - Large granular lymphocyte leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16019510.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  •  go-up   go-down


25. Kennedy GA, Seymour JF, Wolf M, Januszewicz H, Davison J, McCormack C, Ryan G, Prince HM: Treatment of patients with advanced mycosis fungoides and Sézary syndrome with alemtuzumab. Eur J Haematol; 2003 Oct;71(4):250-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of patients with advanced mycosis fungoides and Sézary syndrome with alemtuzumab.
  • OBJECTIVES: Alemtuzumab (anti-CD52, Campath-1H) has recently been shown to be effective in the treatment of a range of hematological malignancies, including B-cell chronic lymphocytic leukemia and T-cell prolymphocytic leukemia.
  • We undertook a phase II study to evaluate the safety, tolerability and efficacy of alemtuzumab in patients with relapsed or refractory advanced stage cutaneous T-cell lymphoma.
  • PATIENTS AND METHODS: A total of eight patients were enrolled, seven with mycosis fungoides/Sézary syndrome (MF/SS) and one with large-cell transformation of MF.
  • Seven patients had disease refractory to multiple previous therapies.
  • Alemzumab (30 mg) was administered intravenously three times per week for 12 wk or until maximum response.
  • RESULTS: The overall response rate was 38%, with three patients achieving partial remission, two patients with stable disease and three patients with progressive disease (PD) during treatment.
  • The time to progression was short, with all patients developing PD within 4 months of starting alemtuzumab.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Antirheumatic Agents / therapeutic use. Mycosis Fungoides / drug therapy. Sezary Syndrome / drug therapy
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Humanized. Disease Progression. Humans. Middle Aged. Remission Induction. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Mycosis fungoides.
  • Genetic Alliance. consumer health - Sezary syndrome.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12950233.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Antirheumatic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


26. Tallman MS: Monoclonal antibody therapies in leukemias. Semin Hematol; 2002 Oct;39(4 Suppl 3):12-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monoclonal antibody therapies in leukemias.
  • Gemtuzumab ozogamicin, a calicheamicin-conjugated anti-CD33 monoclonal antibody, has demonstrated substantial efficacy in patients with acute myeloid leukemia (AML) and has induced remissions in patients with favorable-, intermediate-, and poor-risk cytogenetics.
  • The immunoconjugate BL-22, comprised of an anti-CD22 monoclonal antibody fused to a fragment of pseudomonas exotoxin PE38, has produced high response rates in patients with purine analog-resistant hairy cell leukemia.
  • Campath-1H (Wellcome, Beckenham, UK, and Ilex Oncology, San Antonio, TX), an anti-CD52 monoclonal antibody, has demonstrated significant activity in patients with previously untreated, relapsed, or refractory chronic lymphocytic leukemia (CLL), as well as in patients with T-cell prolymphocytic leukemia.
  • The anti-CD20 monoclonal antibody rituximab also is effective in treating CLL and is being evaluated in combination with chemotherapeutic agents (cyclophosphamide) and fludarabine.
  • Monoclonal antibodies may sensitize cells to chemotherapy.
  • The optimal role of targeted therapy with monoclonal antibodies and immunoconjugates in acute and chronic leukemias has not yet been determined, but these novel therapies are beginning to fulfill their promise.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Humans. Immunoconjugates / therapeutic use. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2002, Elsevier Science (USA). All rights reserved.
  • (PMID = 12447847.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoconjugates
  • [Number-of-references] 39
  •  go-up   go-down


27. Westin EH, Longo DL: T-small cell disorders. Curr Treat Options Oncol; 2001 Jun;2(3):225-35

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-small cell disorders.
  • These include T-cell prolymphocytic leukemia, T-cell granular lymphocytic leukemia, and mycosis fungoides/Sézary syndrome.
  • With the possible exception of early-stage, skin-localized mycosis fungoides, all are considered incurable, although palliation can be achieved with radiation therapy, chemotherapy, biologic therapy, and combinations of these modalities.
  • The T-cell prolymphocytic leukemias, in contrast, are generally refractory to treatment, with a median survival of typically less than 1 year.
  • Although effective therapy remains elusive in most cases, the development of nucleosides as a class of chemotherapeutic agents and biologics, including interferon, monoclonal antibodies, and vitamin A derivatives, offers new hope for at least more effective palliation of these progressive lymphoproliferative disorders.
  • However, rapid improvement in the treatment of these disorders remains hampered by the rarity of these individual entities.
  • More rapid progress in treatment depends on national and international cooperation to accrue patients for definitive trials of sufficient size to evaluate new treatment options quickly.
  • [MeSH-major] Leukemia, T-Cell / therapy. Lymphoma, T-Cell / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Humans. Prognosis. Radiotherapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Am Acad Dermatol. 1998 Jul;39(1):63-73 [9674399.001]
  • [Cites] Haematologica. 1999 Sep;84(9):809-13 [10477454.001]
  • [Cites] Curr Probl Dermatol. 1990;19:144-9 [2153505.001]
  • [Cites] Hematol Oncol. 1988 Jan-Mar;6(1):7-12 [3277904.001]
  • [Cites] Arch Dermatol. 1993 Jun;129(6):747-52 [8507078.001]
  • [Cites] Blood. 1994 Sep 15;84(6):1765-74 [8080984.001]
  • [Cites] Curr Probl Cancer. 1990 Nov-Dec;14(6):293-371 [2245651.001]
  • [Cites] J Clin Oncol. 1987 Feb;5(2):208-15 [3492594.001]
  • [Cites] Oncol Rep. 2000 Nov-Dec;7(6):1197-201 [11032913.001]
  • [Cites] Hematol Oncol Clin North Am. 1995 Oct;9(5):1057-76 [8522484.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3245-6 [8874229.001]
  • [Cites] Br J Cancer Suppl. 1975 Mar;2:29-43 [52366.001]
  • [Cites] J Clin Oncol. 1997 Jul;15(7):2667-72 [9215839.001]
  • [Cites] Am J Surg Pathol. 1992 Jun;16(6):543-52 [1599034.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 2:S46-9 [9178839.001]
  • [Cites] Leuk Lymphoma. 1995 Aug;18(5-6):521-7 [8528063.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Cancer Res. 1992 Oct 1;52(19 Suppl):5496s-5500s [1394162.001]
  • [Cites] Mayo Clin Proc. 1994 Nov;69(11):1085-8 [7967763.001]
  • [Cites] CA Cancer J Clin. 1993 Mar-Apr;43(2):93-115 [8439814.001]
  • [Cites] Am J Pathol. 1988 Aug;132(2):265-77 [3261136.001]
  • [Cites] Br J Haematol. 1986 Sep;64(1):111-24 [3489482.001]
  • [Cites] Leuk Res. 1988;12(1):89-92 [3282128.001]
  • [Cites] Blood. 1998 May 1;91(9):3372-8 [9558395.001]
  • [Cites] Ann Oncol. 1999 Dec;10(12):1419-32 [10643532.001]
  • [Cites] Front Radiat Ther Oncol. 1991;25:80-9; discussion 132-3 [1908426.001]
  • [Cites] J Natl Cancer Inst. 1993 Apr 21;85(8):658-62 [8468724.001]
  • [Cites] Am J Pathol. 1991 Jun;138(6):1545-52 [1828937.001]
  • [Cites] Blood. 1991 Dec 15;78(12):3269-74 [1742486.001]
  • [Cites] Cancer Treat Rep. 1979 Apr;63(4):647-53 [87277.001]
  • [Cites] Arch Dermatol. 1996 Nov;132(11):1309-13 [8915308.001]
  • [Cites] Blood. 1993 Jul 1;82(1):1-14 [8324214.001]
  • [Cites] Leukemia. 1991;5 Suppl 1:46-8 [1716337.001]
  • [Cites] Cancer. 1982 May 15;49(10):2112-35 [6896167.001]
  • [Cites] Ann Oncol. 1998;9 Suppl 5:S25-30 [9926234.001]
  • [Cites] Semin Oncol. 1999 Jun;26(3):276-89 [10375085.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Clin Lymphoma. 2000 Nov;1 Suppl 1:S45-9 [11707864.001]
  • [Cites] J Clin Oncol. 1995 May;13(5):1284-5 [7738636.001]
  • [Cites] Arch Dermatol Res. 1984;276(1):17-26 [6608322.001]
  • [Cites] J Clin Oncol. 1994 Oct;12 (10 ):2051-9 [7931473.001]
  • [Cites] Mod Pathol. 1998 Oct;11(10):978-82 [9796726.001]
  • [Cites] Neth J Med. 1990 Aug;37(1-2):37-43 [2215832.001]
  • [Cites] N Engl J Med. 1989 Dec 28;321(26):1784-90 [2594037.001]
  • [Cites] Semin Cutan Med Surg. 2000 Jun;19(2):91-9 [10892710.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1620-7 [8068951.001]
  • [Cites] Semin Hematol. 1993 Oct;30(4):286-96 [8266115.001]
  • [Cites] Blood. 1994 Oct 1;84(7):2164-70 [7919331.001]
  • [Cites] Blood. 2000 Apr 1;95(7):2212-8 [10733487.001]
  • [Cites] Arch Dermatol. 1998 Feb;134(2):158-64 [9487207.001]
  • [Cites] Blood. 1998 Jan 15;91(2):399-405 [9427692.001]
  • [Cites] Br J Haematol. 1997 Sep;98(4):927-33 [9326191.001]
  • [Cites] Blood. 1998 Jul 15;92(2):368-73 [9657733.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2385-409 [8839829.001]
  • [Cites] Eur J Immunol. 1988 Dec;18(12):1979-83 [3146510.001]
  • [Cites] Dermatology. 2000;201(1):21-8 [10971054.001]
  • [Cites] Blood. 1997 Jan 1;89(1):256-60 [8978299.001]
  • [Cites] Am J Surg Pathol. 2000 Jan;24(1):40-50 [10632486.001]
  • [Cites] J Am Acad Dermatol. 2000 Nov;43(5 Pt 1):793-6 [11050582.001]
  • (PMID = 12057122.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 60
  •  go-up   go-down


