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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pralatrexate-induced tumor cell apoptosis in the epidermis of a patient with HTLV-1 adult T-cell lymphoma/leukemia causing skin erosions.

Pralatrexate is a novel antifolate, which shows increased antitumor activity in human tumor xenograft studies in mice compared with methotrexate.

We investigated the effects of pralatrexate in a patient with adult T-cell lymphoma/leukemia with significant skin involvement.

Atypical lymphocytes in epidermal Pautrier microabscesses were positive for HTLV-1.

Here we present in vivo evidence that pralatrexate-induced erosions in skin affected by adult T-cell lymphoma/leukemia are a manifestation of apoptosis of tumor cells infiltrating the epidermis and are not the result of cytotoxicity by pralatrexate on keratinocytes.

This distinction is critical and may profoundly influence the clinical decision to continue pralatrexate treatment.

[MeSH-major] Aminopterin / analogs & derivatives. Antimetabolites, Antineoplastic / pharmacology. Apoptosis / drug effects. Epidermis / drug effects. Exanthema / chemically induced. Folic Acid Antagonists / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology

[MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Cyclophosphamide / administration & dosage. Diagnosis, Differential. Disease Progression. Doxorubicin / administration & dosage. Drug Eruptions / diagnosis. Etoposide / administration & dosage. Humans. Interferon-alpha / administration & dosage. Male. Prednisone / administration & dosage. Recombinant Proteins. Vincristine / administration & dosage. Zidovudine / administration & dosage

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Hazardous Substances Data Bank. DOXORUBICIN .

Hazardous Substances Data Bank. ZIDOVUDINE .

Hazardous Substances Data Bank. ETOPOSIDE .

Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

Hazardous Substances Data Bank. PREDNISONE .

Hazardous Substances Data Bank. AMINOPTERIN .

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(PMID = 19389878.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / 10-propargyl-10-deazaaminopterin; 0 / Antimetabolites, Antineoplastic; 0 / Folic Acid Antagonists; 0 / Interferon-alpha; 0 / Recombinant Proteins; 4B9XT59T7S / Zidovudine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 99210-65-8 / interferon alfa-2b; JYB41CTM2Q / Aminopterin; VB0R961HZT / Prednisone; CHOP protocol; EPOCH protocol

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Donor cell derived acute myeloid leukemia after allogeneic cord blood transplantation in a patient with adult T-cell lymphoma.

We report a patient with adult T-cell lymphoma who developed acute myeloid leukemia (AML) after allogeneic cord blood transplantation (CBT).

Although 25 cases of donor cell leukemia (DCL) occurring after allogeneic bone marrow transplantation have previously been reported, there have been no reports of DCL after CBT.

[MeSH-major] Cord Blood Stem Cell Transplantation. Leukemia, Myeloid / etiology. Lymphoma, T-Cell / therapy. Neoplasms, Second Primary / etiology

[MeSH-minor] Acute Disease. Chromosomes, Human, X / genetics. Chromosomes, Human, Y / genetics. Fatal Outcome. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Tandem Repeat Sequences. Tissue Donors. Transplantation Chimera. Transplantation, Homologous

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[Copyright] Copyright (c) 2005 Wiley-Liss, Inc.

(PMID = 16044441.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Common genetic variants and risk for non-Hodgkin lymphoma and adult T-cell lymphoma/leukemia in Jamaica.

We evaluated whether risk of non-Hodgkin lymphoma (NHL), particularly adult T-cell leukemia/lymphoma (ATL) related to human T-lymphotropic virus (HTLV) infection was associated with 63 single nucleotide polymorphisms (SNPs) from 38 candidate genes.

The 395 NHL cases registered in Jamaica were matched by age, sex, calendar-year and HTLV serostatus to 309 controls from the same population.

Interleukin 13 (IL13) Ex4+98A>G SNP (rs20541) was associated with decreased NHL risk (OR(AG/AA) = 0.62,95% CI = 0.44-0.87, p = 0.006), as was vascular cell adhesion molecule-1, VCAM1 Ex9+149G>A SNP (rs1041163) (OR(CT) = 0.77, 95% CI = 0.54-1.10, OR(CC) = 0.35, 95% CI = 0.16-0.76, p-trend = 0.007).

Both results were stronger in analyses restricted to ATL cases and HTLV-positive controls, suggesting a role for these genes in ATL etiology (IL13 OR(AG/AA) = 0.54, 95% CI = 0.36-0.84, p = 0.005; VCAM1 OR(CT) = 0.65, 95% CI = 0.42-1.01, OR(CC) = 0.20, 95% CI = 0.08-0.54, p-trend = 0.001).

[MeSH-major] HTLV-I Infections / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Polymorphism, Single Nucleotide / genetics

[MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Genetic Predisposition to Disease. Human T-lymphotropic virus 1 / immunology. Humans. Interleukin-13 / genetics. Interleukin-5 / genetics. Jamaica / epidemiology. Male. Middle Aged. Vascular Cell Adhesion Molecule-1 / genetics. Young Adult

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[Copyright] 2009 UICC

(PMID = 19533685.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / IL5 protein, human; 0 / Interleukin-13; 0 / Interleukin-5; 0 / Vascular Cell Adhesion Molecule-1

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Central nervous system involvement in adult T-cell lymphoma diagnosed with T-cell receptor gene clonality testing of cerebrospinal fluid.

[MeSH-major] Central Nervous System / pathology. Gene Rearrangement, T-Lymphocyte / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration / diagnosis

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(PMID = 20497173.001).

[ISSN] 1365-2141

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Localized nasal cavity, sinus, and massive bilateral orbital involvement by human T cell leukemia virus 1 adult T cell lymphoma, with epidermal hypertrophy due to mite infestation.

HTLV1 adult T cell lymphoma occurs tends to be widely disseminated and aggressive, with only brief responses to chemotherapy.

Aside from cervical adenopathy, involvement of head and neck structures is uncommon and orbital involvement rare.We report a case of nasal cavity HTLV lymphoma with massive bilateral orbital involvement and proptosis, resulting in complete left and partial right eye amaurosis.

No other sites of disease were found.

An associated problem was striking bilateral hypertrophic, hyperkeratotic eyelid and breast lesions due to mite infestation.

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(PMID = 21234251.001).

[ISSN] 2036-3613

[Journal-full-title] Rare tumors

[ISO-abbreviation] Rare Tumors

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Other-IDs] NLM/ PMC3019594

[Keywords] NOTNLM ; HTLV / lymphoma / oncology

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The discovery of the first human retrovirus: HTLV-1 and HTLV-2.

I describe here the history leading up to and including my laboratory's discovery of the first human retrovirus, HTLV-I, and its close relative, HTLV-II.

My efforts were inspired by early work showing a retroviral etiology for leukemias in various animals, including non-human primates.

These efforts finally yielded success following the discovery of IL-2 and its use to culture adult T cell lymphoma/leukemia cells.

[MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 2 / isolation & purification. Leukemia, T-Cell / history. Lymphoma, T-Cell / history

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[CommentIn] Retrovirology. 2005;2:15 [15743525.001]

(PMID = 15743526.001).

[ISSN] 1742-4690

[Journal-full-title] Retrovirology

[ISO-abbreviation] Retrovirology

[Language] eng

[Publication-type] Historical Article; Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC555587

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Rare association of papillary carcinoma of thyroid with adult T-cell lymphoma/leukemia.

But the tumor that arises more frequently in thyroiditis is malignant lymphoma.

We report a rare association of papillary carcinoma of thyroid in an elderly lady with adult T-cell lymphoma/leukemia.

Fine needle aspiration of the thyroid, neck nodes and evaluation of the bone marrow and peripheral blood helped in the diagnosis of papillary cancer coexisting with adult T-cell lymphoma/leukemia.

