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1
adult t cell leukemia lymphomas 2005:2010[pubdate] *count=100
1009 results
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adult t cell leukemia lymphomas
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Items 1 to 100 of about 1009
1.
Kim YM, Ramírez JA, Mick JE, Giebler HA, Yan JP, Nyborg JK:
Molecular characterization of the Tax-containing HTLV-1 enhancer complex reveals a prominent role for CREB phosphorylation in Tax transactivation.
J Biol Chem
; 2007 Jun 29;282(26):18750-7
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[Title]
Molecular characterization of the Tax-containing
HTLV
-1 enhancer complex reveals a prominent role for CREB phosphorylation in Tax transactivation.
Transcriptional activation of
human
T-
cell leukemia
virus
type 1 (
HTLV
-1) is mediated by the viral oncoprotein Tax, which utilizes cellular transcriptional machinery to perform this function.
The coactivator CREB-binding protein (CBP)/p300 binds to this promoter-bound ternary complex, which promotes the initiation of
HTLV
-1 transcription.
Consonant with a fundamental role for CREB phosphorylation in Tax recruitment to the complex, we found that CREB is highly phosphorylated in a panel of
HTLV
-1-infected
human
T-
cell
lines.
Because pCREB has been implicated in leukemogenesis, enhancement of CREB phosphorylation by the
virus
may play a role in the etiology of
adult T
-
cell leukemia
.
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(PMID = 17449469.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA055035; United States / NCI NIH HHS / CA / CA55035; United States / NCI NIH HHS / CA / CA055035-14S1; United States / NCI NIH HHS / CA / CA055035-14; United States / NCI NIH HHS / CA / R01 CA055035-14S1; United States / NCI NIH HHS / CA / CA55035-S1; United States / NCI NIH HHS / CA / R01 CA055035-14
[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 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein
2.
Pais-Correia AM, Sachse M, Guadagnini S, Robbiati V, Lasserre R, Gessain A, Gout O, Alcover A, Thoulouze MI:
Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses.
Nat Med
; 2010 Jan;16(1):83-9
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[Title]
Biofilm-like extracellular viral assemblies mediate
HTLV
-1
cell
-to-
cell
transmission at virological synapses.
Human
T cell leukemia
virus
type 1 (
HTLV
-1) is
a lymphotropic
retrovirus whose
cell
-to-
cell
transmission requires
cell
contacts.
HTLV
-1-infected T lymphocytes form 'virological synapses', but the mechanism of
HTLV
-1 transmission remains poorly understood.
We show here that
HTLV
-1-infected T lymphocytes transiently store viral particles as carbohydrate-rich extracellular assemblies that are held together and attached to the
cell
surface by virally-induced extracellular matrix components, including collagen and agrin, and cellular linker proteins, such as tetherin and galectin-3.
Extracellular viral assemblies rapidly adhere to other cells upon
cell
contact, allowing
virus
spread and infection of target cells.
Their removal strongly reduces the ability of
HTLV
-1-producing cells to infect target cells.
Our findings unveil a novel
virus
transmission mechanism based on the generation of extracellular viral particle assemblies whose structure, composition and function resemble those of bacterial biofilms.
HTLV
-1 biofilm-like structures represent a major route for
virus
transmission from
cell
to
cell
.
[MeSH-major]
CD4-
Positive
T-Lymphocytes / virology. Extracellular Matrix / virology.
HTLV
-I Infections / transmission.
Human
T-
lymphotropic virus
1 / physiology
[MeSH-minor]
Biofilms. Concanavalin A. Gene Products, env / metabolism. Humans. Microscopy, Electron, Transmission.
Virus
Assembly / physiology.
Virus
Attachment.
Virus
Internalization
The Lens.
Cited by Patents in
.
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[CommentIn]
Nat Med. 2010 Jan;16(1):25-7
[
20057417.001
]
(PMID = 20023636.001).
[ISSN]
1546-170X
[Journal-full-title]
Nature medicine
[ISO-abbreviation]
Nat. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Gene Products, env; 11028-71-0 / Concanavalin A
3.
Yu Q, Minoda Y, Yoshida R, Yoshida H, Iha H, Kobayashi T, Yoshimura A, Takaesu G:
HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein.
Biochem Biophys Res Commun
; 2008 Jan 4;365(1):189-94
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[Title]
HTLV
-1 Tax-mediated TAK1 activation involves TAB2 adapter protein.
Human
T cell leukemia
virus
type 1 (
HTLV
-1) Tax is an oncoprotein that plays a crucial role in the proliferation and transformation of
HTLV
-1-infected T lymphocytes.
[MeSH-major]
Adaptor Proteins, Signal Transducing / metabolism. Gene Products, tax / metabolism.
Human
T-
lymphotropic virus
1 / metabolism. MAP Kinase Kinase Kinases / metabolism
[MeSH-minor]
Binding Sites.
Cell
Line. Humans. NF-kappa B / metabolism. Ubiquitin-Protein Ligases / metabolism
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(PMID = 17986383.001).
[ISSN]
1090-2104
[Journal-full-title]
Biochemical and biophysical research communications
[ISO-abbreviation]
Biochem. Biophys. Res. Commun.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / TAB2 protein, human; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP kinase kinase kinase 7; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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4.
Chetaille B:
[Mediastinal lymphomas: histopathology].
Rev Pneumol Clin
; 2010 Feb;66(1):28-31
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[Title]
[Mediastinal
lymphomas
: histopathology].
[Transliterated title]
Lymphomes
médiastinaux: anatomie pathologique.
Mediastinal
lymphomas
are mainly aggressive tumors affecting young patients.
Three main entities summarize this pathology: T lymphoblastic
lymphoma
, mediastinal (thymic) diffuse large B
cell
lymphoma
, and classical Hodgkin
lymphoma
.
Their
diagnosis
is usually performed on tissue collected by mediastinoscopy and requires the implementation of techniques such as classical histopathology, immunohistochemistry, and sometimes molecular biology.
[MeSH-major]
Hodgkin
Disease
/ pathology.
Lymphoma
, Non-Hodgkin / pathology. Mediastinal Neoplasms / pathology
[MeSH-minor]
Adolescent. Biomarkers, Tumor / analysis. Child. Humans.
Lymphoma
, Large B-
Cell
, Diffuse / pathology.
Lymphoma
, Large B-
Cell
, Diffuse / surgery. Mediastinum / pathology. Mediastinum / surgery. Neoplasm Invasiveness. Precursor T-
Cell
Lymphoblastic
Leukemia
-
Lymphoma
/
diagnosis
. Precursor T-
Cell
Lymphoblastic
Leukemia
-
Lymphoma
/ pathology. Prognosis.
Thymus
Neoplasms /
diagnosis
.
Thymus
Neoplasms / pathology. Young
Adult
MedlinePlus Health Information.
consumer health - Hodgkin Disease
.
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[Copyright]
Copyright (c) 2010. Published by Elsevier Masson SAS.
(PMID = 20207293.001).
[ISSN]
0761-8417
[Journal-full-title]
Revue de pneumologie clinique
[ISO-abbreviation]
Rev Pneumol Clin
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
2
5.
Maser RS, Choudhury B, Campbell PJ, Feng B, Wong KK, Protopopov A, O'Neil J, Gutierrez A, Ivanova E, Perna I, Lin E, Mani V, Jiang S, McNamara K, Zaghlul S, Edkins S, Stevens C, Brennan C, Martin ES, Wiedemeyer R, Kabbarah O, Nogueira C, Histen G, Aster J, Mansour M, Duke V, Foroni L, Fielding AK, Goldstone AH, Rowe JM, Wang YA, Look AT, Stratton MR, Chin L, Futreal PA, DePinho RA:
Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers.
Nature
; 2007 Jun 21;447(7147):966-71
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[Title]
Chromosomally unstable mouse tumours have genomic alterations similar to diverse
human
cancers.
Here we engineered
lymphoma
-prone mice with chromosomal instability to assess the usefulness of mouse models in cancer gene discovery and the extent of cross-species overlap in cancer-
associated
copy number aberrations.
Along with targeted
re
-sequencing, our comparative oncogenomic studies identified FBXW7 and PTEN to be commonly deleted both in murine
lymphomas
and in
human
T-
cell
acute
lymphoblastic
leukaemia
/
lymphoma
(T-ALL).
The murine cancers acquire widespread recurrent amplifications and deletions targeting loci syntenic to those not only in
human
T-ALL but also in diverse
human
haematopoietic, mesenchymal and epithelial tumours.
These results indicate that murine and
human
tumours experience common biological processes driven by orthologous genetic events in their malignant evolution.
The highly concordant nature of genomic events encourages the use of genomically unstable murine cancer models in the discovery of biological driver events in the
human
oncogenome.
[MeSH-major]
Chromosomal Instability / genetics. Chromosome Aberrations. Conserved Sequence / genetics.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ genetics.
Lymphoma
, T-
Cell
/ genetics
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
SciCrunch.
OMIM: Data: Gene Annotation
.
The Lens.
Cited by Patents in
.
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(PMID = 17515920.001).
[ISSN]
1476-4687
[Journal-full-title]
Nature
[ISO-abbreviation]
Nature
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE7615
[Grant]
United Kingdom / Wellcome Trust / / 077012; United Kingdom / Wellcome Trust / / 088340; United Kingdom / Medical Research Council / / G0500389; United Kingdom / Wellcome Trust / /
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 3.1.3.67 / PTEN Phosphohydrolase
[Other-IDs]
NLM/ PMC2714968; NLM/ UKMS27310
6.
Gjerdrum LM, Woetmann A, Odum N, Burton CM, Rossen K, Skovgaard GL, Ryder LP, Ralfkiaer E:
FOXP3+ regulatory T cells in cutaneous T-cell lymphomas: association with disease stage and survival.
Leukemia
; 2007 Dec;21(12):2512-8
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[Title]
FOXP3+ regulatory T cells in cutaneous T-
cell lymphomas
: association with
disease
stage and survival.
In solid tumours, high numbers of Tregs are
associated
with a poor prognosis.
In this study, skin biopsies from 86 patients with mycosis fungoides (MF) and cutaneous T-
cell
lymphoma
(CTCL) unspecified were analysed for the expression of FOXP3 on tumour cells and tumour-infiltrating Tregs.
In the remaining 85 cases, the atypical neoplastic infiltrate was either FOXP3 negative (n=80) or contained only very occasional weakly
positive
cells (n=5).
MF with early or infiltrated plaques had significantly higher numbers of FOXP3+ Tregs than CTCL unspecified or advanced MF with tumours or transformation to large
cell
lymphoma
.
An analysis of all patients demonstrated that increasing numbers of FOXP3+ Tregs were
associated
with improved survival in both MF and CTCL unspecified.
In conclusion, our data indicate that the presence of FOXP3+ Tregs in CTCL is
associated
with
disease
stage and patient survival.
[MeSH-major]
Forkhead Transcription Factors / analysis. Lymphocytes, Tumor-Infiltrating / immunology.
Lymphoma
, T-
Cell
, Cutaneous / pathology. Mycosis Fungoides / pathology. Skin Neoplasms / pathology. T-Lymphocytes, Regulatory / immunology
[MeSH-minor]
Adult
. Aged. Aged, 80 and over.
Cell
Line, Tumor. Female. Humans. Jurkat Cells / chemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Prognosis. Proportional Hazards Models. Recombinant Fusion Proteins / analysis. Survival Analysis
Genetic Alliance.
consumer health - Cutaneous T-Cell Lymphoma
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
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Cited by Patents in
.
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(PMID = 17713545.001).
[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 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Recombinant Fusion Proteins
7.
Ohsugi T, Kumasaka T, Okada S, Ishida T, Yamaguchi K, Horie R, Watanabe T, Umezawa K:
Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines.
Cancer Lett
; 2007 Nov 18;257(2):206-15
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[Title]
Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient
adult T
-
cell leukemia
-
derived
cell
lines.
Adult T
-
cell leukemia
(
ATL
) is an aggressive neoplasm caused by
human
T-
cell leukemia
virus
type I (
HTLV
-I), which induces nuclear factor-kappaB (NF-kappaB), a molecule central to the ensuing neoplasia.