28. Flynn JM, Byrd JC: Campath-1H monoclonal antibody therapy. Curr Opin Oncol; 2000 Nov;12(6):574-81
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Campath-1H monoclonal antibody therapy.
  • Monoclonal antibodies are receiving ever-increasing utilization in the treatment of hematologic malignancies.
  • The genetically engineered Campath-1H has been utilized in the treatment of lymphomas and lymphoid leukemias with impressive results.
  • T-cell prolymphocytic leukemia, chronic lymphocytic leukemia, and non-Hodgkin lymphomas appear to be particularly good targets for this agent.
  • The efficacy demonstrated in clinical trials and manageable toxicities make Campath-1H an appealing agent in the treatment of hematologic malignancies.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Hematologic Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11085457.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA81534-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 75
  •  go-up   go-down


29. Zanesi N, Aqeilan R, Drusco A, Kaou M, Sevignani C, Costinean S, Bortesi L, La Rocca G, Koldovsky P, Volinia S, Mancini R, Calin G, Scott CP, Pekarsky Y, Croce CM: Effect of rapamycin on mouse chronic lymphocytic leukemia and the development of nonhematopoietic malignancies in Emu-TCL1 transgenic mice. Cancer Res; 2006 Jan 15;66(2):915-20
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of rapamycin on mouse chronic lymphocytic leukemia and the development of nonhematopoietic malignancies in Emu-TCL1 transgenic mice.
  • Chronic lymphocytic leukemia (CLL) is the most common leukemia in the world.
  • The TCL1 gene, responsible for prolymphocytic T cell leukemia, is also overexpressed in human B cell malignancies and overexpression of the Tcl1 protein occurs frequently in CLL.
  • Aging transgenic mice that overexpress TCL1 under control of the mu immunoglobulin gene enhancer, develop a CD5+ B cell lymphoproliferative disorder mimicking human CLL and implicating TCL1 in the pathogenesis of CLL.
  • In the current study, we exploited this transgenic mouse to investigate two different CLL-related issues: potential treatment of CLL and characterization of neoplasms that accompany CLL.
  • We successfully transplanted CLL cells into syngeneic mice that led to CLL development in the recipient mice.
  • This approach allowed us to verify the involvement of the Tcl1/Akt/mTOR biochemical pathway in the disease by testing the ability of a specific pharmacologic agent, rapamycin, to slow CLL.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Sirolimus / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Humans. Immunohistochemistry. Mice. Mice, Transgenic


30. Singleton CL, Wack RF, Zabka TS, Kent MS, Larsen RS: Diagnosis and treatment of chronic T-lymphocytic leukemia in a spotted hyena (Crocuta crocuta). J Zoo Wildl Med; 2007 Sep;38(3):488-91
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and treatment of chronic T-lymphocytic leukemia in a spotted hyena (Crocuta crocuta).
  • The morphology and distribution of neoplastic T-lymphocytes within the spleen, liver, peripheral blood, and bone marrow was most consistent with chronic T-lymphocytic leukemia.
  • Treatment with chlorambucil and prednisone effectively decreased the lymphocyte count, but was associated with thrombocytopenia, which resolved after chlorambucil treatment was temporarily discontinued.
  • Chemotherapy was resumed with a single dose of L-asparaginase, followed by a lower dosage of chlorambucil and continued prednisone.
  • Two years after initial diagnosis, the hyena developed a hemoabdomen and was euthanized.
  • Neoplastic T-lymphocytes were present in spleen, liver, visceral and peripheral lymph nodes, lungs, heart, kidney, adrenal glands, mesentery, intestines, pancreas, brain, and bone marrow.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hyaenidae. Leukemia, T-Cell / veterinary
  • [MeSH-minor] Animals. Fatal Outcome. Female. Neoplasm Metastasis. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17939362.001).
  • [ISSN] 1042-7260
  • [Journal-full-title] Journal of zoo and wildlife medicine : official publication of the American Association of Zoo Veterinarians
  • [ISO-abbreviation] J. Zoo Wildl. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


31. Lundin J, Karlsson C, Celsing F: Alemtuzumab therapy for severe autoimmune hemolysis in a patient with B-cell chronic lymphocytic leukemia. Med Oncol; 2006;23(1):137-9
Genetic Alliance. consumer health - Leukemia, B-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab therapy for severe autoimmune hemolysis in a patient with B-cell chronic lymphocytic leukemia.
  • B-cell chronic lymphocytic leukemia (B-CLL) is the most common cause of autoimmune hemolytic anemia (AIHA), and a subgroup of these patients who develop both these conditions fail to respond to corticosteroids, cytotoxic drugs, splenectomy, and iv immunoglobulins.
  • Alemtuzumab is a humanized anti-CD52 monoclonal antibody that is an effective therapy for B-CLL, mycosis fungoides, and T-cell prolymphocytic leukemia.
  • Here we present a case report of a 78-yr-old woman with B-CLL and progressive life-threatening AIHA with hemoglobin count 5.5 g/dL following fludarabine treatment, who was treated successfully with alemtuzumab.
  • No infectious complications were noted during or after alemtuzumab therapy.
  • We conclude that alemtuzumab may be indicated for the treatment of AIHA in B-CLL patients who have failed other treatments.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / complications

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 1998 May;16(5):1885-9 [9586905.001]
  • [Cites] Br J Haematol. 1986 Nov;64(3):479-86 [3539172.001]
  • [Cites] Blood. 1993 Aug 1;82(3):807-12 [7687895.001]
  • [Cites] Br J Haematol. 1996 Apr;93(1):151-3 [8611450.001]
  • [Cites] Blood. 1996 May 1;87(9):3869-76 [8611714.001]
  • [Cites] Eur J Haematol. 2003 May;70(5):319-21 [12694169.001]
  • [Cites] Hematol Cell Ther. 1997 Nov;39 Suppl 1:S41-4 [9471060.001]
  • [Cites] Semin Hematol. 1992 Jan;29(1):64-74 [1570545.001]
  • [Cites] Mol Hum Reprod. 1996 Mar;2(3):177-84 [9238677.001]
  • [Cites] J Clin Oncol. 2002 Sep 15;20(18):3891-7 [12228210.001]
  • [Cites] Blood. 2002 Aug 1;100(3):768-73 [12130484.001]
  • [Cites] Leuk Lymphoma. 2002 May;43(5):1007-11 [12148879.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):891-8 [11564082.001]
  • [Cites] Blood. 1989 May 1;73(6):1431-9 [2713487.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):278-81 [14531909.001]
  • [Cites] Blood. 2000 May 1;95(9):2786-92 [10779422.001]
  • [Cites] J Biol Chem. 1995 Mar 17;270(11):6088-99 [7890742.001]
  • [Cites] Immunology. 1998 Nov;95(3):427-36 [9824507.001]
  • [Cites] Semin Oncol. 1998 Feb;25(1):80-97 [9482530.001]
  • [Cites] Semin Oncol. 1998 Feb;25(1):34-41 [9482525.001]
  • [Cites] Leuk Lymphoma. 2002 Sep;43(9):1755-62 [12685828.001]
  • [Cites] Nature. 1988 Mar 24;332(6162):323-7 [3127726.001]
  • [Cites] Semin Hematol. 1992 Jan;29(1):3-12 [1570541.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1567-74 [9193354.001]
  • [Cites] Ann Oncol. 1992 Feb;3(2):171-2 [1606091.001]
  • (PMID = 16645240.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  •  go-up   go-down