[MeSH-major] Carcinoma, Papillary / complications. Leukemia-Lymphoma, Adult T-Cell / complications. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Thyroid Gland / pathology. Thyroid Neoplasms / complications

[MeSH-minor] Adult. Biopsy, Fine-Needle. Bone Marrow / pathology. Female. Histocytochemistry. Humans. Immunohistochemistry. Leukemia. Middle Aged. Neck / radiography. Thyroid Nodule. Tomography

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(PMID = 20090241.001).

[ISSN] 0974-5130

[Journal-full-title] Indian journal of pathology & microbiology

[ISO-abbreviation] Indian J Pathol Microbiol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] India

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adult T-cell lymphoma mimicking Henoch-Schönlein purpura.

We report a male patient with adult T-cell lymphoma, who was initially diagnosed clinically as having Henoch-Schönlein purpura (HSP) with abdominal pain and specific purpura.

Adult T-cell lymphoma-like cells were minimal and abdominal lymph nodes were transiently swollen, and the symptoms were improved by supportive management.

Although the clinical course was compatible with HSP, the histological examination revealed infiltration of lymphocytes rather than neutrophils.

Later he developed lymphoma and was treated with chemotherapy.

This rare case suggests the importance of skin biopsies to seek the underlying pathology in adult HSP.

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(PMID = 17278024.001).

[ISSN] 1439-7595

[Journal-full-title] Modern rheumatology

[ISO-abbreviation] Mod Rheumatol

[Language] ENG

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genomic instability and rapid clinical course in adult T-cell lymphoma/leukemia patient.

Adult T-cell leukemia/lymphoma is a distinct clinical entity characterized by a clonal proliferation of malignant T-lymphocytes.

The etiologic agent of the disease is a Human T-cell lymphotropic virus type I.

It occurs almost exclusively in areas where the virus is endemic; however the disease develops only in the minority of patients who are virus carriers.

Karyotyping findings and their correlation with clinical features are still limited in T-cell malignancies, complicated by clinical heterogeneity and a plethora of secondary abnormalities.

This study describes detailed chromosomal and fluorescence in situ hybridization results observed in a patient with adult T-cell leukemia/lymphoma and correlates them with clinical characteristics.

[MeSH-major] Genomic Instability. HTLV-I Infections / genetics. Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell / genetics. T-Lymphocytes

[MeSH-minor] Adult. Female. Humans. Karyotyping

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[Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.

(PMID = 20211490.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Diffuse normolipaemic plane xanthomatosis associated with adult T-cell lymphoma/leukaemia.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Lipids / blood. Xanthomatosis / complications

[MeSH-minor] Adult. Humans. Male

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(PMID = 18637865.001).

[ISSN] 1468-3083

[Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV

[ISO-abbreviation] J Eur Acad Dermatol Venereol

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Lipids

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Extensive extranodal adult T-cell lymphoma presenting with a lytic arthropathy of the ankle.

A case is presented of a 44-year-old human T-cell lymphotropic virus-1 seropositive Afro-Caribbean man whose adult T-cell lymphoma presented with an ankle arthropathy.

Over a period of weeks he developed subcutaneous tumor masses, osteolytic lesions, sinonasal involvement, and spinal disease culminating in death 4 months after his diagnosis.

The case highlights the extranodal manifestations, generally, and rheumatological complications, specifically, of this very aggressive form of lymphoma with review of the relevant literature.

[MeSH-major] Ankle Joint. Arthritis / etiology. Lymphoma, Extranodal NK-T-Cell / complications

[MeSH-minor] Adult. Biopsy, Needle. Diagnosis, Differential. Fatal Outcome. Follow-Up Studies. Humans. Male. Photomicrography. Tomography, X-Ray Computed

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(PMID = 18176141.001).

[ISSN] 1076-1608

[Journal-full-title] Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases

[ISO-abbreviation] J Clin Rheumatol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adult T-cell lymphoma/leukemia with angioimmunoblastic T-cell lymphomalike features: Report of 11 cases.

In adult T-cell lymphoma/leukemia (ATLL), the neoplastic lymphoid cells are usually medium-sized to large, often with pronounced nuclear pleomorphism compatible with the diagnosis of diffuse pleomorphic peripheral T-cell lymphoma.

We describe here 11 patients with the rare morphologic variant of ATLL, angioimmunoblastic T-cell lymphoma (AILT)-like type.

The lymphoma cells were medium-to-large size with clear cytoplasm.

However, immunohistochemical features of AILT, namely, CD10 and CXCL13 expression in lymphoma cells and proliferation of CD21-positive follicular dendritic cells, were not detected.

Two cases were CXCR3-positive, whereas 9 expressed CCR4, which are usually positive in ATLL.

All patients were positive for antiadult T-cell leukemia/lymphoma-associated antigen, which is a specific antibody for human T-cell lymphotropic virus type-I.

Southern blot analysis revealed proviral DNA integration in lymphoma cells in 9 patients.

Almost all patients showed aggressive clinical course and poor survival (median survival: 5 mo).

This is the first report of ATLL with AILT-like morphologic features.

[MeSH-major] Immunoblastic Lymphadenopathy / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Lymphoma, T-Cell / pathology

[MeSH-minor] Adult. Aged. Antigens, CD / metabolism. Biomarkers, Tumor / metabolism. DNA, Viral / analysis. Female. HTLV-I Infections / virology. Humans. Male. Middle Aged. Survival Rate

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(PMID = 17255766.001).

[ISSN] 0147-5185

[Journal-full-title] The American journal of surgical pathology

[ISO-abbreviation] Am. J. Surg. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / DNA, Viral

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm).

Preclinical research suggests improvements in therapeutic ratio and activity in hematologic and solid tumor models, leading to clinical trials in patients with myeloma, lymphomas, leukemias, and solid tumors.

METHODS: Patients with solid tumor, lymphoma or leukemia diagnoses without standard treatment options were treated with IV NPI on Days 1, 8 and 15 of 28-day cycles in a 3+3 design dose escalation to a Recommended Phase 2 Dose (RP2D).

Enrollment then began in 10 patient lymphoma and CLL RP2D cohorts.

Stable disease was induced in 31% of patients, including one each with mantle cell, Hodgkin's lymphoma, follicular lymphoma, sarcoma, prostate carcinoma, and two with melanoma.

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(PMID = 27961753.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma.

: 8575 Background: Adult T-cell leukemia/lymphoma (ATLL) is associated with human T-cell lymphotropic virus type-I (HTLV-1) described in Southern Japan, Europe, Caribbean and South America.

Risk-stratification tools for ATLL have not been adequately evaluated.

This study attempts to define prognostic factors for patients with ATLL.

Diagnosis was based on clinical history and histological findings consistent with ATLL and either positive HTLV-1 serology or evidence of HTLV-1 integration.

Clinical types were acute (n=45), lymphomatous (n=43), cutaneous (n=10), smoldering (n=3) and chronic (n=1).

Median OS for acute, lymphomatous, smoldering and cutaneous subtype were 2, 11, 17 and 39 months, respectively (log-rank 28.5, p<0.00001).

In the univariate analysis, presence of B symptoms, ECOG performance status 2, clinical stage II or higher, elevated LDH level and bone marrow (BM) involvement were independent factors for survival with p<0.05.

The prognostic index for T-cell lymphoma (PIT) score was determined in 80 patients; 20 (25%), 17 (21%), 33 (41%) and 10 (13%) patients had scores of 0-1, 2, 3 and 4, respectively.

CONCLUSIONS: This retrospective series represents the largest Latin-American experience on ATLL, which is a heterogeneous disease with distinct clinical features and outcomes.

The IPI ant PIT scores, used for risk-stratification of aggressive B-cell and peripheral T-cell lymphomas, respectively, appear as good prognostic indicators for ATLL as well.

Further research is needed to better risk-stratify this unique lymphoma.

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(PMID = 27962272.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country.

: 10046 Background: Acute Lymphatic Leukemia is a curable disease in the range of 80 - 90% in developed countries by aggressive protocol like BFM, St. Judes' but result is much less in adolescence age group (60-70%).