The NF-kappaB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) has been shown to inhibit NF-kappaB activation in Tax-expressing
HTLV
-I-infected cells.
In this study, we used NOD/SCID beta2-microglobulin(null) mice to show that intraperitoneal inoculation with Tax-deficient
ATL
cell
lines caused rapid death, whereas DHMEQ-treated mice survived.
Furthermore, DHMEQ treatment after subcutaneous inoculation inhibited the growth of transplanted
ATL
cells.
These results demonstrate that DHMEQ has therapeutic efficacy on
ATL
cells, regardless of Tax expression.
[MeSH-major]
Benzamides / pharmacology. Cyclohexanones / pharmacology. Gene Products, tax / deficiency.
Leukemia
, T-
Cell
/ prevention & control. Xenograft Model Antitumor Assays / methods
[MeSH-minor]
Adult
. Animals. Apoptosis / drug effects.
Cell
Line, Tumor.
Human
T-
lymphotropic virus
1 / genetics.
Human
T-
lymphotropic virus
1 / metabolism. Humans. Mice. Mice, Inbred NOD. Mice, Knockout. Mice, SCID. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Tumor Burden. beta 2-Microglobulin / genetics. beta 2-Microglobulin / metabolism
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(PMID = 17764832.001).
[ISSN]
0304-3835
[Journal-full-title]
Cancer letters
[ISO-abbreviation]
Cancer Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Benzamides; 0 / Cyclohexanones; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 0 / dehydroxymethylepoxyquinomicin
8.
Toulza F, Nosaka K, Tanaka Y, Schioppa T, Balkwill F, Taylor GP, Bangham CR:
Human T-lymphotropic virus type 1-induced CC chemokine ligand 22 maintains a high frequency of functional FoxP3+ regulatory T cells.
J Immunol
; 2010 Jul 01;185(1):183-9
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[Title]
Human
T-
lymphotropic virus
type 1-induced CC chemokine ligand 22 maintains a high frequency of functional FoxP3+ regulatory T cells.
We recently reported that
human
T-
lymphotropic virus
type 1 (
HTLV
-1) infection is accompanied by a high frequency of CD4(+)FoxP3(+) cells in the circulation.
In asymptomatic carriers of
HTLV
-1 and in patients with
HTLV
-1-
associated
inflammatory and malignant diseases, a high FoxP3(+)
cell
frequency correlated with inefficient cytotoxic
T cell
-mediated killing of
HTLV
-1-infected cells.
In
adult T cell leukemia
/
lymphoma
(
ATLL
), the FoxP3(+) population was distinct from the leukemic
T cell
clones.
However, the cause of the increase in FoxP3(+)
cell
frequency in
HTLV
-1 infection was unknown.
In this study, we report that the plasma concentration of the chemokine CCL22 is abnormally high in
HTLV
-1-infected subjects and that the concentration is strongly correlated with the frequency of FoxP3(+) cells, which express the CCL22 receptor CCR4.
Further, we show that CCL22 is produced by cells that express the
HTLV
-1 transactivator protein Tax, and that the increased CCL22 enhances the migration and survival of FoxP3(+) cells in vitro.
Finally, we show that FoxP3(+) cells inhibit the proliferation of ex vivo, autologous leukemic clones from patients with
ATLL
.
We conclude that
HTLV
-1-induced CCL22 causes the high frequency of FoxP3(+) cells observed in
HTLV
-1 infection; these FoxP3(+) cells may both retard the progression of
ATLL
and
HTLV
-1-
associated
inflammatory diseases and contribute to the immune suppression seen in
HTLV
-1 infection, especially in
ATLL
.
[MeSH-major]
Cell
Proliferation. Chemokine CCL22 / physiology. Forkhead Transcription Factors / physiology.
Human
T-
lymphotropic virus
1 / immunology. T-Lymphocytes, Regulatory / cytology. T-Lymphocytes, Regulatory / immunology
[MeSH-minor]
CD4 Lymphocyte Count.
Cell
Survival / immunology. Cytotoxicity Tests, Immunologic.
HTLV
-I Infections / immunology.
HTLV
-I Infections / pathology. Humans. Jurkat Cells.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ immunology.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ pathology. T-Lymphocytes, Cytotoxic / cytology. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / virology
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Blood. 2001 Aug 1;98(3):721-6
[
11468172.001
]
(PMID = 20525891.001).
[ISSN]
1550-6606
[Journal-full-title]
Journal of immunology (Baltimore, Md. : 1950)
[ISO-abbreviation]
J. Immunol.
[Language]
eng
[Grant]
United Kingdom / Wellcome Trust / / 080871; United Kingdom / Medical Research Council / / G0501974; United Kingdom / Wellcome Trust / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / CCL22 protein, human; 0 / Chemokine CCL22; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
[Other-IDs]
NLM/ EMS51736; NLM/ PMC3575032
9.
Park BB, Kim WS, Lee J, Park KW, Kang JH, Lee SH, Park JO, Kim K, Jung CW, Park YS, Im YH, Kang WK, Ko YH, Lee MH, Park K:
IMVP-16/Pd followed by high-dose chemotherapy and autologous stem cell transplantation as a salvage therapy for refractory or relapsed peripheral T-cell lymphomas.
Leuk Lymphoma
; 2005 Dec;46(12):1743-8
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[Title]
IMVP-16/Pd followed by high-dose chemotherapy and autologous stem
cell
transplantation as a salvage therapy for refractory or relapsed peripheral T-
cell lymphomas
.
The present study aimed to analyse the treatment outcome of IMVP-16/Pd (ifosfamide, methotrexate, etoposide and prednisone) followed by high-dose chemotherapy and autologous stem
cell
transplantation (HDC/ASCT) for patients with peripheral T-
cell lymphomas
(PTCLs) who were previously treated with CHOP.
Considering histopathologic subtypes, 3 of 4 relapsed natural killer (NK)/T-
cell
lymphoma
patients (75%) achieved CR, but only 1 of 6 in non-NK/T-
cell
lymphoma
patients (16.7%) achieved CR (P = 0.19).
These results indicate that IMVP-16/Pd followed by HDC/ASCT appears to be an effective salvage regimen, especially for NK/T-
cell
lymphoma
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Lymphoma
, T-
Cell
/ therapy. Salvage Therapy. Stem
Cell
Transplantation
[MeSH-minor]
Adolescent.
Adult
. Aged. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Ifosfamide / administration & dosage. Male. Methotrexate / administration & dosage. Middle Aged. Neoplasm Staging. Prednisone / administration & dosage. Recurrence. Retrospective Studies. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage
Genetic Alliance.
consumer health - Transplantation
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
IFOSFAMIDE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
Hazardous Substances Data Bank.
METHOTREXATE
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 16263576.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; UM20QQM95Y / Ifosfamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; CHOP protocol; IMVP-16 protocol
10.
Saito M, Mori A, Irie T, Tanaka M, Morioka M, Uchiyama Y, Taukamoto E:
[Picture in clinical hematology no. 41: PET/ CT findings in case of ATLL ].
Rinsho Ketsueki
; 2009 Dec;50(12):1669-70
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[Title]
[Picture in
clinical
hematology no. 41: PET/ CT findings in case of
ATLL
].
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ radiography.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ radionuclide imaging. Positron-Emission Tomography. Tomography, X-Ray Computed
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(PMID = 20068272.001).
[ISSN]
0485-1439
[Journal-full-title]
[Rinshō ketsueki] The Japanese journal of clinical hematology
[ISO-abbreviation]
Rinsho Ketsueki
[Language]
jpn
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
11.
Shiratori S, Yasumoto A, Tanaka J, Shigematsu A, Yamamoto S, Nishio M, Hashino S, Morita R, Takahata M, Onozawa M, Kahata K, Kondo T, Ota S, Wakasa K, Sugita J, Koike T, Asaka M, Kasai M, Imamura M:
A retrospective analysis of allogeneic hematopoietic stem cell transplantation for adult T cell leukemia/lymphoma (ATL): clinical impact of graft-versus-leukemia/lymphoma effect.
Biol Blood Marrow Transplant
; 2008 Jul;14(7):817-23
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[Title]
A retrospective analysis of allogeneic hematopoietic stem
cell
transplantation for
adult T cell leukemia
/
lymphoma
(
ATL
):
clinical
impact of graft-versus-
leukemia
/
lymphoma
effect.
Adult T cell leukemia
/
lymphoma
(
ATL
) is a highly aggressive
T cell
malignancy, and has a poor prognosis.
Recently, allogeneic-hematopoietic stem
cell
transplantation (allo-HSCT) has been suggested to improve the outcome.
We retrospectively analyzed 15 patients with
ATL
who had received allo-HSCT in 2 institutions in Hokkaido, Japan.
Calcineurin inhibitor dosage was reduced and administration was discontinued abruptly in 6 of the 15 patients for
disease
control; as a result, 4 (66.7%) of the 6 patients achieved complete response (CR) or partial response.
Therefore, a graft-versus-
leukemia
/
lymphoma
(GVL) effect might be induced by discontinuation of immunosuppression.
Thirteen of the 15 patients were followed up by monitoring
HTLV
-1 proviral DNA levels.
In 10 of the 11 patients with
positive HTLV
-1 proviral DNA before allo-HSCT,
HTLV
-1 proviral DNA became undetectable at least once after allo-HSCT, and only 1 of the 5 patients in whom
HTLV
-1 proviral DNA became detectable after allo-HSCT relapsed.
Compared to the results of past studies, these results show that allo-HSCT greatly improved the prognosis of
ATL
and suggest a contribution of the induction of a GVL effect.
[MeSH-major]
Graft vs
Leukemia
Effect. Hematopoietic Stem
Cell
Transplantation / methods.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ therapy
[MeSH-minor]
Adult
. Aged.
Disease
-Free Survival. Female. Follow-Up Studies.
HTLV
-I Infections / blood.
HTLV
-I Infections / therapy. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Retrospective Studies. Transplantation, Homologous. Viral Load
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.
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.
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[ErratumIn]
Biol Blood Marrow Transplant. 2008 Sep;14(9):1079
(PMID = 18541202.001).
[ISSN]
1523-6536
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
12.
Uphoff CC, Denkmann SA, Steube KG, Drexler HG:
Detection of EBV, HBV, HCV, HIV-1, HTLV-I and -II, and SMRV in human and other primate cell lines.
J Biomed Biotechnol
; 2010;2010:904767
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[Title]
Detection of EBV, HBV, HCV, HIV-1,
HTLV
-I and -II, and SMRV in
human
and other primate
cell
lines.
The high prevalence of contaminated
cell
cultures suggests that viral contaminations might be distributed among cultures.
We investigated more than 460 primate
cell
lines for Epstein-Barr (EBV), hepatitis B (HBV), hepatitis C (HCV),
human
immunodeficiency
virus
type 1 (HIV-1),
human
T-
cell leukemia
/
lymphoma virus
I and II (
HTLV
-I/-II), and squirrel monkey retrovirus (SMRV) infections for risk assessment.
None of the
cell
lines were infected with HCV, HIV-1, or
HTLV
-I/-II.
However, one
cell
line displayed reverse transcriptase activity.
Thirty-nine
cell
lines harbored EBV DNA sequences.
Studies on the lytic phase of EBV revealed that five
cell
lines produce EBV particles and six further
cell
lines produced EBV upon stimulation.
One
cell
line contained an integrated HBV genome fragment but showed
no virus
production.
Six
cell
lines were SMRV-infected.
Newly established
cell
lines should be tested for EBV infections to detect B-lymphoblastoid
cell
lines (B-LCL).
B-LCLs established with EBV from
cell
line B95-8 should be tested for SMRV infections.
[MeSH-major]
Primates / virology.
Viruses
/ genetics.
Viruses
/ isolation & purification
[MeSH-minor]
Animals. Blotting, Southern.
Cell
Line. DNA, Circular / analysis. HIV-1 / genetics. HIV-1 / isolation & purification. Hepacivirus / genetics. Hepacivirus / isolation & purification. Hepatitis B
virus
/ genetics. Hepatitis B
virus
/ isolation & purification. Herpesvirus 4,
Human
/ genetics. Herpesvirus 4,
Human
/ isolation & purification.
Human
T-
lymphotropic virus
1 / genetics.