32. Jacobs SA, Foon KA: Monoclonal antibody therapy of leukaemias and lymphomas. Expert Opin Biol Ther; 2005 Sep;5(9):1225-43
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monoclonal antibody therapy of leukaemias and lymphomas.
  • Rituximab, which is a chimeric monoclonal antibody produced by recombinant technology, became the first monoclonal antibody to be approved for haematological malignancies by the US Food and Drug Administration.
  • Radioimmunoconjugates are an attractive therapeutic option for lymphomas due to the inherent sensitivity to radiotherapy, the fact that the local emission of ionising radiation by radiolabelled antibodies may kill cells with or without the target antigen in close proximity to the bound antibody, and penetrating radiation may obviate the problem of limited antibody penetration into bulky, poorly vascularised tumours.
  • This paper reviews rituximab, alemtuzumab and gemtuzumab ozogamicin as monoclonal antibody therapies for leukaemias and lymphomas.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antigens, CD / immunology. Antigens, CD20 / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antigens, Neoplasm / immunology. Glycoproteins / immunology. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, T-Cell / drug therapy. Lymphoma, B-Cell / drug therapy. Lymphoma, Follicular / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Randomized Controlled Trials as Topic. Rituximab. Sialic Acid Binding Ig-like Lectin 3

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16120052.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, CD20; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 170
  •  go-up   go-down


33. Hiromura M, Okada F, Obata T, Auguin D, Shibata T, Roumestand C, Noguchi M: Inhibition of Akt kinase activity by a peptide spanning the betaA strand of the proto-oncogene TCL1. J Biol Chem; 2004 Dec 17;279(51):53407-18
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have demonstrated previously that TCL1 (a proto-oncogene underlying human T cell prolymphocytic leukemia) interacts with Akt and functions as an Akt kinase co-activator.
  • Hence, Akt inhibitors create an attractive target for anticancer therapy.
  • However, no effective inhibitors specific for Akt have been developed.
  • [MeSH-minor] Amino Acid Sequence. Animals. Apoptosis. Binding, Competitive. Blood Proteins / chemistry. Cell Line. Cell Line, Tumor. Cell Membrane / metabolism. Cell Proliferation. Dose-Response Relationship, Drug. Glutathione Transferase / metabolism. Humans. Immunoprecipitation. Kinetics. Lipid Metabolism. Magnetic Resonance Spectroscopy. Mice. Mice, Inbred C57BL. Microscopy, Fluorescence. Mitochondria / metabolism. Models, Molecular. Molecular Sequence Data. Neoplasm Transplantation. Neoplasms / metabolism. Permeability. Phosphatidylinositols / metabolism. Phosphoproteins / chemistry. Phosphorylation. Protein Binding. Protein Conformation. Protein Structure, Tertiary. Protein Transport. Proto-Oncogene Proteins c-akt. Sequence Homology, Amino Acid. Time Factors

  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15459205.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Blood Proteins; 0 / Enzyme Inhibitors; 0 / Peptides; 0 / Phosphatidylinositols; 0 / Phosphoproteins; 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human; 0 / platelet protein P47; EC 2.5.1.18 / Glutathione Transferase; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


34. O'Brien S, Ravandi F, Riehl T, Wierda W, Huang X, Tarrand J, O'Neal B, Kantarjian H, Keating M: Valganciclovir prevents cytomegalovirus reactivation in patients receiving alemtuzumab-based therapy. Blood; 2008 Feb 15;111(4):1816-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Valganciclovir prevents cytomegalovirus reactivation in patients receiving alemtuzumab-based therapy.
  • Median age was 58 years (range, 25-83 years); median number of prior therapies was 2 (range, 0-10).
  • Diagnoses included chronic lymphocytic leukemia (29), T-cell prolymphocytic leukemia (3), hairy cell leukemia (1), adult T-cell leukemia/lymphoma (ATLL) (1), marginal zone leukemia (1), large granular lymphocyte leukemia (2), acute lymphoblastic leukemia (1), and T-cell lymphoma (2).
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Antiviral Agents / therapeutic use. Cytomegalovirus / physiology. Cytomegalovirus Infections / prevention & control. Ganciclovir / analogs & derivatives. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Virus Activation / physiology
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal, Humanized. B-Lymphocytes / drug effects. B-Lymphocytes / immunology. Female. Humans. Lymphocyte Depletion. Male. Patient Selection. T-Lymphocytes / drug effects. T-Lymphocytes / immunology

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Cytomegalovirus Infections.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. GANCICLOVIR .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Blood. 2008 Sep 1;112(5):2167 [18725576.001]
  • (PMID = 18039954.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00562770
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / valganciclovir; 3A189DH42V / alemtuzumab; P9G3CKZ4P5 / Ganciclovir
  •  go-up   go-down


35. Dearden CE, Matutes E, Catovsky D: Alemtuzumab in T-cell malignancies. Med Oncol; 2002;19 Suppl:S27-32
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab in T-cell malignancies.
  • We summarize the results of our experience using alemtuzumab to treat a range of clinically aggressive, mature, post-thymic, T-cell malignancies, including T-cell prolymphocytic leukemia (T-PLL), cutaneous T-cell lymphoma (CTCL), T-cell large granular lymphocyte (T-LGL) leukemia, and human T-cell lymphotropic virus I (HTLV-I) associated adult T-cell leukemia-lymphoma (ATLL).
  • Alemtuzumab was administered at a dose of 30 mg, three times a week until maximum response.
  • Apart from first-dose reactions, which were common, treatment was well tolerated, the main complication being infection and viral reactivation associated with the prolonged lymphopenia.
  • Our results indicate that alemtuzumab has activity in T-cell malignancies, particularly in T-PLL and in patients with predominantly blood and bone marrow disease.
  • It may be possible to prolong response duration by the use of high-dose therapy and stem cell transplantation.
  • Alemtuzumab may also have a role in purging minimal residual disease following other chemotherapy and prior to transplantation.
  • We conclude that treatment with alemtuzumab may offer new hope to patients who otherwise have a bleak prognosis.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / drug effects. Antigens, Neoplasm / drug effects. Antineoplastic Agents / therapeutic use. Glycoproteins / drug effects. Lymphoma, T-Cell / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 1997 Jun;97(3):669-72 [9207420.001]
  • [Cites] Blood. 1993 Aug 1;82(3):807-12 [7687895.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1721-6 [11535503.001]
  • [Cites] Br J Haematol. 1998 Nov;103(2):488-94 [9827924.001]
  • [Cites] J Clin Oncol. 1997 Jul;15(7):2667-72 [9215839.001]
  • [Cites] Blood. 1989 May 1;73(6):1431-9 [2713487.001]
  • [Cites] Blood. 1998 Dec 15;92(12):4491-508 [9845514.001]
  • [Cites] Blood. 1991 Dec 15;78(12):3269-74 [1742486.001]
  • [Cites] Blood. 1998 May 15;91(10):3920-6 [9573030.001]
  • [Cites] J Clin Oncol. 1998 Oct;16(10):3257-63 [9779699.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2588-93 [7989933.001]
  • [Cites] Br J Haematol. 1997 Mar;96(3):617-9 [9054672.001]
  • [Cites] Lancet. 1993 Feb 13;341(8842):432-3 [8094189.001]
  • [Cites] Leuk Res. 1998 Feb;22(2):185-91 [9593475.001]
  • [Cites] Oncogene. 1998 Feb 12;16(6):789-96 [9488043.001]
  • [Cites] Leuk Lymphoma. 1990;2(3-4):179-93 [27456733.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1567-74 [9193354.001]
  • (PMID = 12180489.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  • [Number-of-references] 18
  •  go-up   go-down


36. Malani AK, Gupta C, Rangineni R, Singh J, Ammar H: Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia. Acta Oncol; 2007;46(2):247-9
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia.
  • T-cell large granular lymphocyte leukemia (T-LGL) also known as T-cell chronic lymphocytic leukemia is rare and comprises a small minority of all small lymphocytic leukemias.
  • The concomitant presentation of T-LGL with acute myeloid leukemia (AML) has not been previously reported.
  • We present an elderly gentleman with concomitant T-LGL and AML (non-M3) diagnosed by a combination of morphologic evaluation, immunophenotyping by flow cytometry, and T-cell gene rearrangement studies.
  • The patient was managed with combination AML chemotherapy.
  • He remains alive and well seven months after initial diagnosis.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Prolymphocytic, T-Cell / diagnosis
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Antigens, CD / analysis. Flow Cytometry. Humans. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17453377.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 17
  •  go-up   go-down


37. Yee KW, Zeng Z, Konopleva M, Verstovsek S, Ravandi F, Ferrajoli A, Thomas D, Wierda W, Apostolidou E, Albitar M, O'Brien S, Andreeff M, Giles FJ: Phase I/II study of the mammalian target of rapamycin inhibitor everolimus (RAD001) in patients with relapsed or refractory hematologic malignancies. Clin Cancer Res; 2006 Sep 1;12(17):5165-73
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Everolimus (RAD001, Novartis), an oral derivative of rapamycin, inhibits the mammalian target of rapamycin (mTOR), which regulates many aspects of cell growth and division.
  • RESULTS: Twenty-seven patients (9 acute myelogenous leukemia, 5 myelodysplastic syndrome, 6 B-chronic lymphocytic leukemia, 4 mantle cell lymphoma, 1 myelofibrosis, 1 natural killer cell/T-cell leukemia, and 1 T-cell prolymphocytic leukemia) received everolimus.
  • Grade 3 potentially drug-related toxicities included hyperglycemia (22%), hypophosphatemia (7%), fatigue (7%), anorexia (4%), and diarrhea (4%).
  • One patient developed a cutaneous leukocytoclastic vasculitis requiring a skin graft.
  • Phosphorylation of downstream targets of mTOR, eukaryotic initiation factor 4E-binding protein 1, and/or, p70 S6 kinase, was inhibited in six of nine patient samples, including those from the patient with a major platelet response.
  • Studies of everolimus in combination with therapeutic agents directed against other components of the phosphatidylinositol 3-kinase/Akt/mTOR pathway are warranted.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Myelodysplastic Syndromes / drug therapy. Sirolimus / analogs & derivatives
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / antagonists & inhibitors. Administration, Oral. Adolescent. Adult. Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug-Related Side Effects and Adverse Reactions. Everolimus. Female. Humans. Killer Cells, Natural / immunology. Male. Maximum Tolerated Dose. Middle Aged. Phosphoproteins / antagonists & inhibitors. Phosphorylation. Protein Kinases / drug effects. Protein Kinases / metabolism. Recurrence. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Signal Transduction / drug effects. T-Lymphocytes / immunology. TOR Serine-Threonine Kinases. Treatment Outcome. Vasculitis, Leukocytoclastic, Cutaneous / chemically induced