Fever 48 (64.0%), lymphadenopathy 35 (46.7%), and haepatosplenomegaly 28 (37.3%) were the major clinical presentation.

In a follow-up period of 24 - 88 months (with an average of 54 months) the disease-free survival ( DFS) was 42 (56%) patients with an overall survival of 46 (61.34%) patients.

The major cause of the mortality was infection 18% (24.0% patients) followed progressive disease 9 (12.0%) and hemorrhage 2 (2.7%).

CONCLUSIONS: The data of acute lymphatic leukemia in adolescent is not satisfactory as compared to other pediatric patients.

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(PMID = 27962472.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pulmonary metastatic calcification in adult T-cell lymphoma/leukemia.

[MeSH-major] Calcinosis / etiology. Leukemia-Lymphoma, Adult T-Cell / complications. Lung Diseases / etiology

[MeSH-minor] Adult. Fatal Outcome. Humans. Male. Multiple Organ Failure / etiology. Radiopharmaceuticals. Technetium Tc 99m Medronate

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(PMID = 19999398.001).

[ISSN] 1784-3286

[Journal-full-title] Acta clinica Belgica

[ISO-abbreviation] Acta Clin Belg

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Belgium

[Chemical-registry-number] 0 / Radiopharmaceuticals; X89XV46R07 / Technetium Tc 99m Medronate

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adult T-cell lymphoma with HTLV-I and HTLV-II infection.

[MeSH-major] HTLV-I Infections / diagnosis. HTLV-II Infections / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / virology

[MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Male. Middle Aged

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(PMID = 17984755.001).

[ISSN] 0038-4348

[Journal-full-title] Southern medical journal

[ISO-abbreviation] South. Med. J.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Therapeutic and palliative benefit from single-agent irinotecan in multiply treated and highly refractory cases of lymphoma.

: e19554 Background: Multiple reports corroborate a role for irinotecan in the treatment of lymphoma.

This study describes the Memorial Sloan Kettering experience with single-agent irinotecan in the management of heavily pretreated and highly refractory cases of lymphoma.

METHODS: Adult patients with histologically diagnosed relapsed or refractory lymphoma treated with irinotecan between 1/2001 and 8/2008 were identified.

Treatment responses were evaluated based on the Revised Response Criteria for Malignant Lymphoma.

4 patients had Hodgkin Lymphoma (HL) and 26 had Non-Hodgkin lymphoma (NHL): 17 DLBCL, 6 transformed follicular lymphoma, 1 mantle cell lymphoma, 1 T-cell lymphoma and 1 Burkitt's. 25 patients were evaluable for response.

8 patients (32%) had stable disease and 12 (48%) progressed on treatment.

CONCLUSIONS: Irinotecan has utility even in multiply treated and highly refractory cases of lymphoma.

It can mitigate symptoms resulting from bulky disease and shows potential as a palliative treatment option.

Strategies that limit adverse reactions may enhance the agent's effectiveness in refractory lymphoma.

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(PMID = 27961088.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Update on the therapy of highly aggressive non-Hodgkin's lymphoma.

This review focuses on the current understanding of the biology of highly aggressive non-Hodgkin's lymphomas, such as Burkitt's lymphoma, lymphoblastic lymphoma and adult T cell lymphoma/leukaemia.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma. Lymphoma, Non-Hodgkin. Lymphoma, T-Cell. Precursor Cell Lymphoblastic Leukemia-Lymphoma

[MeSH-minor] Adult. Child. Female. Humans. Male

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(PMID = 16805709.001).

[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

[Number-of-references] 95

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Erythema multiforme-like lesions associated with lesional infiltration of tumor cells occurring with adult T-cell lymphoma/leukemia.

[MeSH-major] Erythema Multiforme / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration / pathology. Skin / pathology

[MeSH-minor] Aged. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Immunophenotyping

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(PMID = 18377607.001).

[ISSN] 1365-4632

[Journal-full-title] International journal of dermatology

[ISO-abbreviation] Int. J. Dermatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Isolated central nervous system involvement in adult T-cell lymphoma/leukaemia.

Central nervous system (CNS) presentation of adult T-cell lymphoma/leukaemia is rare, and almost invariably associated with systemic disease.

We report an unusual manifestation of adult T-cell lymphoma/leukaemia, with isolated CNS involvement and unusual imaging findings.

[MeSH-major] Brain Neoplasms / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis

[MeSH-minor] Adult. Antiviral Agents / therapeutic use. Disease Progression. Frontal Lobe / surgery. Humans. Interferons / therapeutic use. Magnetic Resonance Imaging. Male. Palliative Care. Tomography, X-Ray Computed

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[ErratumIn] Br J Haematol. 2005 Nov;131(4):557. Taylor, R [corrected to Tailor, R]

(PMID = 16098064.001).

[ISSN] 0007-1048

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antiviral Agents; 9008-11-1 / Interferons

[Number-of-references] 22

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.

: 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.

METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).

Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).

Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).

Using augmented therapy based on CCG1961 was associated with better outcome.

Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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(PMID = 27962474.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A case of phlegmonous gastritis associated with marked gastric distension.

Phlegmonous gastritis is an acute and severe infectious disease that is occasionally fatal if the diagnosis is delayed.

Alcohol consumption, an immunocompromised state (e.g., due to HIV infection, rheumatoid arthritis, diabetes mellitus, or adult T-cell lymphoma), and mucosal injury of the stomach are reported to be predisposing factors.

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(PMID = 20981225.001).

[ISSN] 2005-1212

[Journal-full-title] Gut and liver

[ISO-abbreviation] Gut Liver

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2956360

[Keywords] NOTNLM ; Gastric outlet obstruction / Phlegmonous gastritis

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Effects of proteasome inhibitors on leukemias].

The abnormality of its activity is sign of tumorigenesis.

Bortezomib, the first proteasome inhibitor, obtained permission of clinical trial and on sale.

A lot of studies on effects of proteasome inhibitors on leukemias, including plasma cell leukemia; chronic lymphocytic leukemia, adult T cell lymphoma/leukemia, chronic myeloid leukemia and acute myeloid leukemia, were reviewed in this article.

MedlinePlus Health Information. consumer health - Leukemia.

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(PMID = 17708829.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] China

[Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib

[Number-of-references] 27

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Analysis of genomic copy number alterations of malignant lymphomas and its application for diagnosis].

Using this technique, we were thus able to reveal disease-specific genomic alterations and the candidate target genes in various lymphomas.

We herein report the characteristic genomic alterations of malignant lymphomas including diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL) and adult T cell lymphoma/leukemia (ATLL).

For instance, we revealed that activated B-cell-like DLBCL is characterized by a gain of chromosome 3, 18q and loss of 9 p21, whereas the germinal center B-cell-like DLBCL is characterized by a gain of 2p15, 7q, and 12q.

Comparison of genome profiles between acute type and lymphoma types of adult T cell lymphoma also demonstrated that acute and lymphoma types are genomically distinct subtypes, and thus may develop tumors via distinct genetic pathways.

In addition to identifying disease-specific genomic alterations, we also discovered several target genes of the genomic gains and losses.

Furthermore,we developed a computer algorithm to classify lymphoma diseases or subtypes on the basis of copy number gains and losses.

These results demonstrate that copy number gains and losses detected by array CGH could be used for classifying lymphomas into biologically and clinically distinct diseases or subtypes.

The genomic copy number alterations detected by array CGH are therefore considered to have the potential to help diagnose or classify different disease entities and tumor subtypes.

[MeSH-major] Gene Dosage. Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Follicular / genetics. Lymphoma, Large B-Cell, Diffuse / genetics

[MeSH-minor] Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / genetics. Genome, Human. Humans. Lymphoma, Mantle-Cell / diagnosis. Lymphoma, Mantle-Cell / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Translocation, Genetic

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(PMID = 17637530.001).