Human
T-
lymphotropic virus
1 / isolation & purification.
Human
T-
lymphotropic virus
2 / genetics.
Human
T-
lymphotropic virus
2 / isolation & purification. Humans. In Situ Hybridization, Fluorescence. Polymerase Chain Reaction. Retroviruses, Simian / genetics. Retroviruses, Simian / isolation & purification. Saimiri / virology. Viral Proteins / analysis
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culture/stock collections - Cell lines described in this publication
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(PMID = 20454443.001).
[ISSN]
1110-7251
[Journal-full-title]
Journal of biomedicine & biotechnology
[ISO-abbreviation]
J. Biomed. Biotechnol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Circular; 0 / Viral Proteins
[Other-IDs]
NLM/ PMC2861168
13.
Okudaira T, Hirashima M, Ishikawa C, Makishi S, Tomita M, Matsuda T, Kawakami H, Taira N, Ohshiro K, Masuda M, Takasu N, Mori N:
A modified version of galectin-9 suppresses cell growth and induces apoptosis of human T-cell leukemia virus type I-infected T-cell lines.
Int J Cancer
; 2007 May 15;120(10):2251-61
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[Title]
A modified version of galectin-9 suppresses
cell
growth and induces apoptosis of
human
T-
cell leukemia
virus
type I-infected T-
cell
lines.
ATL
is a fatal malignancy of T lymphocytes caused by
HTLV
-I infection and remains incurable.
Galectins are a family of animal lectins that function both extracellularly (by interacting with
cell
surface and extracellular matrix glycoproteins and glycolipids) and intracellularly (by interacting with cytoplasmic and nuclear proteins) to modulate signaling pathways.
We found that protease-resistant galectin-9 by modification of its linker peptide, hG9NC(null), prevented
cell
growth of
HTLV
-I-infected T-
cell
lines and primary
ATL
cells.
The suppression of
cell
growth was inhibited by lactose, but not by sucrose, indicating that beta-galactoside binding is essential for hG9NC(null)-induced
cell
growth suppression. hG9NC(null) induced
cell
cycle arrest by reducing the expression of cyclin D1, cyclin D2, cyclin B1, Cdk1, Cdk4, Cdk6, Cdc25C and c-Myc, and apoptosis by reducing the expression of XIAP, c-IAP2 and survivin.
Most of these genes are regulated by NF-kappaB, which plays a critical role in oncogenesis by
HTLV
-I. hG9NC(null) suppressed IkappaBalpha phosphorylation, resulting in suppression of NF-kappaB.
Most importantly, treatment with hG9NC(null) (6.7 mg/kg injected intraperitoneally every day) reduced tumor formation from an
HTLV
-I-infected T-
cell
line when these cells were inoculated subcutaneously into SCID mice.
Our results suggest that hG9NC(null) could be a suitable agent for the management of
ATL
.
[MeSH-major]
Apoptosis / drug effects. Galectins / pharmacology.
HTLV
-I Infections / drug therapy.
Human
T-
lymphotropic virus
1 / growth & development.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ therapy. T-Lymphocytes / pathology. T-Lymphocytes / virology
[MeSH-minor]
Animals. Caspases / metabolism.
Cell
Cycle / drug effects.
Cell
Cycle / physiology.
Cell
Line, Tumor. Female. Galactosides / metabolism. Growth Inhibitors / pharmacology. Humans. Membrane Proteins. Mice. Mice, SCID. NF-kappa B / genetics. NF-kappa B / immunology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors,
Virus
/ biosynthesis. beta-Galactosidase / metabolism
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
[RetractionIn]
Int J Cancer. 2011 Dec 1;129(11):2762-3
[
21960263.001
]
(PMID = 17278100.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
[Publication-country]
United States
[Chemical-registry-number]
0 / Galactosides; 0 / Galectins; 0 / Growth Inhibitors; 0 / HAVCR2 protein, human; 0 / LGALS8 protein, human; 0 / LGALS9 protein, human; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Receptors, Virus; 0 / beta-galactoside; EC 3.2.1.23 / beta-Galactosidase; EC 3.4.22.- / Caspases
14.
Peloponese JM, Yeung ML, Jeang KT:
Modulation of nuclear factor-kappaB by human T cell leukemia virus type 1 Tax protein: implications for oncogenesis and inflammation.
Immunol Res
; 2006;34(1):1-12
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[Title]
Modulation of nuclear factor-kappaB by
human
T cell leukemia
virus
type 1 Tax protein: implications for oncogenesis and inflammation.
Human
T cell leukemia
virus
type 1 (
HTLV
-1) is the causative agent of a fatal malignancy known as
adult T cell leukemia
(
ATL
) and an inflammatory
disease
named tropical spastic paraparesis/
HTLV
-
1 associated
myelopathy (TSP/HAM).
HTLV
-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses.
[MeSH-major]
Cell
Transformation, Neoplastic / immunology. Gene Products, tax / immunology.
HTLV
-I Infections / immunology.
Human
T-
lymphotropic virus
1 / immunology. Inflammation / immunology. NF-kappa B / immunology
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 16720895.001).
[ISSN]
0257-277X
[Journal-full-title]
Immunologic research
[ISO-abbreviation]
Immunol. Res.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Gene Products, tax; 0 / NF-kappa B
[Number-of-references]
102
15.
Sargent JT, Smith OP:
Haematological emergencies managing hypercalcaemia in adults and children with haematological disorders.
Br J Haematol
; 2010 May;149(4):465-77
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Hypercalcaemia is a common metabolic complication of malignant
disease
often requiring emergency intervention.
Although it is more frequently
associated
with solid tumours, malignancy-
associated
hypercalcaemia (MAH) is seen in a significant number of patients with blood diseases.
Its association with myeloma and
adult T
-
cell
leukaemia
/
lymphoma
is well recognized but the incidence of hypercalcaemia in other haematological neoplasms, affecting adults and children, is less clearly defined.
Haematologists need to be familiar with the
clinical
manifestations of, the differential
diagnosis
to be considered and the most effective management strategies that are currently available for MAH.
[MeSH-minor]
Adult
. Bone Density Conservation Agents / therapeutic use. Child. Diphosphonates / therapeutic use. Fluid Therapy / methods. Humans
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(PMID = 20377591.001).
[ISSN]
1365-2141
[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 / Bone Density Conservation Agents; 0 / Diphosphonates
[Number-of-references]
96
16.
Miyano-Kurosaki N, Kira J, Barnor JS, Maeda N, Misawa N, Kawano Y, Tanaka Y, Yamamoto N, Koyanagi Y:
Autonomous proliferation of HTLV-CD4+ T cell clones derived from human T cell leukemia virus type I (HTLV-I)-associated myelopathy patients.
Microbiol Immunol
; 2007;51(2):235-42
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[Title]
Autonomous proliferation of
HTLV
-CD4+
T cell
clones
derived
from
human
T cell leukemia
virus
type I (
HTLV
-I)-
associated
myelopathy patients.
That
HTLV
-I infects CD4(+) T cells and enhances their
cell
growth has been shown as successful long-term in vitro proliferation in the presence of IL-2.
It is known that T cells isolated from HAM patients possess strong ability for
cell
proliferation in vitro and mRNA of various cytokines are abundantly expressed in CNS tissues of HAM patients.
In this study, we examined the relationship between
cell
proliferation and ability of in vitro cytokine production of CD4(+)
T cell
clones isolated from HAM patients.
We started a culture from a single
cell
to isolate
cell
clones immediately after drawing blood from the patients using limiting dilution method, which could allow the
cell
to avoid in vitro
HTLV
-I infection after initiation of culture.
Many
cell
clones were obtained and the rate of proliferation efficiency from a single
cell
was as high as 80%, especially in the 4 weeks' culture cells from HAM patients.
Our results indicate that the ability of
cell
proliferation in HAM patients is not restricted in
HTLV
-I-infected T cells.
HTLV
-Iuninfected CD4(+) T cells, mainly Th0 cells, also have a strong ability to respond to IL-2-stimulation, showing that unusual immune activation on T cells has been observed in HAM patients.
[MeSH-major]
CD4-
Positive
T-Lymphocytes / immunology. CD4-
Positive
T-Lymphocytes / virology.
Human
T-
lymphotropic virus
1 / immunology. Paraparesis, Tropical Spastic / immunology
[MeSH-minor]
Adult
. Aged. Clone Cells. Cytokines / genetics. Cytokines / immunology. DNA, Viral / chemistry. DNA, Viral / genetics. Female. Humans. Lymphocyte Activation. Male. Middle Aged. Polymerase Chain Reaction. Receptors, Antigen, T-
Cell
/ immunology
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(PMID = 17310092.001).
[ISSN]
0385-5600
[Journal-full-title]
Microbiology and immunology
[ISO-abbreviation]
Microbiol. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Cytokines; 0 / DNA, Viral; 0 / Receptors, Antigen, T-Cell
17.
Tanaka Y, Nakasone H, Yamazaki R, Sato K, Sato M, Terasako K, Kimura S, Okuda S, Kako S, Oshima K, Tanihara A, Nishida J, Yoshikawa T, Nakatsura T, Sugiyama H, Kanda Y:
Single-cell analysis of T-cell receptor repertoire of HTLV-1 Tax-specific cytotoxic T cells in allogeneic transplant recipients with adult T-cell leukemia/lymphoma.
Cancer Res
; 2010 Aug 1;70(15):6181-92
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[Title]
Single-
cell
analysis of T-
cell
receptor repertoire of
HTLV
-1 Tax-specific cytotoxic T cells in allogeneic transplant recipients with
adult T
-
cell leukemia
/
lymphoma
.
Adult T
-
cell leukemia
(
ATL
) is a lymphoproliferative malignancy
associated
with
human
T-
cell
lymphotropic virus
type 1 (
HTLV
-1) infection.
Recently, it has been shown that allogeneic hematopoietic stem
cell
transplantation (allo-HSCT) is an effective treatment for
ATL
, and that
HTLV
-1 Tax-specific CD8(+) cytotoxic T cells (CTL) contribute to the graft-versus-
ATL
effect.
In the present study, we, for the first time, analyzed the T-
cell
receptor (TCR) repertoire of isolated Tax(301-309) (SFHSLHLLF)-specific CTLs in HLA-A*2402(+)
ATL
patients before and after allo-HSCT by single-
cell
reverse transcription-PCR.
In addition, a unique conserved amino acid motif of "P-D/P-R" in TCR-beta complementarity-determining region 3 in either BV7- or BV18-expressing CTLs was observed not only in all of the samples from
ATL
patients, but also in samples from the same patient before and after HSCT.
Furthermore, the P-D/P-R motif-bearing CTL clones established from peripheral blood samples after HSCT exhibited strong killing activity against the
HTLV
-1-infected T cells of the patient.
Hence, Tax(301-309)-specific CTLs in
ATL
patients might have a preference for TCR construction and induce strong immune responses against the
HTLV
-1-infected T cells of patients, which contribute to the graft-versus-
ATL
effects after allo-HSCT.
[MeSH-major]
Gene Products, tax / immunology. Hematopoietic Stem
Cell
Transplantation.
Human
T-
lymphotropic virus
1 / immunology.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ immunology. T-Lymphocytes, Cytotoxic / immunology
[MeSH-minor]
Amino Acid Motifs. HLA-A Antigens / immunology. HLA-A24 Antigen. Humans. Peptide Fragments / immunology. Receptors, Antigen, T-
Cell
/ immunology. Receptors, Antigen, T-
Cell
, alpha-beta / immunology
Immune Epitope Database and Analysis Resource.
gene/protein/disease-specific - Related Immune Epitope Information
.
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.
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(PMID = 20647322.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Gene Products, tax; 0 / HLA-A Antigens; 0 / HLA-A*24:02 antigen; 0 / HLA-A24 Antigen; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / tax protein, Human T-lymphotrophic virus 1
18.
Kobayashi H, Ngato T, Sato K, Aoki N, Kimura S, Tanaka Y, Aizawa H, Tateno M, Celis E:
In vitro peptide immunization of target tax protein human T-cell leukemia virus type 1-specific CD4+ helper T lymphocytes.