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16951235.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA55164
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / EIF4EBP1 protein, human; 0 / Phosphoproteins; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


38. Letestu R, Rawstron A, Ghia P, Villamor N, Boeckx N, Boettcher S, Buhl AM, Duerig J, Ibbotson R, Kroeber A, Langerak A, Le Garff-Tavernier M, Mockridge I, Morilla A, Padmore R, Rassenti L, Ritgen M, Shehata M, Smolewski P, Staib P, Ticchioni M, Walker C, Ajchenbaum-Cymbalista F: Evaluation of ZAP-70 expression by flow cytometry in chronic lymphocytic leukemia: A multicentric international harmonization process. Cytometry B Clin Cytom; 2006 Jul 15;70(4):309-14
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of ZAP-70 expression by flow cytometry in chronic lymphocytic leukemia: A multicentric international harmonization process.
  • The clinical course of patients with chronic lymphocytic leukemia (CLL) is heterogeneous with some patients requiring early therapy whereas others will not be treated for years.
  • The evaluation of an individual CLL patient's prognosis remains a problematic issue.
  • Among the available techniques for ZAP-70 detection, flow cytometry is most preferable as it allows the simultaneous quantification of ZAP-70 protein expression levels in CLL cells and residual normal lymphocyte subsets.
  • However, several factors introduce variability in the results reported from different laboratories; these factors include the anti-ZAP-70 antibody clone and conjugate, the staining procedure, the gating strategy, and the method of reporting the results.
  • During this workshop, a technical consensus was reached on the methods for cell permeabilization and immunophenotyping procedures.
  • This procedure was applied to three stabilized blood samples, provided by the UK NEQAS group to all participating members of this study, in order to minimize variability caused by sample storage and shipment.
  • Various gating strategies were used and the ZAP-70 levels were expressed as percentage positive (POS) relative to isotype control or normal B-cells or normal T-cells; in addition the levels were reported as a ratio of expression in CLL cells relative to T-cells.
  • The CLL/T-cell ZAP-70 expression ratio showed a much lower interlaboratory variation than other reporting strategies and is recommended for multicenter studies.
  • We assessed the variation of ZAP-70 expression levels in fresh cells according to storage time, which demonstrated that ZAP-70 is labile but sufficiently stable to allow comparison using fresh samples distributed between labs in Europe.
  • These studies have demonstrated progress toward a consensus reporting procedure, and further work is underway to harmonize the preparation and analysis procedures.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. ZAP-70 Protein-Tyrosine Kinase / analysis
  • [MeSH-minor] Antibodies, Monoclonal / chemistry. Antibody Specificity. Anticoagulants / pharmacology. Antigen-Antibody Reactions. Biomarkers, Tumor / analysis. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / immunology. Consensus. Humans. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. International Cooperation. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Mutation. Reproducibility of Results. T-Lymphocytes / drug effects. T-Lymphocytes / immunology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 International Society for Analytical Cytology.
  • [ErratumIn] Cytometry B Clin Cytom. 2008 Jul;74(4):259. Leuven, Nancy Boeckx [corrected to Boeckx, Nancy]
  • (PMID = 16906588.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Anticoagulants; 0 / Biomarkers, Tumor; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
  •  go-up   go-down


39. Ho AD, Suciu S, Stryckmans P, De Cataldo F, Willemze R, Thaler J, Peetermans M, Döhner H, Solbu G, Dardenne M, Zittoun R: Pentostatin (Nipent) in T-cell malignancies. Leukemia Cooperative Group and the European Organization for Research and Treatment of Cancer. Semin Oncol; 2000 Apr;27(2 Suppl 5):52-7
Hazardous Substances Data Bank. PENTOSTATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pentostatin (Nipent) in T-cell malignancies. Leukemia Cooperative Group and the European Organization for Research and Treatment of Cancer.
  • Within this phase II trial of the European Organization for Research and Treatment of Cancer, we have investigated the safety and efficacy of pentostatin (Nipent; SuperGen, San Ramon, CA) in refractory lymphoid malignancies.
  • Pentostatin was administered at a dosage of 4 mg/m2 every week for the first 3 weeks, then every 14 days, followed by maintenance therapy of 4 mg/m2 monthly for a maximum of 6 months.
  • We have previously reported the results in T- and B-cell prolymphocytic leukemia, B-cell chronic lymphocytic leukemia, and hairy cell leukemia This report focuses on the outcome in T-cell malignancies: T-cell chronic lymphocytic leukemia, Sézary syndrome, mycosis fungoides, and T-zone lymphoma.
  • Of 92 patients with these diagnoses enrolled, 76 were evaluable for response and toxicity, ie, 25 of 28 with T-cell chronic lymphocytic leukemia, 21 of 26 with Sézary syndrome, 22 of 26 with mycosis fungoides, and eight of 12 with T-zone lymphoma.
  • All patients had progressive and advanced disease.
  • Sixteen patients (21%) died during the first 9 weeks of treatment: 12 of progressive disease, two of infectious complications thought to be unrelated to treatment, one of myocardial infarction, and one of renal failure related to administration of intravenous contrast.
  • Better results were achieved in patients with Sézary syndrome or mycosis fungoides (complete remission + partial remission = 33.4% and 22.7%, respectively) than in patients with T-cell chronic lymphocytic leukemia (8%) or T-zone lymphoma (25%).
  • We conclude that pentostatin is active in low-grade T-cell malignancies.
  • A higher dose might be necessary for some T-cell malignancies.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Immunosuppressive Agents / therapeutic use. Leukemia, T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Pentostatin / therapeutic use
  • [MeSH-minor] Adult. Aged. Cause of Death. Disease Progression. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Leukemia, Hairy Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Prolymphocytic / drug therapy. Male. Middle Aged. Mycosis Fungoides / drug therapy. Remission Induction. Sezary Syndrome / drug therapy. Skin Neoplasms / drug therapy. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10877053.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Immunosuppressive Agents; 395575MZO7 / Pentostatin
  •  go-up   go-down


40. Ural AU, Kubar A, Avcu F, Tastan HB, Safali M, Nevruz O, Cetin T: Oral fludarabine treatment of cutaneous infiltration in a patient with B-cell chronic lymphocytic leukaemia. Clin Exp Dermatol; 2007 Mar;32(2):151-4
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oral fludarabine treatment of cutaneous infiltration in a patient with B-cell chronic lymphocytic leukaemia.
  • In B-cell chronic lymphocytic leukaemia (B-CLL), cutaneous infiltration is far less common than in T-cell CLL.
  • However, the effect of fludarabine on cutaneous infiltration in patients with B-CLL is uncertain.
  • We describe a 63-year-old man with B-CLL presenting with cutaneous lesions, who was treated successfully with oral fludarabine.
  • Simultaneously with the normalization of the peripheral blood lymphocytosis, the patient became free of the cutaneous infiltration of CLL after four courses of oral fludarabine.
  • To our knowledge, this is the first case of B-CLL leukaemia cutis treated with oral fludarabine.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemic Infiltration / pathology. Skin / pathology. Vidarabine / analogs & derivatives
  • [MeSH-minor] Administration, Oral. Aged. Humans. Male. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17244344.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


41. Fujino Y, Sawamura S, Kurakawa N, Hisasue M, Masuda K, Ohno K, Tsujimoto H: Treatment of chronic lymphocytic leukaemia in three dogs with melphalan and prednisolone. J Small Anim Pract; 2004 Jun;45(6):298-303
Hazardous Substances Data Bank. PREDNISOLONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of chronic lymphocytic leukaemia in three dogs with melphalan and prednisolone.
  • Three adult dogs with chronic lymphocytic leukaemia (CLL) were successfully treated with melphalan and prednisolone.
  • Based on the immunophenotypic analysis of leukaemic cells, two dogs were diagnosed with B cell CLL and one dog was tentatively diagnosed as having T cell CLL.
  • One dog with B cell CLL had IgM monoclonal gammopathy.
  • The clinical signs and haematological abnormalities associated with CLL in the three dogs improved with the administration of cytoreductive melphalan (3 to 5 mg/m2/day) and prednisolone (4.3 to 30 mg/m2/day) for eight to 210 days.
  • Melphalan and prednisolone therapy may achieve remission with few side effects in dogs with CLL.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Dog Diseases / drug therapy. Glucocorticoids / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / veterinary. Melphalan / administration & dosage. Prednisolone / administration & dosage
  • [MeSH-minor] Animals. Blood Cell Count / veterinary. Blood Chemical Analysis / veterinary. Blood Platelets. Diagnosis, Differential. Dogs. Drug Therapy, Combination. Female. Lymphocytes. Male