[ISSN] 0385-0684

[Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy

[ISO-abbreviation] Gan To Kagaku Ryoho

[Language] jpn

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Japan

[Number-of-references] 13

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Septic shock induced by Serratia marcescens complicating adult T-cell leukemia (ATL)].

Hypercalcemia appeared when of the dose of prednisolone was reduced, and human T-cell lymphotropic virus type-I (HTLV-I) proviral DNA was detected in the leukemic cells by Southern blot analysis, and a diagnosis of acute adult T-cell lymphoma (ATL) was made.

[MeSH-major] Leukemia, T-Cell / complications. Serratia Infections / complications. Serratia marcescens. Shock, Septic / complications

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(PMID = 16780133.001).

[ISSN] 0387-5911

[Journal-full-title] Kansenshōgaku zasshi. The Journal of the Japanese Association for Infectious Diseases

[ISO-abbreviation] Kansenshogaku Zasshi

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Loss of CD7, independent of galectin-3 expression, implies a worse prognosis in adult T-cell leukaemia/lymphoma.

AIMS: Loss of CD7 is characteristic of adult T-cell lymphoma/leukaemia (ATLL).

Galectin-3 (Gal-3) is strongly induced in cultured human T lymphotropic virus-1-infected T lymphocytes, and may cause apoptosis through interaction with CD7.

The aim was to investigate the clinical relevance of the Gal-3-CD7 pathway in ATLL.

METHODS AND RESULTS: Immunohistochemistry for Gal-3 and CD7 was performed on 22 cases of ATLL in the leukaemic phase.

We found that the lymphoma cells were not necessarily Gal-3+, but Gal-3+ stromal cells could always be found.

CONCLUSIONS: These data suggest that, by down-regulating CD7, ATLL cells could have escaped Gal-3-induced apoptosis to run a more aggressive clinical course.

[MeSH-major] Antigens, CD7 / metabolism. Galectin 3 / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology

[MeSH-minor] Adult. Aged. Apoptosis. Cells, Cultured. Chromosome Aberrations. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis

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(PMID = 19207946.001).

[ISSN] 1365-2559

[Journal-full-title] Histopathology

[ISO-abbreviation] Histopathology

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD7; 0 / Galectin 3

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Aberrant NF-kappaB signaling in lymphoma: mechanisms, consequences, and therapeutic implications.

The transcription factor NF-kappaB is a tightly regulated positive mediator of T- and B-cell development, proliferation, and survival.

However, constitutive NF-kappaB activation can promote continuous lymphocyte proliferation and survival and has recently been recognized as a critical pathogenetic factor in lymphoma.

Various molecular events lead to deregulation of NF-kappaB signaling in Hodgkin disease and a variety of T- and B-cell non-Hodgkin lymphomas either up-stream or downstream of the central IkappaB kinase.

These alterations are prerequisites for lymphoma cell cycling and blockage of apoptosis.

This review provides an overview of the NF-kappaB pathway and discusses the mechanisms of NF-kappaB deregulation in distinct lymphoma entities with defined aberrant pathways: Hodgkin lymphoma (HL), diffuse large B-cell lymphoma (DLBCL), mucosa-associated lymphoid tissue (MALT) lymphoma, primary effusion lymphoma (PEL), and adult T-cell lymphoma/leukemia (ATL).

In addition, we summarize recent data that validates the NF-kappaB signaling pathway as an attractive therapeutic target in T- and B-cell malignancies.

[MeSH-major] Lymphoma / physiopathology. NF-kappa B / physiology

[MeSH-minor] Hodgkin Disease / physiopathology. Humans. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Lymphocytes / physiology. Lymphoma, B-Cell / physiopathology. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / physiopathology. Lymphoma, Large B-Cell, Diffuse / physiopathology. Models, Biological. Oncogene Proteins, Viral / physiology. Prognosis. Signal Transduction / physiology. Translocation, Genetic

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(PMID = 17119127.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / NF-kappa B; 0 / Oncogene Proteins, Viral

[Number-of-references] 96

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Osteonecrosis of the femoral head (ONFH) is a devastating disease that can result in a femoral head collapse.

GSEA (gene set enrichment analysis) revealed that proteins overexpressed in ONFH are enriched for gene sets related to multiple myeloma and adult T-cell lymphoma (ATL), and to JAK2-dependent genes.

[MeSH-minor] Adult. Aged. Chromatography, Liquid / methods. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Protein Isoforms / metabolism. Proteomics / methods. Receptors, G-Protein-Coupled / metabolism. Sulfotransferases / metabolism. Tandem Mass Spectrometry / methods

Genetic Alliance. consumer health - Osteonecrosis.

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(PMID = 20001860.001).

[ISSN] 1557-8100

[Journal-full-title] Omics : a journal of integrative biology

[ISO-abbreviation] OMICS

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Protein Isoforms; 0 / Proteome; 0 / Receptors, G-Protein-Coupled; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.- / carbohydrate sulfotransferases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] In vivo analysis of replication and immunogenicity of proviral clones of human T-lymphotropic virus type 1 with selective envelope surface-unit mutations.

Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell lymphoma/leukemia (ATL).

The HTLV-1 envelope gene exhibits limited variability when examined from infected individuals, but has not been tested using infectious clones of the virus in animal models.

In vitro assays indicate that HTLV-1 envelope (Env) Ser75Ile, Asn95Asp, and Asn195Asp surface unit (SU) mutants are able to replicate in and immortalize lymphocytes.

Herein, we examined the effects of these Env mutants in rabbits inoculated with HTLV-1 immortalized ACH.75, ACH.95, or ACH.195 cell lines (expressing full-length molecular clones with the SU mutations) or the ACH.1 cell line (expressing wild-type SU).

However, SU point mutations resulted in decreased antibody responses to viral group-associated antigen (Gag) and Env antigens.

ACH.195 rabbits had a selective decreased antibody response to SU, and one ACH.195 rabbit had an antibody response to both HTLV-1 and HTLV-2 SUs.

However, peripheral-blood mononuclear cell (PBMC) proviral loads did not correlate with antibody responses.

Our data are the first to demonstrate that mutations in critical determinants of HTLV-1 Env SU altered antibody responses and proviral loads, but do not prevent viral replication in vivo.

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(PMID = 16046523.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P01 CA100730-02; United States / NCI NIH HHS / CA / CA-63417; United States / NCI NIH HHS / CA / CA09338; United States / NCI NIH HHS / CA / CA70529

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Viral; 0 / Gene Products, env; 0 / Gene Products, gag

[Other-IDs] NLM/ PMC1895059

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] HTLV-1 related knowledge, attitude and behaviour patterns among mothers who participated in the Jamaica Breastfeeding Intervention Study (1996-2000).

Human T-cell Lymphotropic Virus type-1 (HTLV-1), the first human retrovirus associated with a malignant disease, is endemic in Jamaica.

Women are at greater risk of contracting the virus as it is more efficiently transmitted from male to female than in the reverse.

The study aims to document the knowledge, attitude and behaviour pattern (KABP) of a group of women five years after they had participated in a mother-to-child transmission of HTLV-1 risk reduction study.

There were large deficiencies in the knowledge and practice of women at risk of being infected with HTLV-1.

Only 58% knew that HTLV-1 is sexually transmitted.

A minority was aware of HTLV-1 associated diseases: Adult T-cell lymphoma/leukaemia (ATL) -30.7%; Tropical Spastic Paraparesis (TSP) -42%; Infective dermatitis -42%).

Ten (11.4%) believed that HTLV-1 infection can cause HIV/AIDS and only 33% knew that there was no cure for the virus.

Controlling HTLV-1 spread must be based on interrupting transmission.

In Jamaica, donated blood is screened for HTLV-1 and sharing of infected needle is an insignificant mode of transmission.

However although safe practices in breastfeeding and sexual intercourse are proven ways to reduce HTLV-1 transmission, these data show that knowledge and safe practices among those at risk may not be retained and health education will need to be sustained.