Clin Cancer Res
; 2006 Jun 15;12(12):3814-22
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[Title]
In vitro peptide immunization of target tax protein
human
T-
cell leukemia
virus
type 1-specific CD4+ helper T lymphocytes.
PURPOSE:
Adult T
-
cell leukemia
/
lymphoma
induced by
human
T-
cell leukemia
virus
type 1 (
HTLV
-1) is usually a fatal lymphoproliferative malignant
disease
.
HTLV
-1 Tax protein plays a critical role in
HTLV
-1-
associated
leukemogenesis and is an attractive target for vaccine development.
Although
HTLV
-1 Tax is the most dominant antigen for
HTLV
-1-specific CD8(+) CTLs in
HTLV
-1-infected individuals, few epitopes recognized by CD4(+) helper T lymphocytes in
HTLV
-1 Tax protein have been described.
The aim of the present study was to study T-helper-
cell
responses to
HTLV
-1 Tax and to identify naturally processed MHC class II-restricted epitopes that could be used for vaccine development.
EXPERIMENTAL DESIGN: An MHC class II binding peptide algorithm was used to predict potential T-helper
cell
epitope peptides from
HTLV
-1 Tax.
We assessed the ability of the corresponding peptides to elicit helper T-
cell
responses by in vitro vaccination of purified CD4(+) T lymphocytes.
RESULTS: Peptides Tax(191-205) and Tax(305-319) were effective in inducing T-helper-
cell
responses.
Both these epitopes were found to be naturally processed by
HTLV
-1(+) T-
cell
lymphoma
cells and by autologous antigen-presenting cells that were pulsed with
HTLV
-1 Tax(+) tumor lysates.
Notably, the two newly identified helper T-
cell
epitopes are found to lie proximal to known CTL epitopes, which will facilitate the development of prophylactic peptide-based vaccine capable of inducing simultaneous CTL and T-helper responses.
CONCLUSION: Our data suggest that
HTLV
-1 Tax protein could serve as tumor-
associated
antigen for CD4(+) helper T cells and that the present epitopes might be used for T-
cell
-based immunotherapy against tumors expressing
HTLV
-1.
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.
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(PMID = 16778109.001).
[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 CA103921; United States / NCI NIH HHS / CA / R01CA80782; United States / NCI NIH HHS / CA / R01CA103921; United States / NCI NIH HHS / CA / R01 CA080782; United States / NCI NIH HHS / CA / P50CA91956; United States / NCI NIH HHS / CA / P50 CA091956
[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 / Gene Products, tax; 0 / HLA-D Antigens; 0 / Peptides
[Other-IDs]
NLM/ NIHMS14245; NLM/ PMC1986724
19.
Larousserie F, Bardel E, Pflanz S, Arnulf B, Lome-Maldonado C, Hermine O, Brégeaud L, Perennec M, Brousse N, Kastelein R, Devergne O:
Analysis of interleukin-27 (EBI3/p28) expression in Epstein-Barr virus- and human T-cell leukemia virus type 1-associated lymphomas: heterogeneous expression of EBI3 subunit by tumoral cells.
Am J Pathol
; 2005 Apr;166(4):1217-28
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[Title]
Analysis of interleukin-27 (EBI3/p28) expression in Epstein-Barr
virus
- and
human
T-
cell leukemia
virus
type 1-
associated
lymphomas
: heterogeneous expression of EBI3 subunit by tumoral cells.
Interleukin (IL)-27 is a novel heterodimeric cytokine of the IL-12 family that is composed of two subunits, Epstein-Barr
virus
(EBV)-induced gene 3 (EBI3) and p28.
EBI3 is expressed at high levels in EBV-transformed B-
cell
lines and is induced in vitro by the EBV oncogene LMP1 in a nuclear factor (NF)-kappaB-dependent manner.
We show here that EBI3 expression is up-regulated in
human
T-
cell leukemia
virus
type 1 (
HTLV
-1)-infected
cell
lines and IL-2-dependent leukemic cells from
adult T
-
cell leukemia
/
lymphoma
(
ATL
) patients, compared to normal activated T cells.
EBI3 expression was decreased in
HTLV
-1-transformed cells after treatment with the NF-kappaB inhibitor BAY11-7082 and was induced in Jurkat cells by expression of
HTLV
-1 wild-type Tax oncoprotein, but not by the Tax mutant M22, which is defective for NF-kappaB activation.
In situ analysis of EBI3 and p28 expression in Hodgkin's
lymphomas
(HLs), in various EBV-
associated
lymphoproliferative disorders (LPDs) (including post-transplant LPDs and nasal-type NK/T-
cell lymphomas
), and in
ATL
showed that EBI3 was expressed by neoplastic cells in all cases of HL and of LMP1-
positive
EBV-
associated
LPD, at variable levels in
ATL
cases, but rarely in control T-
cell lymphomas
.
In contrast, in all
lymphomas
tested, no or few tumoral cells expressed p28.
Consistent with these data, no significant p28 or IL-27 expression was detected in HL-
derived
cell
lines, or in EBV- or
HTLV
-1-transformed
cell
lines.
[MeSH-major]
Epstein-Barr
Virus
Infections / metabolism. Interleukins / biosynthesis.
Lymphoma
/ virology. Tumor
Virus
Infections / metabolism
[MeSH-minor]
Blotting, Western. Deltaretrovirus / metabolism. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Herpesvirus 4,
Human
/ metabolism. Humans. Immunohistochemistry. In Situ Hybridization. Jurkat Cells. NF-kappa B / metabolism
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(PMID = 15793300.001).
[ISSN]
0002-9440
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / C19orf10 protein, human; 0 / IL27 protein, human; 0 / Interleukins; 0 / NF-kappa B
[Other-IDs]
NLM/ PMC1602381
20.
Tözsér J, Weber IT:
The protease of human T-cell leukemia virus type-1 is a potential therapeutic target.
Curr Pharm Des
; 2007;13(12):1285-94
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[Title]
The protease of
human
T-
cell leukemia
virus
type-1 is a potential therapeutic target.
Human
T-
cell leukemia
virus
type-1 (
HTLV
-1) is
associated
with a number of
human
diseases.
Although the mechanism by which the
virus
causes diseases is still not known, studies indicate that viral replication is critical for the development of
HTLV
-
1 associated
myelopathy, and initial studies suggested that blocking replication with reverse transcriptase inhibitors had a therapeutic effect.
Therefore, based on the success of HIV-1 protease inhibitors, the
HTLV
-1 protease is also a potential target for chemotherapy.
Furthermore, mutated residues in HIV-1 protease that confer drug resistance are frequently seen in equivalent positions of other retroviral proteases, like
HTLV
-1 protease.
Therefore, comparison of
HTLV
-1 and HIV-1 proteases is expected to aid the rational design of broad spectrum inhibitors effective against various retroviral proteases, including the mutant HIV-1 enzymes appearing in drug resistance.
This review describes the characteristics of
HTLV
-1 protease, makes comparison with HIV-1 protease, and discusses the status of inhibitor development for the
HTLV
-1 protease.
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(PMID = 17504236.001).
[ISSN]
1873-4286
[Journal-full-title]
Current pharmaceutical design
[ISO-abbreviation]
Curr. Pharm. Des.
[Language]
ENG
[Grant]
United States / NIGMS NIH HHS / GM / R01 GM062920; United States / NIGMS NIH HHS / GM / GM 062920; United States / FIC NIH HHS / TW / TW01001
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Protease Inhibitors; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / HTLV-1 protease
[Number-of-references]
45
21.
Yang J, Zhang F, Fang H, Ye Z, Lin S, Han A:
Clinicopathologic features of primary lymphoma in soft tissue.
Leuk Lymphoma
; 2010 Nov;51(11):2039-46
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[Title]
Clinicopathologic features of primary
lymphoma
in soft tissue.
By reviewing 3725
lymphomas
diagnosed in our institution from 1999 to 2010, we found eight cases (0.21%) of primary
lymphoma
in soft tissue with comprehensive histologic and immunohistochemical studies.
Of the eight cases of primary
lymphoma
in soft tissue, two patients were male and six were female.
Six cases were diffuse large B-
cell
lymphoma
(DLBCL), subclassified as three DLBCL non-germinal center B-
cell
phenotype, one DLBCL germinal center B-
cell
phenotype, and two (Epstein-Barr
Virus
) EBV-
positive
DLBCL of the elderly; one case was anaplastic large
cell
lymphoma
, ALK-
positive
; and one case was peripheral
T cell
lymphoma
, not otherwise specified.
One patient who refused further therapy died of the
disease
at 2 months after
diagnosis
.
The other three patients with follow-up were alive without recurrence and metastatic
disease
at 9, 36, and 48 months, respectively, after excisional biopsy combined with appropriate chemotherapy and/or radiation therapy.
[MeSH-major]
Lymphoma
/ pathology. Soft Tissue Neoplasms / pathology
[MeSH-minor]
Adult
. Aged.
Diagnosis
, Differential. Female. Follow-Up Studies. Humans. Immunophenotyping. Male. Middle Aged. Retrospective Studies. Young
Adult
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(PMID = 20929318.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
22.
Aiello A, Fattorusso E, Luciano P, Menna M, Calzado MA, Muñoz E, Bonadies F, Guiso M, Sanasi MF, Cocco G, Nicoletti R:
Synthesis of structurally simplified analogues of aplidinone A, a pro-apoptotic marine thiazinoquinone.
Bioorg Med Chem
; 2010 Jan 15;18(2):719-27
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The study evidenced one of the synthetic analogues (11) as a potent cytotoxic and pro-apoptotic agent against several tumor
cell
lines which also inhibits the TNFalpha-induced NF-kappaB activation in
a human
leukemia T cell
line.
[MeSH-minor]
Animals.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Computer Simulation. Drug Screening Assays, Antitumor. Humans. Molecular Structure. NF-kappa B / metabolism. Structure-Activity Relationship. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / pharmacology
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[Copyright]
Copyright 2009 Elsevier Ltd. All rights reserved.
(PMID = 20031419.001).
[ISSN]
1464-3391
[Journal-full-title]
Bioorganic & medicinal chemistry
[ISO-abbreviation]
Bioorg. Med. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Quinones; 0 / Tumor Necrosis Factor-alpha; 0 / aplidinone A
23.
Gómez-Acevedo H, Li MY:
Backward bifurcation in a model for HTLV-I infection of CD4+ T cells.
Bull Math Biol
; 2005 Jan;67(1):101-14
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[Title]
Backward bifurcation in a model for
HTLV
-I infection of CD4+ T cells.
Human
T-
cell
Lymphotropic Virus
Type I (
HTLV
-I) primarily infects CD4+ helper T cells.
HTLV
-I infection is clinically linked to the development of
Adult T
-
cell Leukemia
/
Lymphoma
and of
HTLV
-
I Associated
Myelopathy/Tropical Spastic Paraparesis, among other illnesses.
HTLV
-I transmission can be either horizontal through
cell
-to-
cell
contact, or vertical through mitotic division of infected CD4+ T cells.
It has been observed that
HTLV
-I infection has a high proviral load but a low rate of proviral genetic variation.
We consider and analyze a mathematical model for
HTLV
-I infection of CD4+ T cells that incorporates both horizontal and vertical transmission.
[MeSH-major]
CD4-
Positive
T-Lymphocytes / virology. Computer Simulation.
Human
T-
lymphotropic virus
1 / growth & development. Models, Biological
[MeSH-minor]
Algorithms.
Cell
Death.
Cell
Proliferation. Humans
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(PMID = 15691541.001).
[ISSN]
0092-8240
[Journal-full-title]
Bulletin of mathematical biology
[ISO-abbreviation]
Bull. Math. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
24.
Mahieux R, Gessain A:
Adult T-cell leukemia/lymphoma and HTLV-1.
Curr Hematol Malig Rep
; 2007 Oct;2(4):257-64
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[Title]
Adult T
-
cell leukemia
/
lymphoma
and
HTLV
-1.
Human
T-
cell leukemia
/
lymphoma virus
type 1 (
HTLV
-1) was the first oncogenic
human
retrovirus to be discovered, more than 25 years ago.
HTLV
-1 infects 15 to 20 million individuals worldwide.