  • MedlinePlus Health Information. consumer health - Steroids.
  • Hazardous Substances Data Bank. MELPHALAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15206475.001).
  • [ISSN] 0022-4510
  • [Journal-full-title] The Journal of small animal practice
  • [ISO-abbreviation] J Small Anim Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Glucocorticoids; 9PHQ9Y1OLM / Prednisolone; Q41OR9510P / Melphalan
  •  go-up   go-down


42. Kim K, Kim WS, Jung CW, Im YH, Kang WK, Lee MH, Park CH, Ko YH, Ree HJ, Park K: Clinical features of peripheral T-cell lymphomas in 78 patients diagnosed according to the Revised European-American lymphoma (REAL) classification. Eur J Cancer; 2002 Jan;38(1):75-81
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical features of peripheral T-cell lymphomas in 78 patients diagnosed according to the Revised European-American lymphoma (REAL) classification.
  • The aim of this study was to analyse the clinical characteristics and prognostic factors of peripheral T-cell lymphomas (PTCLs) according to the Revised European-American Lymphoma (REAL) classification.
  • From 1994 to 1999, 78 patients were diagnosed with PTCLs, excluding cutaneous T-cell lymphomas and T-cell chronic lymphocytic leukaemia.
  • The distribution of the histological subgroups were: PTCL unspecified (PTCL-U), 40%; angiocentric lymphoma, 32%; anaplastic large cell lymphoma (ALCL), 17%; angioimmunoblastic T-cell lymphoma (AILD), 6%; intestinal T-cell lymphoma, 3%; and panniculitic T-cell lymphoma, 3%.
  • Most patients were treated with doxorubicin-containing combination chemotherapy (with or without radiation therapy).
  • PTCL responds poorly to treatment with low survival rates and the IPI is a useful prognostic factor for PTCL.
  • [MeSH-major] Lymphoma, T-Cell, Peripheral / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Female. Hematopoietic Stem Cell Transplantation / methods. Humans. Male. Middle Aged. Prednisone / administration & dosage. Radiotherapy, Adjuvant / methods. Retrospective Studies. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Peripheral T-cell lymphoma.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11750843.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  •  go-up   go-down


43. Gandhi V, Tam C, O'Brien S, Jewell RC, Rodriguez CO Jr, Lerner S, Plunkett W, Keating MJ: Phase I trial of nelarabine in indolent leukemias. J Clin Oncol; 2008 Mar 1;26(7):1098-105
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of nelarabine in indolent leukemias.
  • PURPOSE: To test whether nelarabine is an effective agent for indolent leukemias and to evaluate whether there is a relationship between cellular pharmacokinetics of the analog triphosphate and clinical responses.
  • PATIENTS AND METHODS: Thirty-five patients with relapsed/refractory leukemias (n = 24, B-cell chronic lymphocytic leukemia and n = 11, T-cell prolymphocytic leukemia) were entered onto three different protocols.
  • Histologic category, number of prior therapies, and fludarabine refractoriness did not influence the response rate.
  • Pharmacokinetics of plasma nelarabine and arabinosylguanine (ara-G) and of cellular ara-G triphosphate (ara-GTP) were similar in the two groups of diagnoses, and the elimination of ara-GTP from leukemia cells was slow (median, > 24 hours).
  • CONCLUSION: Nelarabine is an effective regimen against indolent leukemias, and combining it with fludarabine was most promising.
  • Determination of tumor cell ara-GTP levels may provide a predictive test for response to nelarabine.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Prolymphocytic, T-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Arabinonucleotides / metabolism. DNA (Cytosine-5-)-Methyltransferase / antagonists & inhibitors. Drug Therapy, Combination. Female. Guanosine Triphosphate / analogs & derivatives. Guanosine Triphosphate / metabolism. Humans. Male. Middle Aged. Tumor Cells, Cultured. Vidarabine / analogs & derivatives. Vidarabine / pharmacokinetics. Vidarabine / therapeutic use

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18309944.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA57629; United States / NCI NIH HHS / CA / CA81534
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 0 / Arabinonucleotides; 60158CV180 / nelarabine; 72490-81-4 / 9-beta-D-arabinofuranosylguanosine 5'-triphosphate; 86-01-1 / Guanosine Triphosphate; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


44. Kreitman RJ: Recombinant immunotoxins for the treatment of chemoresistant hematologic malignancies. Curr Pharm Des; 2009;15(23):2652-64
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recombinant immunotoxins for the treatment of chemoresistant hematologic malignancies.
  • No agents of this class are approved yet for medical use, although a related molecule, denileukin diftitox, composed of interleukin-2 fused to truncated diphtheria toxin, is approved for relapsed/refractory cutaneous T-cell lymphoma.
  • Recombinant immunotoxins which have been tested in patients with chemotherapy-pretreated hematologic malignancies include LMB-2 (anti-CD25), BL22 (CAT-3888, anti-CD22) and HA22 (CAT-8015, anti-CD22), each containing an Fv fragment fused to truncated Pseudomonas exotoxin.
  • Major responses were observed with LMB-2 in adult T-cell leukemia, chronic lymphocytic leukemia (CLL), cutaneous T-cell lymphoma, Hodgkin's disease, and hairy cell leukemia (HCL).
  • HA22, an improved version of BL22 with higher affinity to CD22, is now undergoing phase I testing in HCL, CLL, non-Hodgkin's lymphoma, and pediatric acute lymphoblastic leukemia.
  • [MeSH-major] Drug Discovery / methods. Drug Resistance, Neoplasm / drug effects. Hematologic Neoplasms / drug therapy. Immunotoxins / therapeutic use. Recombinant Proteins / therapeutic use

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19689336.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Immunotoxins; 0 / Leukocidins; 0 / Pseudomonas aeruginosa Cytotoxins; 0 / Recombinant Proteins; 0 / Toxins, Biological
  • [Number-of-references] 190
  •  go-up   go-down


45. Ho AD, Hensel M: Pentostatin and purine analogs for indolent lymphoid malignancies. Future Oncol; 2006 Apr;2(2):169-83
Hazardous Substances Data Bank. PENTOSTATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pentostatin has been shown to be active in a variety of B- and T-cell malignancies.
  • The drug is a tight inhibitor of adenosine deaminase, a key degradative enzyme of purine metabolism present in all human tissues, with the highest levels found in the lymphoid system.
  • Early clinical trials indicated that this agent was highly active in acute lymphoblastic leukemias with high intracellular adenosine deaminase levels.
  • Relatively high doses of the drug were needed, which was associated with severe adverse events.
  • Through the efforts of a few investigators, better tolerated, low-dose regimens have been shown to be extremely active in lymphoproliferative diseases with very low intracellular adenosine deaminase levels such as hairy cell leukemia, B- and T-cell chronic leukemias, T-cell cutaneous lymphomas and low-grade non-Hodgkin lymphomas.
  • Clinical as well as experimental data have indicated that this drug induces lymphocyte-specific cytotoxicity, and myelosuppressive adverse events have been minimal.
  • Although all the purine analogs have shown similar activity, the advantage of pentostatin is the relatively specific cytotoxicity against lymphocytes, which permits treatment even in patients with severe cytopenias.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Leukemia, Hairy Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Prolymphocytic / drug therapy. Pentostatin / therapeutic use. Purine Nucleosides / therapeutic use

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16563086.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenosine Deaminase Inhibitors; 0 / Antibiotics, Antineoplastic; 0 / Purine Nucleosides; 395575MZO7 / Pentostatin
  • [Number-of-references] 92
  •  go-up   go-down


46. Ayuk F, Maywald N, Hannemann S, Larsen U, Zander A, Kröger N: Comparison of the cytotoxicity of 4 preparations of anti-T-cell globulins in various hematological malignancies. Anticancer Res; 2009 Apr;29(4):1355-60
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of the cytotoxicity of 4 preparations of anti-T-cell globulins in various hematological malignancies.
  • MATERIALS AND METHODS: Myeloma, myeloid leukaemia and lymphoma cell lines as well as primary CLL and T-cell samples were used.
  • Cell viability was analyzed by flow cytometry.
  • RESULTS: All ATG preparations had potent and similar cytotoxic activity against T-cells, primary CLL cells, NHL cell lines and myeloma cell lines.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antilymphocyte Serum / pharmacology. Hematologic Neoplasms / therapy. Immunoglobulins / pharmacology. T-Lymphocytes / immunology
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / immunology. Cytotoxicity, Immunologic. Flow Cytometry. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19414387.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antilymphocyte Serum; 0 / Immunoglobulins; 0 / lymphoglobuline; 0 / thymoglobulin
  •  go-up   go-down