[MeSH-major] Breast Feeding. HTLV-I Infections / transmission. Health Knowledge, Attitudes, Practice. Human T-lymphotropic virus 1. Mothers

[MeSH-minor] Adult. Chi-Square Distribution. Cross-Sectional Studies. Demography. Female. Focus Groups. Health Education. Humans. Infectious Disease Transmission, Vertical. Jamaica / epidemiology. Male. Middle Aged. Regression Analysis. Surveys and Questionnaires

MedlinePlus Health Information. consumer health - Breastfeeding.

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(PMID = 20931911.001).

[ISSN] 0043-3144

[Journal-full-title] The West Indian medical journal

[ISO-abbreviation] West Indian Med J

[Language] eng

[Publication-type] Journal Article

[Publication-country] Jamaica

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression patterns of programmed cell death 4 protein in normal human skin and some representative skin lesions.

Expression of a tumor suppressor gene, programmed cell death 4 (PDCD4), was investigated at the protein level in the human skin.

Immunohistochemically, PDCD4 protein expressed mainly in suprabasal layers, while PDCD4-positive and -negative areas were observed discontinuously in the basal cell layer of the epidermis.

In hair follicles, the suprabulbar area including the hair and inner root sheath was immunoreactive, while the bulbar area, containing germinative cells which were strongly proliferating cell nuclear antigen (PCNA)-positive, was not or less.

PDCD4-positive cells were localized in the inside layers while PCNA-positive cells were located in the basal layer in the outer root sheath of hair follicles.

The cells of sebaceous glands and sweat glands also were PDCD4-positive.

PDCD4 expression was found to be suppressed in the epidermis overlying an adult T-cell lymphoma (ATL), possibly reflecting a paracrine effect of factors produced by ATL cells.

PDCD4 expression was suppressed in the keratinocyte cell line HaCaT by exposure of cultures to epidermal growth factor, transforming growth factor-beta1 or hepatocyte growth factor.

[MeSH-minor] Cell Line. Cell Nucleus / metabolism. Hair Follicle / immunology. Hair Follicle / metabolism. Humans. Immunohistochemistry. Keratinocytes / cytology. Keratinocytes / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Sebaceous Glands / cytology. Sebaceous Glands / metabolism. Sweat Glands / cytology. Sweat Glands / metabolism

MedlinePlus Health Information. consumer health - Skin Conditions.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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(PMID = 17286809.001).

[ISSN] 0906-6705

[Journal-full-title] Experimental dermatology

[ISO-abbreviation] Exp. Dermatol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Denmark

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / PDCD4 protein, human; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA-Binding Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Central nervous system leukemia mimicking rapidly progressive HTLV-1 associated myelopathy].

After one month, she showed flaccid paraplegia and hyperreflexia in the lower limbs with positive Babinski signs.

Anti-HTLV-1 antibody titer was elevated in the serum, but negative in the cerebrospinal fluid (CSF).

Adult T cell lymphoma (ATL)-like cells were seen in the CSF.

A tentative diagnosis of rapidly progressive HTLV-1 associated myelopathy (HAM) was given, but intravenous methylprednisolone was ineffective.

Six months later, she developed pneumonia, and abundant ATL cells were seen in the peripheral blood, suggesting a diagnosis of ATL.

Direct infiltration of ATL cells to central nervous system was therefore suggested to have caused neurological abnormalities in this case.

One may consider central nervous system leukemia when rapidly progressive HAM-like symptoms and signs are recognized, especially without positive anti-HTLV-1 antibody in the CSF.

[MeSH-major] Central Nervous System Neoplasms / diagnosis. HTLV-I Infections / complications. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Spinal Cord Diseases / diagnosis

[MeSH-minor] Aged. Diagnosis, Differential. Female. Humans

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(PMID = 19491526.001).

[ISSN] 0300-9173

[Journal-full-title] Nihon Ronen Igakkai zasshi. Japanese journal of geriatrics

[ISO-abbreviation] Nihon Ronen Igakkai Zasshi

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Mutation of the p53 tumour suppressor gene and overexpression of its protein in 62 Japanese non-Hodgkin's lymphomas.

To clarify whether p53 mutation could be involved in the pathogenesis of various subtypes of lymphoma, we investigated 62 Japanese cases of non-Hodgkin's lymphomas (NHLs) for p53 gene mutations and their relationship with the expression of p53 protein.

Missense and/or nonsense mutations of p53 were detected in 3 (10.7%) of 28 diffuse large B-cell lymphomas (DLBLs) and 2 (15.4%) of 13 T-cell NHLs (15.4%).

A single missense mutation at codon 157 (Val to Phe) in exon 5 and at codon 273 (Arg to Pro) in exon 8 was found respectively in 2 DLBLs and in one peripheral T-cell lymphoma (unspecified).

Double transversion mutations comprising of a missense mutation at codon 167 (Gln to His) in exon 5 and a nonsense mutation at codon 183 (Ser to stop codon) in exon 5 were detected in one DLBL that had apparently transformed from follicular lymphoma and in one advanced adult T-cell lymphoma (ATL).

In these two cases harbouring p53 nonsense mutation, no cells positive for p53 protein immunostaining were detected, as well as lymphomas without p53 mutation.

[MeSH-major] Asian Continental Ancestry Group. Gene Expression Regulation, Neoplastic / genetics. Lymphoma, Non-Hodgkin / genetics. Lymphoma, Non-Hodgkin / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Child. Exons / genetics. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mutation / genetics. Ribonucleases / metabolism

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(PMID = 17609875.001).

[ISSN] 1591-8890

[Journal-full-title] Clinical and experimental medicine

[ISO-abbreviation] Clin. Exp. Med.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 3.1.- / Ribonucleases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] CD26, together with cell surface adenosine deaminase, is selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma.

CD26/dipeptidyl peptidase IV is a cell surface antigen with multiple biological functions.

Although its involvement in tumor biology has been suggested, the significance of its expression in malignant lymphoma has not been clarified in detail.

This study examined the expression of CD26 and cell surface adenosine deaminase (ADA) in 42 cases of Hodgkin's lymphoma (HL) and T-cell lymphoma by immunohistochemistry on frozen sections.

CD26 was expressed in three of 14 cases of HL, in four of eight cases of anaplastic large cell lymphoma (ALCL), in two of nine cases of peripheral T-cell lymphoma, in one of six cases of lymphoblastic lymphoma and in none of three cases of adult T-cell lymphoma/leukemia.

Expression of cell surface ADA was fully correlated with the expression of CD26 and expression of CD26/ADA in ALCL and HL was also completely correlated with the expression of p80 and epithelial membrane antigen.

Of 10 CD26-positive patients, seven had fever and elevated CRP at initial diagnosis and over a median follow-up of 61 months (range, 7 - 152 months) only three survived.

This study suggested that CD26 is selectively expressed on ALK-positive, but not on ALK-negative, ALCL and HL.

This is also the first report to demonstrate that ADA is coexpressed with CD26 on the cell surface of malignant neoplasms in vivo.

[MeSH-major] Adenosine Deaminase / biosynthesis. Cell Membrane / enzymology. Dipeptidyl Peptidase 4 / biosynthesis. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / biosynthesis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD3 / biosynthesis. Female. Humans. Jurkat Cells. Male. Middle Aged. Receptor Protein-Tyrosine Kinases

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(PMID = 17071493.001).

[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, CD3; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.5.4.4 / Adenosine Deaminase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of tumor invasion factors determines systemic engraftment and induction of humoral hypercalcemia in a mouse model of adult T-cell leukemia.

Infection with human T-cell leukemia virus type 1 (HTLV-1) leads sometimes to the development of adult T-cell lymphoma/leukemia (ATL), which is invariably fatal and often associated with humoral hypercalcemia of malignancy.