HTLV
-1 causes two major diseases:
adult T
-
cell leukemia
/
lymphoma
(
ATLL
) and tropical spastic paraparesis/
HTLV
-1-
associated
myelopathy (TSP/HAM).
ATLL
can be classified into four major subtypes: a smoldering type, a chronic type,
a lymphoma
type, and a leukemic type.
Because of intrinsic chemoresistance and severe immunosuppression, the survival rate of
ATLL
patients, especially those who develop the
acute
leukemic or
lymphoma
forms, is very poor, and such clonal malignant CD4 expansion remains one of the most severe lymphoproliferations.
[MeSH-major]
Human
T-
lymphotropic virus
1 / pathogenicity.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ virology
[MeSH-minor]
Adult
. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arsenicals / therapeutic use. CD4-
Positive
T-Lymphocytes / virology.
Clinical
Trials as Topic. Drug Resistance, Neoplasm. Endemic Diseases. Female. Gene Products, tax / physiology. Genes, pX. Humans. Immunoglobulin G / therapeutic use. Immunophenotyping. Immunotherapy. Infant, Newborn. Infectious
Disease
Transmission, Vertical. Interferon-alpha / therapeutic use. Male. Oxides / therapeutic use. Paraparesis, Tropical Spastic / epidemiology. Paraparesis, Tropical Spastic / virology. Pregnancy. Pregnancy Complications, Infectious. Zidovudine / therapeutic use
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[ISSN]
1558-822X
[Journal-full-title]
Current hematologic malignancy reports
[ISO-abbreviation]
Curr Hematol Malig Rep
[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; 0 / Arsenicals; 0 / Gene Products, tax; 0 / Immunoglobulin G; 0 / Interferon-alpha; 0 / Oxides; 0 / tax protein, Human T-lymphotrophic virus 1; 3A189DH42V / alemtuzumab; 4B9XT59T7S / Zidovudine; CUJ2MVI71Y / daclizumab; S7V92P67HO / arsenic trioxide
[Number-of-references]
63
25.
Yoshie O:
Expression of CCR4 in adult T-cell leukemia.
Leuk Lymphoma
; 2005 Feb;46(2):185-90
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[Title]
Expression of CCR4 in
adult T
-
cell leukemia
.
Adult T
-
cell leukemia
(
ATL
) is a malignancy of mature T cells that is etiologically
associated
with
human
T-
cell leukemia
virus
type 1 (
HTLV
-1).
The frequent manifestation of
ATL
is infiltration of leukemic cells into various organs.
Besides certain
cell
adhesion molecules and matrix metalloproteineses, chemokine receptors may play important roles in tissue infiltration of
ATL
.
Identification of a unique set of chemokine receptors expressed by
ATL
would thus provide valuable information about the molecular mechanism of tissue infiltration of
ATL
.
This may also reveal that
ATL
frequently develops from a certain subset of T cells that express a particular set of chemokine receptors.
Since
HTLV
-1 encodes a potent viral transcriptional activator Tax, which is known to induce various cellular genes, expression of some chemokine receptors may be affected by Tax.
This, however, may relate more to
HTLV
-1-infected T cells, since
ATL
cells usually do not express Tax.
Finally, identification of a unique set of chemokine receptors expressed by
ATL
may also provide a new therapeutic target.
These considerations prompted us to examine the chemokine receptor expression in
ATL
.
We found that in the majority of
ATL
cases, leukemic cells consistently express CCR4.
Since CCR4 is known to be involved in
T cell
migration into skin, this may in part explain the frequent skin infiltration in
ATL
.
Thus, the majority of
ATL
may predominantly originate from either Th2 or regulatory T cells.
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ immunology. Receptors, Chemokine / analysis
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(PMID = 15621800.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / Receptors, Chemokine
[Number-of-references]
44
26.
Hieshima K, Nagakubo D, Nakayama T, Shirakawa AK, Jin Z, Yoshie O:
Tax-inducible production of CC chemokine ligand 22 by human T cell leukemia virus type 1 (HTLV-1)-infected T cells promotes preferential transmission of HTLV-1 to CCR4-expressing CD4+ T cells.
J Immunol
; 2008 Jan 15;180(2):931-9
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[Title]
Tax-inducible production of CC chemokine ligand 22 by
human
T cell leukemia
virus
type 1 (
HTLV
-1)-infected T cells promotes preferential transmission of
HTLV
-1 to CCR4-expressing CD4+ T cells.
Adult T cell leukemia
is a mature CD4+
T cell
malignancy which predominantly expresses CCR4 and is etiologically
associated
with
human
T cell leukemia
virus
type 1 (
HTLV
-1).
Because
HTLV
-1 transmission depends on close
cell
-
cell
contacts,
HTLV
-1-infected T cells may preferentially interact with CCR4+CD4+ T cells for efficient viral transmission.
In terms of gene expression and protein secretion, we found a strong correlation between
HTLV
-1 Tax oncoprotein and CCL22, a CCR4 ligand, in
HTLV
-1-infected T cells.
Transient Tax expression in an
HTLV
-1-negative
T cell
line activated the CCL22 promoter and induced CCL22.
In chemotaxis assays, the culture supernatants of
HTLV
-1-infected T cells selectively attracted CCR4+CD4+ T cells in PBMCs.
Finally, anti-CCL22 Ab treatment also blocked
HTLV
-1 transmission to primary CD4+ T cells in coculture experiments with
HTLV
-1 producer cells.
Thus,
HTLV
-1-infected T cells produce CCL22 through Tax and selectively interact with CCR4+CD4+ T cells, resulting in preferential transmission of
HTLV
-1 to CCR4+CD4+ T cells.
[MeSH-major]
CD4-
Positive
T-Lymphocytes / virology. Chemokine CCL22 / genetics. Gene Expression Regulation, Viral. Gene Products, tax / metabolism.
Human
T-
lymphotropic virus
1 / physiology.
Virus
Internalization
[MeSH-minor]
Cell
Adhesion / drug effects.
Cell
Adhesion / genetics.
Cell
Line. Humans. Pertussis Toxin / pharmacology. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Receptors, CCR4 / antagonists & inhibitors. Receptors, CCR4 / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / virology
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
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[ErratumIn]
J Immunol. 2008 Jun 15;180(12):8470
(PMID = 18178833.001).
[ISSN]
0022-1767
[Journal-full-title]
Journal of immunology (Baltimore, Md. : 1950)
[ISO-abbreviation]
J. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / CCL22 protein, human; 0 / CCR4 protein, human; 0 / Chemokine CCL22; 0 / Gene Products, tax; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, CCR4; EC 2.4.2.31 / Pertussis Toxin
27.
D'Agostino DM, Silic-Benussi M, Hiraragi H, Lairmore MD, Ciminale V:
The human T-cell leukemia virus type 1 p13II protein: effects on mitochondrial function and cell growth.
Cell Death Differ
; 2005 Aug;12 Suppl 1:905-15
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[Title]
The
human
T-
cell leukemia
virus
type 1 p13II protein: effects on mitochondrial function and
cell
growth.
p13(II) of
human
T-
cell leukemia
virus
type 1 (
HTLV
-1) is an 87-amino-acid protein that is targeted to the inner mitochondrial membrane. p13(II) alters mitochondrial membrane permeability, producing a rapid, membrane potential-dependent influx of K(+).
At the cellular level, p13(II) has been found to interfere with
cell
proliferation and transformation and to promote apoptosis induced by ceramide and Fas ligand.
Assays carried out in T cells (the major targets of
HTLV
-1 infection in vivo) demonstrate that p13(II)-mediated sensitization to Fas ligand-induced apoptosis can be blocked by an inhibitor of Ras farnesylation, thus implicating Ras signaling as a downstream target of p13(II) function.
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(PMID = 15761473.001).
[ISSN]
1350-9047
[Journal-full-title]
Cell death and differentiation
[ISO-abbreviation]
Cell Death Differ.
[Language]
ENG
[Grant]
United States / PHS HHS / / 100730; United States / FIC NIH HHS / TW / TW005705-03; United States / FIC NIH HHS / TW / TW 05705; United States / FIC NIH HHS / TW / R03 TW005705; United States / FIC NIH HHS / TW / R03 TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-02; United States / FIC NIH HHS / TW / R03 TW005705-03; United States / FIC NIH HHS / TW / R03 TW005705-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Retroviridae Proteins; 0 / rof protein, Human T-lymphotropic virus 1; 0 / tof protein, Human T-lymphotropic virus 1; SY7Q814VUP / Calcium
[Number-of-references]
84
[Other-IDs]
NLM/ NIHMS183534; NLM/ PMC3057663
28.
Lyell V, Khatamzas E, Allain T:
Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report.
J Med Case Rep
; 2007;1:56
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[Title]
Severe hypercalcaemia and
lymphoma
in an
HTLV
-
1 positive
Jamaican woman: a case report.
Human
T cell
lymphotrophic virus
type-1 infection is endemic in the Afro-Caribbean community in Britain, with carriage rates of about 3%.
Although there is a long latency, carriers have
a 1
-5% chance of developing
adult T cell
leukaemia
/
lymphoma
, a condition frequently complicated by marked and refractory hypercalcaemia, and with a poor prognosis.
We present the case of an elderly Jamaican woman with severe hypercalcaemia and a raised PTHrP who was found to have
lymphoma
and was
positive
for
HTLV
-1.
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1752-1947
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Journal of medical case reports
[ISO-abbreviation]
J Med Case Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC1950877
29.
Schlecht-Louf G, Renard M, Mangeney M, Letzelter C, Richaud A, Ducos B, Bouallaga I, Heidmann T:
Retroviral infection in vivo requires an immune escape virulence factor encrypted in the envelope protein of oncoretroviruses.
Proc Natl Acad Sci U S A
; 2010 Feb 23;107(8):3782-7
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Here, we genetically "switched off' the envelope-mediated immunosuppression of an infectious retrovirus, the Friend murine
leukemia
virus
, while preserving mutant envelope infectivity both ex vivo and in vivo, thus allowing us to test the functional importance of envelope-mediated immunosuppression in retrovirus physiology.
Remarkably, we show, in vivo, that the non-IS mutant
virus
displays the same propagation kinetics as its WT counterpart in irradiated immunocompromised mice but that it is rapidly and totally cleared from normal immunocompetent mice, which become fully protected against a challenge with the WT retrovirus.
Using
cell
depletion strategies, we further establish that envelope-mediated immunosuppression enables the retrovirus to escape innate (natural killer cells) and adaptive (CD8 T cells) antiviral effectors.
In conclusion, our work demonstrates the critical role of Env-induced immunosuppression for retrovirus propagation in vivo and identifies a unique definite target for antiretroviral therapies and vaccine strategies, also characterized in the
human
T-
cell leukemia
virus
(
HTLV
) and xenotropic murine
leukemia
virus
-related
virus
(XMRV) retroviruses, opening unprecedented prospects for the treatment of retroviral diseases.
[MeSH-major]
Friend murine
leukemia
virus
/ immunology. Immune Tolerance.
Leukemia
, Experimental / immunology. Retroviridae Infections / immunology. Tumor
Virus
Infections / immunology. Viral Envelope Proteins / immunology. Virulence Factors / immunology
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[ISSN]
1091-6490
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Viral Envelope Proteins; 0 / Viral Vaccines; 0 / Virulence Factors
[Other-IDs]
NLM/ PMC2840525
30.
Miyamura F, Kako S, Yamagami H, Sato K, Sato M, Terasako K, Kimura S, Nakasone H, Aoki S, Okuda S, Yamazaki R, Oshima K, Yoshinaga K, Higuchi T, Nishida J, Demitsu T, Kakehashi A, Kanda Y:
Successful treatment of young-onset adult T cell leukemia/lymphoma and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem cell transplantation.
Int J Hematol
; 2009 Oct;90(3):397-401
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[Title]
Successful treatment of young-onset
adult T cell leukemia
/
lymphoma
and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem
cell
transplantation.
Only some carriers of
human
T cell
lymphotropic virus
type I (
HTLV
-1) develop
adult T cell leukemia
/
lymphoma
(
ATLL
) after a long latency period, and an association has been reported between chronic refractory eczema, known as infective dermatitis, and young-onset
ATLL
.