47. Meyers JA, Taverna J, Chaves J, Makkinje A, Lerner A: Phosphodiesterase 4 inhibitors augment levels of glucocorticoid receptor in B cell chronic lymphocytic leukemia but not in normal circulating hematopoietic cells. Clin Cancer Res; 2007 Aug 15;13(16):4920-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phosphodiesterase 4 inhibitors augment levels of glucocorticoid receptor in B cell chronic lymphocytic leukemia but not in normal circulating hematopoietic cells.
  • Type 4 cyclic AMP (cAMP) phosphodiesterase (PDE4) inhibitors, a class of compounds in clinical development that activate cAMP-mediated signaling by inhibiting cAMP catabolism, offer a feasible means by which to potentiate glucocorticoid-mediated apoptosis in lymphoid malignancies such as B-cell chronic lymphocytic leukemia (B-CLL).
  • In this study, we show that PDE4 inhibitors up-regulate glucocorticoid receptor (GRalpha) transcript levels in B-CLL cells but not T-CLL cells or Sezary cells or normal circulating T cells, B cells, monocytes, or neutrophils.
  • Because GRalpha transcript half-life does not vary in CLL cells treated with the prototypic PDE4 inhibitor rolipram, the 4-fold increase in GRalpha mRNA levels observed within 4 h of rolipram treatment seems to result from an increase in GRalpha transcription.
  • Rolipram treatment increases levels of transcripts derived from the 1A3 promoter to a greater extent than the 1B promoter.
  • Treatment of B-CLL cells with two other PDE4 inhibitors currently in clinical development also augments GR transcript levels and glucocorticoid-mediated apoptosis.
  • Washout studies show that simultaneous treatment with both drug classes irreversibly augments apoptosis over the same time frame that GR up-regulation occurs.
  • Although treatment of B-CLL cells with glucocorticoids reduces basal GRalpha transcript levels in a dose-related manner, cotreatment with rolipram maintained GRalpha transcript levels above baseline.
  • Our results suggest that as a result of their unusual sensitivity to PDE4 inhibitor-mediated up-regulation of GRalpha expression, treatment of B-CLL patients with combined PDE4 inhibitor/glucocorticoid therapy may be of therapeutic benefit in this disease.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • SciCrunch. DrugBank: Data: Chemical .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Endocrinol. 2001 Aug;15(8):1381-95 [11463861.001]
  • [Cites] J Clin Pharmacol. 2002 Mar;42(3):297-303 [11865966.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):919-29 [12648060.001]
  • [Cites] Blood. 2003 May 15;101(10):4122-30 [12531792.001]
  • [Cites] Biochemistry. 2003 Sep 23;42(37):10978-90 [12974633.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2661-7 [14615375.001]
  • [Cites] Biochemistry. 2004 Aug 31;43(34):10851-8 [15323545.001]
  • [Cites] J Immunol. 2004 Sep 15;173(6):3816-24 [15356129.001]
  • [Cites] Cancer. 1973 Mar;31(3):502-8 [4693581.001]
  • [Cites] Blood. 1977 Dec;50(6):1049-59 [336116.001]
  • [Cites] Cancer Res. 1983 Aug;43(8):3865-73 [6134583.001]
  • [Cites] Leuk Res. 1984;8(4):579-85 [6590931.001]
  • [Cites] J Biol Chem. 1986 Apr 15;261(11):4909-14 [3007479.001]
  • [Cites] Mol Cell Biol. 1987 Dec;7(12):4211-7 [2830485.001]
  • [Cites] Mol Endocrinol. 1987 Jan;1(1):68-74 [2842660.001]
  • [Cites] J Biol Chem. 1989 Aug 15;264(23):13679-83 [2547771.001]
  • [Cites] Mol Endocrinol. 1989 Dec;3(12):2119-27 [2628744.001]
  • [Cites] Blood. 1992 Jan 1;79(1):213-22 [1728309.001]
  • [Cites] Mol Endocrinol. 1993 Jan;7(1):104-13 [8383286.001]
  • [Cites] Blood. 1993 Oct 15;82(8):2304-9 [8400283.001]
  • [Cites] Am J Hematol. 1994 Dec;47(4):334 [7977310.001]
  • [Cites] J Immunol. 1995 Nov 15;155(10):4525-8 [7594448.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 1995;103(3):175-83 [7584520.001]
  • [Cites] Curr Biol. 1998 Jul 30-Aug 13;8(16):935-8 [9707409.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2484-94 [9746789.001]
  • [Cites] J Steroid Biochem Mol Biol. 1998 Oct;67(2):89-94 [9877208.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Jan 27;254(3):559-65 [9920778.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1378-85 [10096574.001]
  • [Cites] Leuk Lymphoma. 1999 Jun;34(1-2):167-70 [10350345.001]
  • [Cites] Biochem Pharmacol. 2005 Feb 1;69(3):473-83 [15652238.001]
  • [Cites] Pulm Pharmacol Ther. 2005;18(4):277-84 [15777610.001]
  • [Cites] Mol Cell. 2005 Apr 29;18(3):331-42 [15866175.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jun;90(6):3505-9 [15755863.001]
  • [Cites] Pediatr Blood Cancer. 2005 Aug;45(2):121-7 [15704223.001]
  • [Cites] Cancer Res. 2005 Nov 1;65(21):9712-8 [16266991.001]
  • [Cites] Biochem J. 2006 Jan 1;393(Pt 1):21-41 [16336197.001]
  • [Cites] Chest. 2006 Jan;129(1):56-66 [16424413.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):11893-8 [11027313.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(23):9009-17 [11073999.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):3937-41 [11358809.001]
  • [Cites] Mol Endocrinol. 2001 Jul;15(7):1093-103 [11435610.001]
  • (PMID = 17699872.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106705; United States / NCI NIH HHS / CA / R01 CA106705-03; United States / NCI NIH HHS / CA / CA 106705; United States / NHLBI NIH HHS / HL / T32 HL007501-26; United States / NCI NIH HHS / CA / CA106705-03; United States / NHLBI NIH HHS / HL / HL007501-26; United States / NHLBI NIH HHS / HL / T32 HL007501
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminopyridines; 0 / Benzamides; 0 / Carboxylic Acids; 0 / Cyclohexanecarboxylic Acids; 0 / Cyclopropanes; 0 / Nitriles; 0 / Phosphodiesterase Inhibitors; 0 / Receptors, Glucocorticoid; 0 / glucocorticoid receptor alpha; 0P6C6ZOP5U / Roflumilast; 7S5I7G3JQL / Dexamethasone; 8ATB1C1R6X / Cilomilast; EC 3.1.4.17 / 3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 4; K676NL63N7 / Rolipram
  • [Other-IDs] NLM/ NIHMS91850; NLM/ PMC2656255
  •  go-up   go-down


48. Lecureur V, Le Thiec A, Le Meur A, Amiot L, Drenou B, Bernard M, Lamy T, Fauchet R, Fardel O: Potassium antimonyl tartrate induces caspase- and reactive oxygen species-dependent apoptosis in lymphoid tumoral cells. Br J Haematol; 2002 Dec;119(3):608-15
Hazardous Substances Data Bank. ANTIMONY POTASSIUM TARTRATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The metalloid salt potassium antimonyl tartrate (PAT), previously used as an antiparasitic agent, has recently been shown to exert cytotoxicity towards acute promyelocytic leukaemia cells like arsenical compounds.
  • Like As2O3, PAT was found to inhibit cell growth of various lymphoid cell lines, deriving from either acute lymphoid leukaemias (Jurkat, Molt-4 and Nalm-6) or lymphomas (Daudi, Raji and Rec1).
  • It was enhanced by co-treatment with the pro-oxidant buthionine sulphoximine and abolished in response to the antioxidant N-acetylcysteine, thus underlining that PAT toxicity, similarly to that of As2O3, is probably modulated by the redox status of the cells.
  • PAT, used at concentrations in the micromolar range that are thought to be clinically achievable, was also demonstrated to markedly decrease the viability of primary cultured tumoral B cells that originated from 18 patients suffering from chronic lymphoid leukaemia whereas normal lymphocytes were less sensitive.
  • These data therefore suggest that PAT may deserve to be evaluated in the treatment of some lymphoid malignancies.
  • [MeSH-major] Antimony Potassium Tartrate / therapeutic use. Antineoplastic Agents / therapeutic use. Caspases / physiology. Lymphoma / drug therapy. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Apoptosis / drug effects. Arsenicals / therapeutic use. Blotting, Western. Cell Survival. Coumarins / pharmacology. Cysteine Proteinase Inhibitors / pharmacology. Fluorescent Dyes / pharmacology. Humans. Oligopeptides / pharmacology. Oxides / therapeutic use. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12437633.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Coumarins; 0 / Cysteine Proteinase Inhibitors; 0 / Fluorescent Dyes; 0 / Oligopeptides; 0 / Oxides; 0 / Reactive Oxygen Species; 0 / acetyl-aspartyl-glutamyl-valyl-aspartyl-amino-4-methylcoumarin; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; DL6OZ476V3 / Antimony Potassium Tartrate; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