The transformation of infected CD4 T cells and the pathogenesis of leukemia have been studied with great limitation in tissue culture and patients.

To better understand the pathogenesis and perform preclinical drug studies, animal models of ATL are urgently needed.

In mice, inoculation of HTLV-1 cell lines mostly leads to development of localized lymphomas.

To develop an ATL animal model with leukemic spread of ATL cells, mouse strains with different well-defined immune deficiencies were inoculated intraperitoneally with different HTLV-1-infected cell lines (ACH.2, C8166, MT-2, MET-1).

Inoculation of MET-1 cells into NOD/SCID mice provided the best model system for slowly developing T-cell leukemia with multiple organ involvement.

In contrast to the other cell lines that did not spread systemically, MET-1 expressed both the adhesion molecules CD11a (LFA-1alpha) and CD49d (VLA-4alpha) and produced or induced expression of matrix metalloproteinases 1, 2, 3, and 9, thus underlining the importance of these molecules in the spread of adult T-cell leukemia cells.

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(PMID = 19429977.001).

[ISSN] 1544-2217

[Journal-full-title] Veterinary pathology

[ISO-abbreviation] Vet. Pathol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P01 CA100730-07; United States / NCI NIH HHS / CA / CA100730-07S19003; United States / NCI NIH HHS / CA / P01 CA100730-07S19003; United States / NCI NIH HHS / CA / CA100730-07; United States / NCI NIH HHS / CA / P01 CA100730

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD11a; 0 / Bsg protein, mouse; 0 / Parathyroid Hormone-Related Protein; 0 / RANK Ligand; 0 / Receptors, Chemokine; 0 / Tnfsf11 protein, mouse; 0 / macrophage inflammatory protein 1alpha receptor; 136894-56-9 / Antigens, CD147; 143198-26-9 / Integrin alpha4; 63231-63-0 / RNA; EC 3.4.24.- / Mmp9 protein, mouse; EC 3.4.24.35 / Matrix Metalloproteinase 9

[Other-IDs] NLM/ NIHMS175834; NLM/ PMC2852243

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Development of a cytotoxic T-cell assay in rabbits to evaluate early immune response to human T-lymphotropic virus type 1 infection.

Human T-lymphotropic virus type 1 (HTLV-1) infection causes adult T-cell lymphoma/leukemia (ATL) following a prolonged clinical incubation period, despite a robust adaptive immune response against the virus.

We have developed a cytotoxic T-lymphocyte (CTL) assay to monitor the early events of HTLV-1 infection in rabbits.

Rabbit skin fibroblast cell lines were established by transformation with a plasmid expressing simian virus 40 (SV40) large T antigen and used as autochthonous targets (derived from same individual animal) to measure CTL activity against HTLV-1 infection in rabbits.

Recombinant vaccinia virus (rVV) constructs expressing either HTLV-1 envelope surface unit (SU) glycoprotein 46 or Tax proteins were used to infect fibroblast targets in a (51)Cr-release CTL assay.

Rabbits inoculated with Jurkat T cells or ACH.2 cells (expressing ACH HTLV-1 molecule clone) were monitored at 0, 2, 4, 6, 8, 13, 21, and 34 wk post-infection.

Proviral load analysis indicated that rabbits with higher proviral loads had significant CTL activity against HTLV-1 SU as early as 2 wk post-infection, while both low- and high-proviral-load groups had minimal Tax-specific CTL activity throughout the study.

This first development of a stringent assay to measure HTLV-1 SU and Tax-specific CTL assay in the rabbit model will enhance immunopathogenesis studies of HTLV-1 infection.

Our data suggest that during the early weeks following infection, HTLV-1-specific CTL responses are primarily targeted against Env-SU.

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(PMID = 19951176.001).

[ISSN] 1557-8976

[Journal-full-title] Viral immunology

[ISO-abbreviation] Viral Immunol.

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / RR014324-05; United States / NCI NIH HHS / CA / CA100730-02S1; United States / NCI NIH HHS / CA / P01 CA100730-02S1; United States / NCI NIH HHS / CA / P01 CA100730-07; United States / NCI NIH HHS / CA / CA100730; United States / NCI NIH HHS / CA / CA100730-03S1; United States / NCI NIH HHS / CA / P01 CA100730-04S1; United States / NCRR NIH HHS / RR / R01 RR014324-05; United States / NCI NIH HHS / CA / CA100730-04S1; United States / NCI NIH HHS / CA / P01 CA100730-03S1; United States / NCI NIH HHS / CA / CA100730-07

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Gene Products, env; 0 / Gene Products, tax; 0 / Recombinant Fusion Proteins; 0 / Retroviridae Proteins, Oncogenic; 0 / gp46 protein, Human T-cell leukemia virus type I; 0 / tax protein, Human T-lymphotrophic virus 1

[Other-IDs] NLM/ NIHMS175831; NLM/ PMC2852241

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Population differences in immune marker profiles associated with human T-lymphotropic virus type I infection in Japan and Jamaica.

The natural history of human T-lymphotropic virus type I (HTLV-I) has been shown to differ markedly by geographic area.

The differences include contrasting patterns of risk of adult T-cell lymphoma (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), which may be due in part to differences in host immune response to infection.

To characterize variations in host immunity across populations, we compared serologic immune marker patterns in HTLV-I-endemic populations in Japan and Jamaica.

We matched 204 participants with archived blood from the Miyazaki Cohort Study (Japan) and the Food Handlers Study (Jamaica)-i.e., 51 HTLV-I-positive ("carriers") and 51 HTLV-I-negative individuals ("noncarriers") from each population-by age, sex and blood collection year.

We compared plasma concentrations of markers of T-cell-mediated (antigen-specific) and nonspecific immunity using regression models and correlation coefficients.

Compared to Jamaican HTLV-I noncarriers, Japanese noncarriers had higher covariate-adjusted mean levels of T-cell activation markers, including antibody to Epstein-Barr virus nuclear antigen-1 (reciprocal titer 27 vs. 71, respectively, p=0.005), soluble interleukin-2 receptor-alpha (477 vs. 623 pg/mL, p=0.0008) and soluble CD30 (34 vs. 46 U/mL, p=0.0001) and lower levels of C-reactive protein (1.1 vs. 0.43 microg/mL, p=0.0004).

HTLV-I infection was associated with activated T-cell immunity in Jamaicans but with diminished T-cell immunity in Japanese persons.

The observed population differences in background and HTLV-I-related host immunity correspond closely to the divergent natural histories of infection observed among HTLV-I carriers in Japan and Jamaica and corroborate a role for host immune status in the contrasting patterns of ATL and HAM/TSP risk.

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[Copyright] Copyright (c) 2008 Wiley-Liss, Inc.

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(PMID = 18989900.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA038450-15; United States / NCI NIH HHS / CA / CA115687-01A1; United States / NCI NIH HHS / CA / R01 CA038450-15; United States / NCI NIH HHS / CA / K07 CA115687-01A1; United States / NCI NIH HHS / CA / K07 CA115687; United States / NCI NIH HHS / CA / CA115687-02; United States / NCI NIH HHS / CA / R01 CA038450-14; United States / NCI NIH HHS / CA / K07 CA115687-03; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / CA115687-03; United States / NCI NIH HHS / CA / CA115687; United States / NCI NIH HHS / CA / CA09001; United States / NCI NIH HHS / CA / CA038450-14; United States / NCI NIH HHS / CA / T32 CA009001; United States / NCI NIH HHS / CA / CA38450; United States / NCI NIH HHS / CA / K07 CA115687-02

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Viral; 0 / Antigens, Viral

[Other-IDs] NLM/ NIHMS99048; NLM/ PMC2701897

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] HTLV-1 Tax: centrosome amplification and cancer.

During interphase, each cell contains a single centrosome that acts as a microtubule organizing center for cellular functions in interphase and in mitosis.

Centrosome amplification during the S phase of the cell cycle is a tightly regulated process to ensure that each daughter cell receives the proper complement of the genome.