A 25-year-old female developed
ATLL
and underwent allogeneic hematopoietic stem
cell
transplantation (HSCT) in non-remission.
She had chronic refractory eczema and corneal injury at the onset of
ATLL
.
Remission of
ATLL
was achieved, and the
HTLV
-1 proviral load decreased after HSCT.
More than a year has passed since the transplantation was performed, and she has had no recurrence of either
ATLL
or lesions in the skin and eye.
Her
clinical
course suggests a possible association between skin and eye lesions and
HTLV
-1 infection.
Special attention is needed when
HTLV
-1 carriers develop eye or skin lesions.
[MeSH-major]
Corneal Diseases / therapy. Eczema / therapy. Hematopoietic Stem
Cell
Transplantation.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ therapy
[MeSH-minor]
Adult
. Chronic
Disease
. Female.
HTLV
-I Infections / complications.
Human
T-
lymphotropic virus
1. Humans. Transplantation, Homologous. Treatment Outcome. Viral Load
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.
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.
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.
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consumer health - Eczema
.
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1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
31.
Roy S, Josephson SA, Fridlyand J, Karch J, Kadoch C, Karrim J, Damon L, Treseler P, Kunwar S, Shuman MA, Jones T, Becker CH, Schulman H, Rubenstein JL:
Protein biomarker identification in the CSF of patients with CNS lymphoma.
J Clin Oncol
; 2008 Jan 1;26(1):96-105
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[Title]
Protein biomarker identification in the CSF of patients with CNS
lymphoma
.
PURPOSE: Elucidation of the CSF proteome may yield insights into the pathogenesis of CNS
disease
.
We tested the hypothesis that individual CSF proteins distinguish CNS
lymphoma
from benign focal brain lesions.
METHODS: We used a liquid chromatography/mass spectrometry-based method to differentially quantify and identify several hundred CSF proteins in CNS
lymphoma
and control patients.
ATIII RNA transcripts were identified within CNS
lymphomas
, and ATIII protein was localized selectively to tumor neovasculature.
We propose that the discovery of CSF protein biomarkers will facilitate early and noninvasive
diagnosis
in patients with lesions not amenable to brain biopsy, as well as provide improved surrogates of prognosis and treatment response in CNS
lymphoma
and brain metastasis.
[MeSH-major]
Biomarkers, Tumor / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid.
Lymphoma
/ cerebrospinal fluid. Neoplasm Proteins / cerebrospinal fluid
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Antithrombin III / genetics. Antithrombin III / metabolism. Case-Control Studies. Chromatography, Liquid.
Diagnosis
, Differential. Enzyme-Linked Immunosorbent Assay. Female. Humans. Immunoblotting. Immunoenzyme Techniques.
Leukemia
, Myeloid / cerebrospinal fluid.
Leukemia
, Myeloid / pathology.
Lymphoma
, B-
Cell
/ cerebrospinal fluid.
Lymphoma
, B-
Cell
/ pathology.
Lymphoma
, B-
Cell
, Marginal Zone / cerebrospinal fluid.
Lymphoma
, B-
Cell
, Marginal Zone / pathology.
Lymphoma
, Large B-
Cell
, Diffuse / cerebrospinal fluid.
Lymphoma
, Large B-
Cell
, Diffuse / pathology.
Lymphoma
, Non-Hodgkin / cerebrospinal fluid.
Lymphoma
, Non-Hodgkin / pathology. Male. Middle Aged. Proteomics. Sensitivity and Specificity. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Survival Rate
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[CommentIn]
J Clin Oncol. 2009 May 1;27(13):2302-3; author reply 2303-4
[
19332721.001
]
(PMID = 18056677.001).
[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 / K23 CA100291
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 9000-94-6 / Antithrombin III
[Other-IDs]
NLM/ NIHMS612770; NLM/ PMC4134101
32.
Nicot C, Harrod RL, Ciminale V, Franchini G:
Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions.
Oncogene
; 2005 Sep 5;24(39):6026-34
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[Title]
Human
T-
cell leukemia
/
lymphoma virus
type 1 nonstructural genes and their functions.
The
human
T-
cell leukemia
/
lymphoma virus
(
HTLV
) genome, in addition to the structural Gag and Env proteins and retroviral enzymes, carries a region at its 3' end originally designated pX.
To date, we know that this region encodes two essential transcriptional and post-transcriptional
positive
regulators of viral expression, the Tax and Rex proteins, respectively (reviewed elsewhere in this issue).
[MeSH-major]
Human
T-
lymphotropic virus
1 / genetics. Viral Nonstructural Proteins / genetics
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(PMID = 16155609.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United States / NIAID NIH HHS / AI / R01 AI058944; United States / NCI NIH HHS / CA / R01 CA106258
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Viral Nonstructural Proteins
[Number-of-references]
54
33.
Patronas M, Smith JA, Levy-Clarke GA, Reed GF, Buggage RR:
Hypergammaglobulinemia and corneal opacities in patients with human T-cell lymphotrophic virus type-1.
Am J Ophthalmol
; 2006 Dec;142(6):1088-9
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[Title]
Hypergammaglobulinemia and corneal opacities in patients with
human
T-
cell
lymphotrophic virus
type-1.
PURPOSE: To investigate the relationship between serum immunoglobulin levels and corneal opacities in a cohort of patients with
human
T-
cell
lymphotrophic virus
type-1 (
HTLV
-1).
METHODS: Complete ophthalmologic examination was performed on 44 patients with
HTLV
-1 infection (25 patients with
adult T
-
cell leukemia
/
lymphoma
[
ATL
], 18 patients with
HTLV
-1 that was
associated
myelopathy/tropical spastic paraparesis [HAM/TSP], and one patient who was asymptomatic).
RESULTS: Corneal opacities were identified in 15 of 25 patients (60%) with
ATL
and five of 18 patients (28%) with HAM/TSP.
The prevalence of corneal opacities was
associated
statistically with elevated IgG level (P = .023) in patients with
ATL
, but not in patients with HAM/TSP (P > .99).
CONCLUSION: Although the mechanism remains unclear, hypergammaglobulinemia is
associated
with the development of the corneal opacities in patients of African descent with
ATL
.
[MeSH-major]
Corneal Opacity / etiology.
HTLV
-I Infections / complications. Hypergammaglobulinemia / etiology
[MeSH-minor]
Human
T-
lymphotropic virus
1 / isolation & purification. Humans. Immunoglobulin A / blood. Immunoglobulin G / blood. Immunoglobulin M / blood. Nephelometry and Turbidimetry. Prevalence. Retrospective Studies
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(PMID = 17157606.001).
[ISSN]
0002-9394
[Journal-full-title]
American journal of ophthalmology
[ISO-abbreviation]
Am. J. Ophthalmol.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Immunoglobulin A; 0 / Immunoglobulin G; 0 / Immunoglobulin M
34.
Wada T, Yoshinaga E, Oiso N, Kawara S, Kawada A, Kozuka T:
Adult T-cell leukemia-lymphoma associated with follicular mucinosis.
J Dermatol
; 2009 Dec;36(12):638-42
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[Title]
Adult T
-
cell leukemia
-
lymphoma associated
with follicular mucinosis.
Follicular mucinosis (alopecia mucinosa) is often
associated
with malignancies including mycosis fungoides and Sézary syndrome, but not
adult T
-
cell leukemia
-
lymphoma
(
ATLL
).
The patient showed 11% of flower-shaped atypical lymphocytes in blood examination and
positive human
T-
cell leukemia
virus
type 1 antibody in serology, consistent with the chronic type of
ATLL
.
This case seems to be a very rare association of follicular mucinosis and chronic
ATLL
, suggesting that malignant T cells may have a feature of folliculotropism as well as epidermotropism.
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ complications. Mucinosis, Follicular / complications
[MeSH-minor]
DNA, Viral / genetics. DNA, Viral / isolation & purification.
Human
T-
lymphotropic virus
1 / genetics.
Human
T-
lymphotropic virus
1 / isolation & purification. Humans. Male. Middle Aged
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(PMID = 19958447.001).
[ISSN]
1346-8138
[Journal-full-title]
The Journal of dermatology
[ISO-abbreviation]
J. Dermatol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Viral
35.
Shahnaz S, Reich D, Arévalo-Valencia D, Kucinska S, Tulczynska J, Fleischman J:
HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia.
J Gen Intern Med
; 2007 Mar;22(3):420-3
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[Title]
HTLV
-1-
associated
adult T cell leukemia
lymphoma
presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia.
BACKGROUND: Since the initial description of
human
T cell
lymphotropic virus
(
HTLV
-1), clusters of this infection have been detected globally.
Unlike HIV infection, most patients infected with
HTLV
-1 remain asymptomatic throughout their lifetime.
CASE REPORT: We report the case of a 39-year-old Afro-Caribbean man with
HTLV
-1 infection presenting as hypercalcemia and granulomatous pneumocystis jiroveci pneumonia.
HTLV
-1-
associated
adult T cell leukemia
lymphoma
(
ATLL
) was diagnosed in this patient by bone marrow and lymph node biopsy.
This is believed to be the first description of this type of reaction to pneumocystis jiroveci in
a HTLV
-1-infected
ATLL
patient.
[MeSH-major]
HTLV
-I Infections /
diagnosis
. Hypercalcemia /
diagnosis
.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/
diagnosis
. Pneumocystis jirovecii. Pneumonia, Pneumocystis /
diagnosis
[MeSH-minor]
Aged.
Diagnosis
, Differential. Female. Humans
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 17356979.001).
[ISSN]
1525-1497
[Journal-full-title]
Journal of general internal medicine
[ISO-abbreviation]
J Gen Intern Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1824742
36.
Ohkura S, Yamashita M, Ishida T, Babu PG, Koyanagi Y, Yamamoto N, Miura T, Hayami M:
Phylogenetic heterogeneity of new HTLV type 1 isolates from southern India in subgroup A.
AIDS Res Hum Retroviruses
; 2005 Apr;21(4):325-30
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[Title]
Phylogenetic heterogeneity of new
HTLV
type 1 isolates from southern India in subgroup A.
Seven isolates of
human
T cell leukemia
virus
type 1 (
HTLV
-1) were taken in southern India and phylogenetically analyzed to gain new insights into the origin and dissemination of
HTLV
-1 in the subcontinent.
The new Indian
HTLV
-1s were found to be members of subgroup A (Transcontinental subgroup) of the Cosmopolitan group.
These results demonstrate that Indian
HTLV
-1s are genetically heterogeneous and include the most divergent strain of subgroup A.
On the basis of these results, we speculate that subgroup
A HTLV
- 1s may have been present for thousands of years in India.
[MeSH-major]
HTLV
-I Infections / virology.
Human
T-
lymphotropic virus
1 / genetics. Polymorphism, Genetic
[MeSH-minor]
Adult
. Child. DNA, Viral / chemistry. Female. Humans. India. Male. Middle Aged. Molecular Sequence Data. Phylogeny. Sequence Analysis, DNA. Terminal Repeat Sequences / genetics
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(PMID = 15943577.001).
[ISSN]
0889-2229
[Journal-full-title]
AIDS research and human retroviruses
[ISO-abbreviation]
AIDS Res. Hum. Retroviruses
[Language]
eng
[Databank-accession-numbers]
GENBANK/ AY607576/ AY607577/ AY607578/ AY607579/ AY607580/ AY607581/ AY607582
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Viral
37.
Aster JC:
Deregulated NOTCH signaling in acute T-cell lymphoblastic leukemia/lymphoma: new insights, questions, and opportunities.
Int J Hematol
; 2005 Nov;82(4):295-301
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[Title]
Deregulated NOTCH signaling in
acute
T-
cell
lymphoblastic
leukemia
/
lymphoma
: new insights, questions, and opportunities.
Recent work has shown that the majority of
human acute
T-
cell
lymphoblastic
leukemias
and
lymphomas
(T-ALL) have gain-of-function mutations in NOTCH1, a type I transmembrane receptor that normally signals through a gamma-secretase-dependent mechanism that relies on ligand-induced regulated intramembranous proteolysis.
Cleavage by gamma-secretase releases the intracellular domain of NOTCH1 (ICN1), permitting it to translocate to the nucleus and form a short-lived transcriptional activation complex that is essential for normal T-
cell
development.