49. Nahimana A, Attinger A, Aubry D, Greaney P, Ireson C, Thougaard AV, Tjørnelund J, Dawson KM, Dupuis M, Duchosal MA: The NAD biosynthesis inhibitor APO866 has potent antitumor activity against hematologic malignancies. Blood; 2009 Apr 2;113(14):3276-86
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Intracellular NAD is essential for cell survival, and NAD depletion resulting from APO866 treatment elicits tumor cell death.
  • Here, we determine the in vitro and in vivo sensitivities of hematologic cancer cells to APO866 using a panel of cell lines (n = 45) and primary cells (n = 32).
  • Most cancer cells (acute myeloid leukemia [AML], acute lymphoblastic leukemia [ALL], mantle cell lymphoma [MCL], chronic lymphocytic leukemia [CLL], and T-cell lymphoma), but not normal hematopoietic progenitor cells, were sensitive to low concentrations of APO866 as measured in cytotoxicity and clonogenic assays.
  • Treatment with APO866 decreased intracellular NAD and adenosine triphosphate (ATP) at 24 hours and 48 to72 hours, respectively.
  • The NAD depletion led to cell death.
  • At 96 hours, APO866-mediated cell death occurred in a caspase-independent mode, and was associated with mitochondrial dysfunction and autophagy.
  • Further, in vivo administration of APO866 as a single agent prevented and abrogated tumor growth in animal models of human AML, lymphoblastic lymphoma, and leukemia without significant toxicity to the animals.
  • [MeSH-major] Acrylamides / therapeutic use. Antineoplastic Agents / therapeutic use. Cytokines / antagonists & inhibitors. Hematologic Neoplasms / drug therapy. NAD / biosynthesis. Nicotinamide Phosphoribosyltransferase / antagonists & inhibitors. Piperidines / therapeutic use
  • [MeSH-minor] Animals. Cell Death / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Cells, Cultured. U937 Cells. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Blood. 2009 Jun 4;113(23):6035-7; author reply 6037-8 [19498032.001]
  • (PMID = 19196867.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acrylamides; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human
  •  go-up   go-down


50. Pawson R, Potter MN, Theocharous P, Lawler M, Garg M, Yin JA, Rezvani K, Craddock C, Rassam S, Prentice HG: Treatment of relapse after allogeneic bone marrow transplantation with reduced intensity conditioning (FLAG +/- Ida) and second allogeneic stem cell transplant. Br J Haematol; 2001 Dec;115(3):622-9
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of relapse after allogeneic bone marrow transplantation with reduced intensity conditioning (FLAG +/- Ida) and second allogeneic stem cell transplant.
  • Acute leukaemias in relapse after allogeneic stem cell transplantation (SCT) respond poorly to donor leucocyte infusions (DLI) compared with chronic myeloid leukaemia (CML), at least in part because of faster disease kinetics.
  • Fludarabine-containing 'non-myeloablative' chemotherapy followed by further allo SCT may offer more rapid and effective disease control.
  • We report 14 patients with relapse after allo SCT for acute leukaemia [seven acute myeloid leukaemia (AML), five acute lymphoblastic leukaemia (ALL)] or refractory anaemia with excess blasts in transformation (RAEB-t, n = 2) treated with fludarabine, high-dose cytosine arabinoside (ara-C) and granulocyte colony-simulating factor (G-CSF) with (n = 10) or without (n = 2) idarubicin (FLAG +/- Ida) or DaunoXome (FLAG-X) (n = 2) and second allo SCT from the original donor.
  • Donors were fully human leucocyte antigen (HLA) -matched in 13 cases with a single class A mismatch in one.
  • Actuarial overall survival was 60% and disease-free survival was 26% at 58 months.
  • Transplants were well tolerated with no treatment-related deaths.
  • The major complication was graft-versus-host disease (GvHD, acute >/= grade II-2 cases, chronic - eight cases, two limited, six extensive) although there have been no deaths attributable to this.
  • FLAG +/- Ida and second allo SCT is a safe and useful approach and may be more effective than DLI in the treatment of acute leukaemias relapsing after conventional allo SCT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bone Marrow Transplantation. Cytarabine / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Idarubicin / administration & dosage. Leukemia / therapy. Transplantation Conditioning / methods. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Anemia, Refractory, with Excess of Blasts / therapy. Child. Child, Preschool. Disease-Free Survival. Female. Filgrastim. Graft vs Host Disease / immunology. Graft vs Host Disease / prevention & control. Humans. Leukemia, Myeloid / therapy. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Recombinant Proteins. Recurrence. Reoperation. Retrospective Studies. Survival Rate. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. Filgrastim .
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11736947.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; PVI5M0M1GW / Filgrastim; ZRP63D75JW / Idarubicin; Ida-FLAG protocol
  •  go-up   go-down


51. Rousseau RF, Bollard CM, Heslop HE: Gene therapy for paediatric leukaemia. Expert Opin Biol Ther; 2001 Jul;1(4):663-74
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene therapy for paediatric leukaemia.
  • Improvements in the chemotherapeutic and transplant regimens have had a significant impact in improving survival rates for paediatric leukaemia.
  • However, there are still important problems to address including what options are available for patients with chemoresistant disease and what strategies are available to avoid the concerns regarding the toxicity associated with highly cytotoxic treatment regimens.
  • Gene therapy and immunotherapy protocols hold great promise.
  • Using gene transfer of a marker gene, a number of biological issues in the therapy of leukaemia have been addressed.
  • For example, by gene marking autologous bone marrow grafts it has been possible to demonstrate that infused marrow contributes to relapse in acute and chronic myeloid leukaemias.
  • In the allogeneic transplant setting, genetically modified T-cells have proven valuable for the prophylaxis and treatment of viral diseases and may have an important role in preventing or treating disease relapse.
  • Gene transfer is also being used to modify tumour function, enhance immunogenicity, and confer drug-resistance to normal haematopoietic stem cells.
  • With the continued scientific advancements in this field, gene therapy will almost certainly have a major impact on the treatment of paediatric leukaemia in the future.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Genetic Therapy / methods. Leukemia / therapy
  • [MeSH-minor] Child. Clinical Trials, Phase I as Topic. Dendritic Cells / immunology. Dendritic Cells / metabolism. Gene Transfer Techniques. Genes, MDR. Genetic Vectors. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / physiology. Humans. Immunotherapy / methods. Immunotherapy, Adoptive. Oncogenes

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11727502.001).
  • [ISSN] 1471-2598
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines
  • [Number-of-references] 139
  •  go-up   go-down


52. Kindler T, Meyer RG, Fischer T: BCR-ABL as a target for novel therapeutic interventions. Expert Opin Ther Targets; 2002 Feb;6(1):85-101
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BCR-ABL as a target for novel therapeutic interventions.
  • There is good experimental evidence demonstrating that BCR-ABL is the single causative abnormality in chronic myeloid leukaemia (CML), making it a unique model for the development of molecular targets.
  • In addition to CML, BCR-ABL transcripts can be found in a minority of acute lymphoblastic leukaemias and very rarely in acute myeloid leukaemia (AML).
  • Elucidating the molecular mechanisms and downstream pathways of BCR-ABL has led to the design of several novel therapeutic approaches.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Genes, abl / genetics. Neoplasms / drug therapy. Neoplasms / genetics. Protein-Tyrosine Kinases / drug effects
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / drug effects. Fusion Proteins, bcr-abl. Humans. Signal Transduction / drug effects. T-Lymphocytes / drug effects

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11901483.001).
  • [ISSN] 1472-8222
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


53. Ravandi F, O'Brien S: Alemtuzumab. Expert Rev Anticancer Ther; 2005 Feb;5(1):39-51
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Over the past several years, a number of clinical trials have demonstrated the clinical activity of alemtuzumab in treating patients with chronic lymphocytic leukemia, T-cell malignancies such as T-prolymphocytic leukemia and cutaneous T-cell lymphoma, as well as in the prevention and therapy of graft-versus-host disease in the setting of allogeneic stem cell transplantation.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Autoimmune Diseases / drug therapy. Hematologic Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15757437.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  • [Number-of-references] 91
  •  go-up   go-down