The controls that ensure that centrosomes are duplicated exactly once in the cell cycle are not well understood.

These phenotypes are also observed in cancers induced by viruses, including adult T cell lymphoma which is caused by the human T cell lymphotrophic virus Type 1 (HTLV-1).

Several reports have indicated that the HTLV-1 transactivator, Tax, is directly responsible for the centrosomal abnormalities observed in ATL cells.

A recent paper in Nature Cell Biology by Ching et al. has shed some new light into how Tax may be inducing centrosome abnormalities.

The authors demonstrated that 30% of ATL cells contained more than two centrosomes and expression of Tax alone induced supernumerary centrosomes.

These results suggest that Tax1BP2 may be an important block to centrosome re-duplication that is observed in normal cells.

Presently, a specific cellular protein that prevents centrosome re-duplication has not been identified.

This paper has provided further insight into how Tax induces centrosome abnormalities that lead to ATL.

Lastly, additional work on Tax1BP2 will also provide insight into how the cell suppresses centrosome re-duplication during the cell cycle and the role that Tax1BP2 plays in this important cellular pathway.

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(PMID = 16899128.001).

[ISSN] 1742-4690

[Journal-full-title] Retrovirology

[ISO-abbreviation] Retrovirology

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / AI44357; United States / NIAID NIH HHS / AI / R01 AI043894; United States / PHS HHS / / 13969; United States / NIAID NIH HHS / AI / AI43894; United States / NIAID NIH HHS / AI / R29 AI044357

[Publication-type] Editorial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Gene Products, tax; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / VAC14 protein, human

[Other-IDs] NLM/ PMC1555608

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cutaneous tumor lysis syndrome in a patient with HTLV-1 adult T-cell lymphoma/leukemia.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Skin Diseases / pathology. Tumor Lysis Syndrome / pathology

Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.

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(PMID = 19892727.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cytomegalovirus in cutaneous ulcers in a patient with adult T-cell lymphoma.

[MeSH-major] Cytomegalovirus / isolation & purification. Cytomegalovirus Infections / complications. Lymphoma, T-Cell / complications. Skin Ulcer / virology

Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.

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(PMID = 16648934.001).

[ISSN] 0001-5555

[Journal-full-title] Acta dermato-venereologica

[ISO-abbreviation] Acta Derm. Venereol.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Norway

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adult T-cell lymphoma/leukaemia developing in a patient with psoriasis treated with long-term cyclosporine.

[MeSH-major] Cyclosporine / adverse effects. Dermatologic Agents / adverse effects. Leukemia-Lymphoma, Adult T-Cell / chemically induced. Psoriasis / drug therapy

Genetic Alliance. consumer health - Psoriasis.

MedlinePlus Health Information. consumer health - Psoriasis.

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(PMID = 16648935.001).

[ISSN] 0001-5555

[Journal-full-title] Acta dermato-venereologica

[ISO-abbreviation] Acta Derm. Venereol.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Norway

[Chemical-registry-number] 0 / Dermatologic Agents; 83HN0GTJ6D / Cyclosporine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL.

Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease.

In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Proteins / physiology. Receptors, Notch / physiology. T-Lymphocytes / pathology

[MeSH-minor] Animals. Apoptosis / physiology. Cell Cycle / physiology. F-Box Proteins / physiology. Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. Humans. Ikaros Transcription Factor / genetics. Ikaros Transcription Factor / physiology. Ligands. Mice. Mice, Transgenic. Oncogenes. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / physiology. Signal Transduction / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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(PMID = 18758476.001).

[ISSN] 1476-5594

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Grant] United States / NCI NIH HHS / CA / T32 CA09171

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] England

[Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / IKZF1 protein, human; 0 / Ligands; 0 / Neoplasm Proteins; 0 / Receptors, Notch; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 148971-36-2 / Ikaros Transcription Factor; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / Ubiquitin-Protein Ligases

[Number-of-references] 84

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.

This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.

In addition, we identified deletions and associated mutations in the WT1 tumor suppressor gene in 2 of 9 samples.

Subsequent analysis showed WT1 mutations in 28 of 211 (13.2%) of pediatric and 10 of 85 (11.7%) of adult T-ALL cases.

Survival analysis demonstrated that WT1 mutations do not confer adverse prognosis in pediatric and adult T-ALL.

[MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

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(PMID = 19494353.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Databank-accession-numbers] GEO/ GSE15931

[Grant] United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins

[Other-IDs] NLM/ PMC2721784

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Identification of two new HLA-A*1101-restricted tax epitopes recognized by cytotoxic T lymphocytes in an adult T-cell leukemia patient after hematopoietic stem cell transplantation.

We previously reported that Tax-specific CD8(+) cytotoxic T lymphocytes (CTLs), directed to single epitopes restricted by HLA-A2 or A24, expanded in vitro and in vivo in peripheral blood mononuclear cells (PBMC) from some adult T-cell leukemia (ATL) patients after but not before allogeneic hematopoietic stem cell transplantation (HSCT).

Here, we demonstrated similar Tax-specific CTL expansion in PBMC from another post-HSCT ATL patient without HLA-A2 or A24, whose CTLs equally recognized two newly identified epitopes, Tax88-96 and Tax272-280, restricted by HLA-A11, suggesting that these immunodominant Tax epitopes are present in the ATL patient in vivo.

[MeSH-major] Epitopes / immunology. Gene Products, tax / immunology. HLA-A Antigens / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / therapy. Stem Cell Transplantation. T-Lymphocytes, Cytotoxic / immunology

[MeSH-minor] Amino Acid Sequence. Coculture Techniques. Human T-lymphotropic virus 1 / immunology. Humans. Leukocytes, Mononuclear. Male. Middle Aged. Molecular Sequence Data. Peptides / genetics. T-Cell Antigen Receptor Specificity. Transplantation, Homologous

Genetic Alliance. consumer health - Transplantation.

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(PMID = 16014972.001).

[ISSN] 0022-538X

[Journal-full-title] Journal of virology

[ISO-abbreviation] J. Virol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Epitopes; 0 / Gene Products, tax; 0 / HLA-A Antigens; 0 / Peptides

[Other-IDs] NLM/ PMC1181560

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children.

The C-Myb transcription factor is essential for hematopoiesis, including in the T-cell lineage.

The C-Myb locus is a common site of retroviral insertional mutagenesis, however no recurrent genomic involvement has been reported in human malignancies.

Here, we identified 2 types of genomic alterations involving the C-MYB locus at 6q23 in human T-cell acute leukemia (T-ALL).

Expression analysis, including allele-specific approaches, showed stronger C-MYB expression in the MYB-rearranged cases compared with other T-ALLs, and a dramatically skewed C-MYB allele expression in the TCRB-MYB cases, which suggests that a translocation-driven deregulated expression may overcome a cellular attempt to down-regulate C-MYB.

Strikingly, profiling of the T-ALLs by clinical, genomic, and large-scale gene expression analyses shows that the TCRB-MYB translocation defines a new T-ALL subtype associated with a very young age for T-cell leukemia (median, 2.2 years) and with a proliferation/mitosis expression signature.

By contrast, the MYB(dup) alteration was associated with the previously defined T-ALL subtypes.

[MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Proto-Oncogene Proteins c-myb / genetics. Translocation, Genetic

[MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Base Sequence. Child. Child, Preschool. Female. Gene Dosage. Gene Expression Profiling. Genome, Human. Humans. Infant. Male. Middle Aged. Molecular Sequence Data. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Sequence Homology, Nucleic Acid

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(PMID = 17452517.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA101859

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.

Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del(19)(p13.2).

From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases.

[MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion

[MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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(PMID = 18185524.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Delineation of immunoregulatory properties of adult T-cell leukemia cells.