Two types of mutations are prevalent in
human
T-ALL: extracellular domain mutations that increase ICN1 production and C-terminal mutations that sustain ICN1 action.
Inhibitors of ICN1 production and activity abrogate the growth of established T-ALL
cell
lines, and
a clinical
trial of a NOTCH pathway inhibitor in patients with refractory T-ALL has opened recently.
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ genetics.
Lymphoma
, T-
Cell
/ genetics. Receptor, Notch1 / genetics. Signal Transduction / genetics
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[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Receptor, Notch1
[Number-of-references]
74
38.
Ravandi F, Aribi A, O'Brien S, Faderl S, Jones D, Ferrajoli A, Huang X, York S, Pierce S, Wierda W, Kontoyiannis D, Verstovsek S, Pro B, Fayad L, Keating M, Kantarjian H:
Phase II study of alemtuzumab in combination with pentostatin in patients with T-cell neoplasms.
J Clin Oncol
; 2009 Nov 10;27(32):5425-30
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[Title]
Phase II study of alemtuzumab in combination with pentostatin in patients with T-
cell
neoplasms.
PURPOSE: To examine the efficacy and safety of the combination of alemtuzumab and pentostatin in patients with T-
cell
neoplasms.
PATIENTS AND METHODS: We treated 24 patients with a variety of T-
cell
leukemias
and
lymphomas
with a combination of alemtuzumab 30 mg intravenously (IV) three times weekly for up to 3 months and pentostatin 4 mg/m(2) IV weekly for 4 weeks followed by alternate weekly administration for up to 6 months.
Monoclonal T-
cell
receptor chain gene rearrangements were detected by polymerase chain reaction in bone marrow of 20 of 22 evaluable patients and became negative in five of seven evaluable patients in CR.
Opportunistic infections caused by pathogens
associated
with severe T-
cell
dysfunction were common.
CONCLUSION: The combination of alemtuzumab and pentostatin is feasible and effective in T-
cell
neoplasms.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
, T-
Cell
/ drug therapy.
Lymphoma
, T-
Cell
/ drug therapy
[MeSH-minor]
Adult
. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / administration & dosage. Antibodies, Neoplasm / adverse effects. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Neutropenia / chemically induced. Pentostatin / administration & dosage. Pentostatin / adverse effects. Sepsis / chemically induced. Survival Analysis. Thrombocytopenia / chemically induced. Treatment Outcome. Young
Adult
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Hazardous Substances Data Bank.
PENTOSTATIN
.
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(PMID = 19805674.001).
[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 / P30 CA016672
[Publication-type]
Clinical Trial, Phase II; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab
[Other-IDs]
NLM/ PMC4881363
39.
Jabbour E, Koscielny S, Sebban C, Peslin N, Patte C, Gargi T, Biron P, Fermé C, Bourhis JH, Vantelon JM, Arnaud P, Ribrag V:
High survival rate with the LMT-89 regimen in lymphoblastic lymphoma (LL), but not in T-cell acute lymphoblastic leukemia (T-ALL).
Leukemia
; 2006 May;20(5):814-9
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[Title]
High survival rate with the LMT-89 regimen in lymphoblastic
lymphoma
(LL), but not in T-
cell
acute
lymphoblastic
leukemia
(T-ALL).
The most appropriate treatment for lymphoblastic
lymphomas
(LL) remains uncertain.
Four patients had central nervous system involvement and 12 had bone marrow involvement and 24/27 (89%) had advanced Ann Arbor stage III-IV
disease
.
Bone marrow involvement was
associated
with a poor outcome.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ drug therapy. Precursor
Cell
Lymphoblastic
Leukemia
-
Lymphoma
/ drug therapy
[MeSH-minor]
Adolescent.
Adult
. Bone Marrow / pathology.
Disease
Progression.
Disease
-Free Survival. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Remission Induction. Survival Rate. Treatment Outcome
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(PMID = 16511514.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article
[Publication-country]
England
40.
Phillips AA, Shapira I, Willim RD, Sanmugarajah J, Solomon WB, Horwitz SM, Savage DG, Bhagat G, Soff G, Zain JM, Alobeid B, Seshan VE, O'Connor OA:
A critical analysis of prognostic factors in North American patients with human T-cell lymphotropic virus type-1-associated adult T-cell leukemia/lymphoma: a multicenter clinicopathologic experience and new prognostic score.
Cancer
; 2010 Jul 15;116(14):3438-46
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[Title]
A critical analysis of prognostic factors in North American patients with
human
T-
cell
lymphotropic virus
type-1-
associated
adult T
-
cell leukemia
/
lymphoma
: a multicenter clinicopathologic experience and new prognostic score.
BACKGROUND: To define the clinicopathologic and prognostic features of patients with
human
T-
cell
lymphotropic virus
type-1 (
HTLV
-1)-
associated
adult T
-
cell leukemia
/
lymphoma
(
ATLL
) in North America, standard criteria were used to identify patients with
ATLL
.
The
acute
subtype predominated (68.5%).
Although the International Prognostic Index and Prognostic Index for peripheral T-
cell
lymphoma
unspecified identified subsets of patients, these models were not completely predictive.
A recursive partitioning analysis was performed on the data, which successfully identified 3 prognostic categories based on Eastern Cooperative Oncology Group performance status, stage, age, and calcium level at
diagnosis
.
CONCLUSIONS: This series proposed a new prognostic model for patients with
HTLV
-1-
associated ATLL
and confirmed a poor outcome for these patients in North America.
[MeSH-major]
Human
T-
lymphotropic virus
1.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged. Prognosis. United States
Genetic Alliance.
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[Copyright]
Copyright (c) 2010 American Cancer Society.
(PMID = 20564100.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
41.
Jardin F, Ruminy P, Parmentier F, Picquenot JM, Courel MN, Bertrand P, Buchonnet G, Tilly H, Bastard C:
Clinical and biological relevance of single-nucleotide polymorphisms and acquired somatic mutations of the BCL6 first intron in follicular lymphoma.
Leukemia
; 2005 Oct;19(10):1824-30
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[Title]
Clinical
and biological relevance of single-nucleotide polymorphisms and acquired somatic mutations of the BCL6 first intron in follicular
lymphoma
.
Genetic modifications of the BCL6 gene in
lymphoma
include translocations, deletions, and somatic mutations (SM) of the 5' noncoding region.
Clinical
and biological relevance of these SNPs are unknown.
Based on a case-control study, BCL6 SNPs frequencies were assessed in 97 t(14;18) follicular
lymphomas
(FL) and in 54
lymphomas
with 3q27 rearrangement.
[MeSH-major]
Chromosomes,
Human
, Pair 3 / genetics. DNA-Binding Proteins / genetics. Introns / genetics.
Lymphoma
, Follicular / genetics. Mutation. Polymorphism, Single Nucleotide / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Case-Control Studies. Chromosomes,
Human
, Pair 14 / genetics. Chromosomes,
Human
, Pair 18 / genetics. DNA / genetics. DNA / metabolism. DNA Mutational Analysis. Electrophoretic Mobility Shift Assay. Female. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Humans.
Lymphoma
, Large B-
Cell
, Diffuse / genetics. Male. Middle Aged. Proto-Oncogene Proteins c-bcl-6
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(PMID = 16094416.001).
[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 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-6; 0 / Transcription Factors; 9007-49-2 / DNA
42.
Nasr R, El-Sabban ME, Karam JA, Dbaibo G, Kfoury Y, Arnulf B, Lepelletier Y, Bex F, de Thé H, Hermine O, Bazarbachi A:
Efficacy and mechanism of action of the proteasome inhibitor PS-341 in T-cell lymphomas and HTLV-I associated adult T-cell leukemia/lymphoma.
Oncogene
; 2005 Jan 13;24(3):419-30
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[Title]
Efficacy and mechanism of action of the proteasome inhibitor PS-341 in T-
cell lymphomas
and
HTLV
-
I associated
adult T
-
cell leukemia
/
lymphoma
.
HTLV
-
I associated
adult T
-
cell leukemia
(
ATL
) and
HTLV
-I-negative peripheral T-
cell lymphomas
are
associated
with poor prognosis.
Using pharmacological concentrations of the proteasome inhibitor PS-341, we demonstrate inhibition of
cell
proliferation and induction of apoptosis in fresh
ATL
cells,
HTLV
-I transformed and
HTLV
-I-negative malignant T cells, while normal resting or activated T lymphocytes were resistant.
In
HTLV
-I-negative malignant cells, PS-341 treatment significantly downregulated the antiapoptotic protein X-IAP and to a lesser extent c-IAP-1 and bcl-X(L) and resulted in caspase-dependent apoptosis.
In
HTLV
-I transformed cells, the inhibition of the proteasomal degradation of Tax by PS-341 likely explains the relative protection of
HTLV
-I infected cells against caspase-dependent apoptosis.
In both
HTLV
-I-
positive
and -negative cells, PS-341 treatment induced ceramide accumulation that correlated with apoptosis.
We conclude that PS-341 affects multiple pathways critical for the survival of
HTLV
-I-
positive
and -negative malignant T cells supporting a potential therapeutic role for PS-341 in both
ATL
and
HTLV
-I-negative T-
cell lymphomas
, whether alone or in combination with chemotherapy.
[MeSH-major]
Antineoplastic Agents / toxicity. Boronic Acids / toxicity.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ pathology.
Lymphoma
, T-
Cell
/ pathology. Protease Inhibitors / toxicity. Proteasome Inhibitors. Pyrazines / toxicity
[MeSH-minor]
Adult
. Apoptosis / drug effects. Bortezomib.
Cell
Division / drug effects.
Cell
Line.
Cell
Line, Tumor.
Cell
Survival / drug effects. Ceramides / metabolism. Humans. Jurkat Cells
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(PMID = 15543232.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Ceramides; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
43.
Javier RT:
Cell polarity proteins: common targets for tumorigenic human viruses.
Oncogene
; 2008 Nov 24;27(55):7031-46
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[Title]
Cell
polarity proteins: common targets for tumorigenic
human viruses
.
Loss of polarity and disruption of
cell
junctions are common features of epithelial-
derived
cancer cells, and mounting evidence indicates that such defects have a direct function in the pathology of cancer.
Supporting this idea, results with several different
human
tumor
viruses
indicate that their oncogenic potential depends in part on a common ability to inactivate key
cell
polarity proteins.
For example, adenovirus (Ad) type 9 is unique among
human
Ads by causing exclusively estrogen-dependent mammary tumors in experimental animals and in having E4 region-encoded open reading frame 1 (E4-ORF1) as its primary oncogenic determinant.
Most notably, the E4-ORF1 PBM mediates interactions with a selected group of cellular PDZ proteins, three of which include the
cell
polarity proteins Dlg1, PATJ and ZO-2.
Data further indicate that these interactions promote disruption of
cell
junctions and a loss of
cell
polarity.
In addition, one or more of the E4-ORF1-interacting
cell
polarity proteins, as well as the
cell
polarity protein Scribble, are common targets for the high-risk
human
papillomavirus (HPV) E6 or
human
T-
cell leukemia
virus
type 1 (
HTLV
-1) Tax oncoproteins.
Underscoring the significance of these observations, in humans, high-risk HPV and
HTLV
-1 are causative agents for cervical cancer and
adult T
-
cell leukemia
, respectively.
Consequently,
human
tumor
viruses
should serve as powerful tools for deciphering mechanisms whereby disruption of
cell
junctions and loss of
cell
polarity contribute to the development of many
human
cancers.
This review article discusses evidence supporting this hypothesis, with an emphasis on the
human
Ad E4-ORF1 oncoprotein.
[MeSH-major]
Cell
Polarity. Membrane Proteins / physiology. Neoplasms / etiology.
Virus
Attachment.
Virus
Diseases / complications
[MeSH-minor]
Adenovirus Infections,
Human
/ virology. Adenoviruses,
Human
/ physiology. Animals.
Cell
Transformation, Viral / physiology. Gene Products, tax / physiology.
Human
T-
lymphotropic virus
1 / metabolism.
Human
T-
lymphotropic virus
1 / physiology.
Human
papillomavirus 6 / metabolism.