54. Wierda WG, Castro JE, Aguillon R, Sampath D, Jalayer A, McMannis J, Prussak CE, Keating M, Kipps TJ: A phase I study of immune gene therapy for patients with CLL using a membrane-stable, humanized CD154. Leukemia; 2010 Nov;24(11):1893-900
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of immune gene therapy for patients with CLL using a membrane-stable, humanized CD154.
  • Ligation of CD40 on chronic lymphocytic leukemia (CLL) cells induces phenotypic and biochemical changes that facilitate CLL cell-T cell interactions and enhances the sensitivity of CLL cells to clearance by adaptive and innate immune-effector mechanisms.
  • CLL cells can be transduced to express CD40 ligand (CD154) using a replication-defective adenovirus vector, thereby cross-linking CD40 on transduced and non-transduced, bystander CLL cells.
  • In a previous study, patients received infusions of autologous CLL cells, transduced to express murine CD154 (mCD154), which induced anti-leukemic immune responses, but also anti-mCD154 antibodies.
  • In this study, we report a phase I study, in which patients were infused with 1 × 10(8), 3 × 10(8) or 1 × 10(9) autologous CLL cells transduced ex vivo to express ISF35, a humanized, membrane-stable CD154.
  • After infusion, circulating CLL cells had enhanced or de novo expression of CD95, DR5, p73 and Bid, which enhanced their susceptibility to death-receptor-mediated or drug-induced apoptosis, including CLL cells with deletions at 17p13.1 (del(17p)).
  • Two patients who had CLL with del(17p) had subsequent chemoimmunotherapy and responded well to treatment.
  • In summary, infusions of autologous, ISF35-transduced CLL cells were well tolerated, had biological and clinical activity, and might enhance the susceptibility of CLL cells with del(17p) to chemoimmunotherapy.
  • [MeSH-major] CD40 Ligand / therapeutic use. Genetic Therapy / methods. Leukemia, Lymphocytic, Chronic, B-Cell / therapy

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20882050.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Antigens, CD95; 147205-72-9 / CD40 Ligand
  • [Other-IDs] NLM/ NIHMS718310; NLM/ PMC4556366
  •  go-up   go-down


55. Thursky KA, Worth LJ, Seymour JF, Miles Prince H, Slavin MA: Spectrum of infection, risk and recommendations for prophylaxis and screening among patients with lymphoproliferative disorders treated with alemtuzumab*. Br J Haematol; 2006 Jan;132(1):3-12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There is an increasing use of monoclonal antibodies in the treatment of haematological malignancies.
  • Alemtuzumab (Campath-1H; Ilex Pharmaceuticals, San Antonio, TX, USA) is a monoclonal antibody reactive with the CD52 antigen used as first and second line therapy for two types of lymphoproliferative disorders: chronic lymphocytic leukaemia (CLL), and T-cell lymphomas [both peripheral (PTCL) and cutaneous (CTCL)].
  • With alemtuzumab therapy, viral, bacterial and fungal infectious complications are frequent, and may be life threatening.
  • This review discusses the infection risks associated with these lymphoproliferative disorders and their treatment, and provide detailed recommendations for screening and prophylaxis.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antibodies, Neoplasm / adverse effects. Antineoplastic Agents / adverse effects. Lymphoproliferative Disorders / drug therapy. Opportunistic Infections / chemically induced
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antiviral Agents / therapeutic use. Humans. Immunocompromised Host

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16371014.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 83
  •  go-up   go-down


56. Smith KJ, Welsh M, Skelton H: Trichophyton rubrum showing deep dermal invasion directly from the epidermis in immunosuppressed patients. Br J Dermatol; 2001 Aug;145(2):344-8
Hazardous Substances Data Bank. FLUCONAZOLE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Trichophyton rubrum is the most widely encountered dermatophyte infection, and is usually regarded as exclusively keratinophilic often leading to chronic cutaneous and nail infections, even in healthy individuals.
  • We present three patients with acute leukaemias, with ill-defined pre-existent cutaneous eruptions that were treated with a potent topical corticosteroid.
  • All three patients received aggressive marrow toxic chemotherapy.
  • These patients had progression of their cutaneous disease, which showed deep dermal invasion of T. rubrum, invading directly from the epidermis with no evidence of systemic spread.
  • [MeSH-minor] Adolescent. Adult. Amphotericin B / therapeutic use. Anti-Inflammatory Agents / therapeutic use. Antifungal Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Fluconazole / therapeutic use. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / immunology. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / immunology. Male. Middle Aged. Naphthalenes / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Steroids. Treatment Outcome. Trichophyton / immunology

  • MedlinePlus Health Information. consumer health - Tinea Infections.
  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11531807.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antifungal Agents; 0 / Naphthalenes; 0 / Steroids; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole; G7RIW8S0XP / terbinafine
  •  go-up   go-down


57. Valiev TT, Vinogradova IuE, Chernova NG, Mar'in DS, Volkova IaK, Petrova VI, Bulanov AIu, Kalinin NN, Semenova EA, Gretsov EM, Kravchenko SK, Kremenetskaia AM, Vorob'ev AI: [Remission in T-cell prolymphocytic leukemia during the FMC treatment course]. Ter Arkh; 2006;78(7):87-90
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Remission in T-cell prolymphocytic leukemia during the FMC treatment course].
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy
  • [MeSH-minor] Cyclophosphamide / administration & dosage. Cyclophosphamide / therapeutic use. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / therapeutic use. Remission Induction. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16944758.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


58. Sohani AR, Ferry JA, Chang PS, Abramson JS: Epstein-barr virus-positive diffuse large B-cell lymphoma during therapy with alemtuzumab for T-cell prolymphocytic leukemia. J Clin Oncol; 2010 Feb 10;28(5):e69-72
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epstein-barr virus-positive diffuse large B-cell lymphoma during therapy with alemtuzumab for T-cell prolymphocytic leukemia.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antibodies, Neoplasm / adverse effects. Antineoplastic Agents / adverse effects. Herpesvirus 4, Human / isolation & purification. Leukemia, Prolymphocytic, T-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / chemically induced
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Examination. Disease Progression. Fatal Outcome. Female. Humans. Magnetic Resonance Imaging. Middle Aged. Treatment Failure

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • Genetic Alliance. consumer health - B Cell Prolymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19917859.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


59. Abbi KK, Rizvi SM, Sivik J, Thyagarajan S, Loughran T, Drabick JJ: Guillain-Barré syndrome after use of alemtuzumab (Campath) in a patient with T-cell prolymphocytic leukemia: a case report and review of the literature. Leuk Res; 2010 Jul;34(7):e154-6
MedlinePlus Health Information. consumer health - Guillain-Barre Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Guillain-Barré syndrome after use of alemtuzumab (Campath) in a patient with T-cell prolymphocytic leukemia: a case report and review of the literature.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antibodies, Neoplasm / adverse effects. Guillain-Barre Syndrome / chemically induced. Leukemia, Prolymphocytic, T-Cell / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, Neoplasm / immunology. Autoimmunity / drug effects. Combined Modality Therapy. Complement Pathway, Classical. Dendritic Cells / drug effects. Glycoproteins / antagonists & inhibitors. Glycoproteins / immunology. Humans. Immunoglobulins, Intravenous / therapeutic use. Male. Plasmapheresis. Respiration, Artificial. T-Lymphocyte Subsets / drug effects

  • Genetic Alliance. consumer health - Guillain-Barre Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20362332.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Immunoglobulins, Intravenous; 3A189DH42V / alemtuzumab
  •  go-up   go-down


60. Ramsay AG, Gribben JG: Immune dysfunction in chronic lymphocytic leukemia T cells and lenalidomide as an immunomodulatory drug. Haematologica; 2009 Sep;94(9):1198-202
Hazardous Substances Data Bank. THALIDOMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immune dysfunction in chronic lymphocytic leukemia T cells and lenalidomide as an immunomodulatory drug.
  • [MeSH-major] Immunologic Factors / therapeutic use. Leukemia, T-Cell / drug therapy. Leukemia, T-Cell / immunology. Thalidomide / analogs & derivatives
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Chronic Disease. Humans

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2002 Jul 1;100(1):167-73 [12070023.001]
  • [Cites] Haematologica. 2009 Sep;94(9):1266-73 [19734418.001]
  • [Cites] J Clin Invest. 2005 Jul;115(7):1797-805 [15965501.001]
  • [Cites] Lancet Oncol. 2006 Jun;7(6):480-8 [16750498.001]
  • [Cites] J Clin Oncol. 2006 Dec 1;24(34):5343-9 [17088571.001]
  • [Cites] Nat Rev Immunol. 2007 Feb;7(2):131-43 [17259969.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2811-8 [17638850.001]
  • [Cites] J Clin Oncol. 2008 Mar 20;26(9):1544-52 [18285605.001]
  • [Cites] J Clin Oncol. 2008 May 20;26(15):2519-25 [18427150.001]
  • [Cites] Blood. 2008 Jun 1;111(11):5291-7 [18334676.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2427-37 [18551193.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4650-7 [18628480.001]
  • [Cites] Blood. 2008 Aug 15;112(4):975-80 [18411418.001]
  • [Cites] J Clin Oncol. 2008 Oct 10;26(29):4851-2; author reply 4852-3 [18779599.001]
  • [Cites] Blood. 2008 Dec 15;112(13):5180-9 [18772452.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 Jan;15(1 Suppl):53-8 [19147079.001]
  • [Cites] Br J Haematol. 2009 Mar;144(6):848-55 [19183192.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6250-5 [19332800.001]
  • [Cites] Blood. 2002 Sep 15;100(6):2123-31 [12200376.001]
  • (PMID = 19734414.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Number-of-references] 19
  • [Other-IDs] NLM/ PMC2738710
  •  go-up   go-down






Advertisement