We characterized leukemic cells from 20 adult T-cell leukemia (ATL) cases and 7 ATL-derived cell lines in terms of Foxp3 messenger RNA (mRNA) expression, cytokine production, cell surface markers associated with regulatory T-cells (Treg), and in vitro immunoregulatory activity and compared the results with those of cells from 3 T-cell-type chronic lymphocytic leukemia (T-CLL) patients and normal CD4+ T-cells.

Real-time polymerase chain reaction analysis showed that cells from 10 ATL cases, 1 T-CLL case, and 1 ATL cell line had higher Foxp3 mRNA levels than CD4+ T-cells.

In 5 ATL cases, Foxp3 levels were comparable to those of CD4+CD25+ T-cells.

Flow cytometric analysis revealed that CTLA-4 expression correlated with Foxp3 mRNA level in ATL cells.

The cells of all ATL cases examined produced no interleukin 2 or interferon gamma after iono-mycin and phorbolmyristate acetate stimulation.

An in vitro inhibition assay showed that the proliferation of normal CD4+CD25- T-cells stimulated with anti-CD3 monoclonal antibody and autologous dendritic cells was significantly suppressed by coculture with Foxp3-high ATL cells.

These results indicate that Foxp3 expression is variable in ATL cases and that Foxp3-high ATL cells, which resemble Treg phenotypically as well as functionally, may be involved in immune suppression in ATL.

[MeSH-major] Gene Expression Regulation, Leukemic / immunology. Immune Tolerance. Leukemia-Lymphoma, Adult T-Cell / immunology

[MeSH-minor] Aged. Cell Line, Tumor. Coculture Techniques. Female. Humans. Male. Middle Aged. T-Lymphocytes, Regulatory / immunology

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(PMID = 16867905.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The identification of activating mutations in NOTCH1 in over 50% of T-cell acute lymphoblastic leukemias (T-ALL) has generated major interest in the elucidation of the mechanisms of transformation downstream of oncogenic NOTCH and in the targeting of the NOTCH signaling pathway in this disease.

Small molecule gamma-secretase inhibitors (GSIs) block NOTCH1 signaling in T-ALL lymphoblasts, yet the clinical development of GSIs has been held back by the development of gastrointestinal toxicity and their weak antileukemic effects against human T-ALL.

This review focuses on the molecular basis of NOTCH1-induced transformation, the mechanisms of action of oncogenic NOTCH1 and clinical significance of NOTCH1 mutations in T-ALL.

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(PMID = 20008221.001).

[ISSN] 1520-4383

[Journal-full-title] Hematology. American Society of Hematology. Education Program

[ISO-abbreviation] Hematology Am Soc Hematol Educ Program

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA129382-02; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01 CA129382-02

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases

[Number-of-references] 40

[Other-IDs] NLM/ NIHMS168983; NLM/ PMC2847371

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor.

NF-kappaB is constitutively activated in adult T-cell leukemia (ATL) and is considered responsible for cell growth and prevention of cell death.

In this study, we demonstrate that NF-kappaB is constitutively activated in various HTLV-1-infected T-cell lines and ATL-derived cell lines irrespectively of Tax expression as evidenced by the phosphorylation of IkappaBalpha and p65 subunit of NF-kappaB, activation of NF-kappaB DNA binding, and upregulation of various target genes including bcl-xL, bcl-2, XIAP, c-IAP1, survivin, cyclinD1, ICAM-1 and VCAM-1.

The effects of a novel IkappaB kinase (IKK) inhibitor, 2-amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-piperidin-4-yl nicotinonitrile (ACHP), were examined on cell growth of these cell lines and fresh ATL leukemic cells.

We found that ACHP could inhibit the phosphorylation of IkappaBalpha and p65, as well as NF-kappaB DNA-binding, associated with downregulation of the NF-kappaB target genes and induce cell growth arrest and apoptosis in these cells.

When Tax-active and Tax-inactive cell lines were compared, ACHP could preferentially inhibit cell growth of Tax-active cells.

Moreover, ACHP exhibited strong apoptosis-inducing activity in fresh ATL cells.

These findings indicate that ACHP and its derivatives are effective in inducing ATL cell death and thus feasible candidates for the treatment of ATL.

[MeSH-major] Enzyme Inhibitors / pharmacology. I-kappa B Kinase / antagonists & inhibitors. Leukemia-Lymphoma, Adult T-Cell / metabolism. Nicotinic Acids / pharmacology. Nitriles / pharmacology. T-Lymphocytes / drug effects

[MeSH-minor] Apoptosis / drug effects. Binding Sites. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA / metabolism. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Enzyme Activation / genetics. Enzyme Activation / physiology. Gene Expression Regulation, Enzymologic / drug effects. Human T-lymphotropic virus 1 / metabolism. Humans. In Vitro Techniques. Phosphorylation. Protein Subunits / antagonists & inhibitors. Protein Subunits / genetics. Protein Subunits / metabolism. Structure-Activity Relationship. Transcription Factor RelA / antagonists & inhibitors. Transcription Factor RelA / genetics. Transcription Factor RelA / metabolism

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(PMID = 16453001.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / 2-amino-6-(2-(cyclopropylmethoxy)-6-hydroxyphenyl)-4-piperidin-4-yl nicotinonitrile; 0 / Enzyme Inhibitors; 0 / Nicotinic Acids; 0 / Nitriles; 0 / Protein Subunits; 0 / Transcription Factor RelA; 9007-49-2 / DNA; EC 2.7.11.10 / I-kappa B Kinase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Soy-derived isoflavones inhibit the growth of adult T-cell leukemia cells in vitro and in vivo.

Adult T-cell leukemia occurs in human T-lymphotropic virus type I-infected individuals and is endemic to the south-western area of Kyushu in Japan.

In this communication, we examined the effect of soy isoflavones on the growth of adult T-cell leukemia cells in vitro and in vivo.

Among the isoflavones studied, genistein had the highest growth-inhibitory effect; however, genistein did not exert an apparent growth-inhibitory effect on Jurkat and Molt-4 cells, which were non-adult T-cell leukemia cells.

The in vivo studies demonstrated that soy-derived isoflavones significantly inhibit ED-40515 cell growth and infiltration into various organs in non-obese diabetic severe combined-immunodeficiency common gamma-chain knockout mice.

Taken together, it is evident that soy isoflavones might serve as a promising compound for the treatment of adult T-cell leukemia.

[MeSH-major] Isoflavones / pharmacology. Isoflavones / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Soybeans

[MeSH-minor] Animals. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Genistein / pharmacology. Humans. Jurkat Cells. Mice. Mice, Knockout. Mice, SCID. Transplantation, Heterologous

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(PMID = 17727682.001).

[ISSN] 1349-7006

[Journal-full-title] Cancer science

[ISO-abbreviation] Cancer Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Isoflavones; 6287WC5J2L / daidzein; 92M5F28TVF / glycitein; DH2M523P0H / Genistein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10.

Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL).

The overexpression of HOXA genes was associated with overexpression of its cofactor MEIS1 in CALM-AF10+ T-ALL, reaching levels of expression similar to those observed in MLL-t AL.

We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.

[MeSH-major] Homeodomain Proteins / biosynthesis. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis

[MeSH-minor] Adolescent. Adult. Cell Proliferation. Cell Transformation, Neoplastic. Child. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Polycomb Repressive Complex 1. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation

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(PMID = 16107895.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Recent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1.

We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1.

Cell lines derived from these tumors undergo G(0)/G(1) arrest and apoptosis when treated with a gamma-secretase inhibitor.

In addition, we found activating Notch1 mutations in 31% of thymic lymphomas that occur in mice deficient for various combinations of the H2AX, Tp53, and Rag2 genes.

Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations.

[MeSH-major] Disease Models, Animal. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma / genetics. Mutation / genetics. Receptor, Notch1 / genetics. Thymus Neoplasms / genetics

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(PMID = 16166587.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA096899

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / H2AX protein, mouse; 0 / Histones; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse

[Other-IDs] NLM/ PMC1895623