Human
papillomavirus 6 / physiology. Humans. Models, Biological. Oncogene Proteins, Viral / metabolism. Oncogene Proteins, Viral / physiology. Protein Binding
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[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA058541
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / E4 protein, Adenovirus 9; 0 / Gene Products, tax; 0 / Membrane Proteins; 0 / Oncogene Proteins, Viral; 0 / tax protein, Human T-lymphotrophic virus 1
[Number-of-references]
233
[Other-IDs]
NLM/ NIHMS411909; NLM/ PMC3501650
44.
Masuda M, Maruyama T, Ohta T, Ito A, Hayashi T, Tsukasaki K, Kamihira S, Yamaoka S, Hoshino H, Yoshida T, Watanabe T, Stanbridge EJ, Murakami Y:
CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells.
J Biol Chem
; 2010 May 14;285(20):15511-22
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[Title]
CADM1 interacts with Tiam1 and promotes invasive phenotype of
human
T-
cell leukemia
virus
type I-transformed cells and
adult T
-
cell leukemia
cells.
CADM1 encodes a multifunctional immunoglobulin-like
cell
adhesion molecule whose cytoplasmic domain contains a type II PSD95/Dlg/ZO-1 (PDZ)-binding motif (BM) for associating with other intracellular proteins.
Although CADM1 lacks expression in T lymphocytes of healthy individuals, it is overexpressed in
adult T
-
cell leukemia
-
lymphoma
(
ATL
) cells.
It has been suggested that the expression of CADM1 protein promotes infiltration of leukemic cells into various organs and tissues, which is one of the frequent
clinical
manifestations of
ATL
.
Amino acid sequence alignment revealed that Tiam1 (T-
lymphoma
invasion and metastasis 1), a Rac-specific guanine nucleotide exchange factor, has a type II PDZ domain similar to those of membrane-
associated
guanylate kinase homologs (MAGUKs) that are known to bind to the PDZ-BM of CADM1.
In this study, we demonstrated that the cytoplasmic domain of CADM1 directly interacted with the PDZ domain of Tiam1 and induced formation of lamellipodia through Rac activation in
HTLV
-I-transformed
cell
lines as well as
ATL
cell
lines.
Our results indicate that Tiam1 integrates signals from CADM1 to regulate the actin cytoskeleton through Rac activation, which may lead to tissue infiltration of leukemic cells in
ATL
patients.
[MeSH-major]
Guanine Nucleotide Exchange Factors / metabolism.
Human
T-
lymphotropic virus
1 / pathogenicity. Immunoglobulins / metabolism.
Leukemia
, T-
Cell
/ pathology. Membrane Proteins / metabolism. Neoplasm Invasiveness. Tumor Suppressor Proteins / metabolism
[MeSH-minor]
Amino Acid Sequence. Base Sequence.
Cell
Adhesion Molecules.
Cell
Line, Tumor. Humans. Immunohistochemistry. Microscopy, Confocal. Molecular Sequence Data. Protein Binding. RNA Interference. RNA, Small Interfering. Sequence Homology, Amino Acid
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(PMID = 20215110.001).
[ISSN]
1083-351X
[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 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Guanine Nucleotide Exchange Factors; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / TIAM1 protein, human; 0 / Tumor Suppressor Proteins
[Other-IDs]
NLM/ PMC2865322
45.
Sugita S, Takase H, Yoshida T, Sugamoto Y, Watanabe T, Mochizuki M:
Intraocular soluble IL-2 receptor alpha in a patient with adult T cell leukaemia with intraocular invasion.
Br J Ophthalmol
; 2006 Sep;90(9):1204-6
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[Title]
Intraocular soluble IL-2 receptor alpha in a patient with
adult T cell
leukaemia
with intraocular invasion.
[MeSH-major]
Biomarkers, Tumor / analysis. Eye / pathology.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ pathology. Leukemic Infiltration / immunology. Receptors, Interleukin-2 / analysis
MedlinePlus Health Information.
consumer health - Eye Care
.
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[Cites]
Am J Ophthalmol. 2002 Oct;134(4):616-8
[
12383828.001
]
[Cites]
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Rinsho Ketsueki. 1992 Apr;33(4):537-41
[
1318431.001
]
(PMID = 16929066.001).
[ISSN]
0007-1161
[Journal-full-title]
The British journal of ophthalmology
[ISO-abbreviation]
Br J Ophthalmol
[Language]
eng
[Publication-type]
Case Reports; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / IL2RA protein, human; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Interleukin-2
[Other-IDs]
NLM/ PMC1857395
46.
Zhang J, Yamada O, Matsushita Y, Chagan-Yasutan H, Hattori T:
Transactivation of human osteopontin promoter by human T-cell leukemia virus type 1-encoded Tax protein.
Leuk Res
; 2010 Jun;34(6):763-8
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[Title]
Transactivation of
human
osteopontin promoter by
human
T-
cell leukemia
virus
type 1-encoded Tax protein.
We report here that OPN gene is transactivated by Tax protein of
human
T-
cell leukemia
virus
type 1 (
HTLV
-1).
This study suggests that OPN is one of the downstream mediators of aberrantly activated PI3K/AKT signaling by Tax, which may partially contribute to
HTLV
-1-
associated
leukemogenesis.
[MeSH-minor]
Base Sequence. Binding Sites. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology.
Cell
Line, Tumor.
Cell
Transformation, Viral / genetics. Gene Expression Regulation, Neoplastic.
Human
T-
lymphotropic virus
1 / genetics.
Human
T-
lymphotropic virus
1 / physiology. Humans. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Phosphatidylinositol 3-Kinases / metabolism. Phosphatidylinositol 3-Kinases / physiology. Promoter Regions, Genetic / physiology. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-akt / physiology. Signal Transduction / genetics. Transcription Factor AP-1 / metabolism
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
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author profiles
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.
NCI CPTC Antibody Characterization Program.
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NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[Copyright]
Copyright 2009 Elsevier Ltd. All rights reserved.
(PMID = 19767100.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Gene Products, tax; 0 / Transcription Factor AP-1; 0 / tax protein, Human T-lymphotrophic virus 1; 106441-73-0 / Osteopontin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
47.
Peloponese JM Jr, Yeung ML, Jeang KT:
Modulation of nuclear factor-ϰB by human T cell leukemia virus type 1 tax protein : Implications for oncogenesis and inflammation.
Immunol Res
; 2006 Jan;34(1):1-12
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[Title]
Modulation of nuclear factor-ϰB by
human
T cell leukemia
virus
type 1 tax protein : Implications for oncogenesis and inflammation.
Human
T cell leukemia
virus
type 1 (
HTLV
-1) is the causative agent of a fatal malignancy known as
adult T cell leukemia
(
ATL
) and an inflammatory
disease
named tropical spastic paraparesis/
HTLV
-
1 associated
myelopathy (TSP/HAM).
HTLV
-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
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.
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[ISSN]
0257-277X
[Journal-full-title]
Immunologic research
[ISO-abbreviation]
Immunol. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Keywords]
NOTNLM ; Adult T cell leukemia (ATL) / HTLV-1 Tax / Human T cell leukemia virus (HTLV-1) / IKK / Inflammation / NF-ϰB / NIK
48.
de Larrinoa AF, del Cura J, Zabala R, Fuertes E, Bilbao F, Lopez JI:
Value of ultrasound-guided core biopsy in the diagnosis of malignant lymphoma.
J Clin Ultrasound
; 2007 Jul-Aug;35(6):295-301
[Fulltext service]
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[Source]
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[Title]
Value of ultrasound-guided core biopsy in the
diagnosis
of malignant
lymphoma
.
PURPOSE: Ultrasound-guided core needle biopsy for the
diagnosis
and management of malignant
lymphomas
is controversial and has not been accepted as an alternative to surgical biopsy.
We investigate the
clinical
usefulness of this procedure in a large series of patients.
METHODS: Over a 5-year period (2000-2004), ultrasound-guided core needle biopsies were performed in 102 malignant
lymphomas
.
Five diagnostic categories were considered: large B-
cell lymphomas
(LBCL), small B-
cell lymphomas
(SBCL), Hodgkin's
disease
(HD),
T cell lymphomas
, and miscellaneous.
SBCL (39), LBCL (36), HD (15),
T cell lymphomas
(5), and miscellaneous (7) [including
T cell
-rich B
cell
(2), natural killer
cell
(1), Burkitt's
lymphoma
(1), and non-Hodgkin's
lymphoma
of the B
cell
type,
NOS
(3)] were correctly diagnosed.
Three HDs, 1 natural killer
cell
lymphoma
, 1 follicular
lymphoma
, and 1 LBCL were not correctly diagnosed.
CONCLUSIONS: Ultrasound-guided core needle biopsy is effective in the
diagnosis
of malignant
lymphomas
and can be used as the first diagnostic approach in selected
clinical
situations.
[MeSH-major]
Biopsy / methods.
Lymphoma
/
diagnosis
. Ultrasonography, Interventional
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Burkitt
Lymphoma
/
diagnosis
. Burkitt
Lymphoma
/ pathology. Female. Hodgkin
Disease
/
diagnosis
. Humans. Killer Cells, Natural / pathology.
Leukemia
, Lymphocytic, Chronic, B-
Cell
/
diagnosis
. Lymph Nodes / pathology.
Lymphoma
, B-
Cell
/
diagnosis
.
Lymphoma
, Follicular /
diagnosis
.
Lymphoma
, Large B-
Cell
, Diffuse /
diagnosis
.
Lymphoma
, T-
Cell
/
diagnosis
. Male. Middle Aged. Prospective Studies
MedlinePlus Health Information.
consumer health - Biopsy
.
MedlinePlus Health Information.
consumer health - Lymphoma
.
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[Copyright]
(c) 2007 Wiley Periodicals, Inc.
(PMID = 17486566.001).
[ISSN]
0091-2751
[Journal-full-title]
Journal of clinical ultrasound : JCU
[ISO-abbreviation]
J Clin Ultrasound
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
49.
Fahim S, Prokopetz R, Jackson R, Faught C, McCarthy AE, Andonov A, Coulthart M, Daw Z, Olberg B, Giulivi A, Padmore R:
Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut.
CMAJ
; 2006 Sep 12;175(6):579
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[Title]
Human
T-
cell
lymphotropic virus
type 1-
associated
adult T
-
cell leukemia
/
lymphoma
in the Inuit people of Nunavut.
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ ethnology
[MeSH-minor]
Adult
. Aged. Fatal Outcome. Female. Humans. Indians, North American. Lymphocytosis / blood. Medical History Taking. Middle Aged. Physical Examination. Practice Guidelines as Topic
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
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author profiles
.
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[Cites]
Tissue Antigens. 1998 Nov;52(5):444-51
[
9864034.001
]
[Cites]
CMAJ. 2006 Jan 17;174(2):150-1
[
16415454.001
]
[Cites]
Am J Hematol. 2005 Mar;78(3):232-9
[
15726602.001
]
(PMID = 16966657.001).
[ISSN]
1488-2329
[Journal-full-title]
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne
[ISO-abbreviation]
CMAJ
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Canada
[Other-IDs]
NLM/ PMC1559419
50.
Mesnard JM, Barbeau B, Devaux C:
HBZ, a new important player in the mystery of adult T-cell leukemia.
Blood
; 2006 Dec 15;108(13):3979-82
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[Title]
HBZ, a new important player in the mystery of
adult T
-
cell leukemia
.
Adult T
-
cell leukemia
(
ATL
) was first described in 1977.
A link between
ATL
and
human
T-
cell leukemia
virus
type 1 (
HTLV
-1) was clearly established in the early 1980s.
Over the years, many aspects of
HTLV
-1-induced cellular dysfunctions have been clarified.
However, the detailed mechanism behind
ATL
occurrence remains unsolved.
Presently, we are still unable to explain the absence of viral Tax protein (thought to play a central role in T-
cell
transformation) in more than 50% of
ATL
cells.
A novel
HTLV
-1 HBZ protein, encoded on the negative strand, was characterized by our group and is currently the subject of intensive research efforts to determine its function in viral replication and/or pathophysiology.
Recently, 4 studies reported on the existence of different HBZ isoforms and have investigated on their function in both
ATL
cells or animal models.
[MeSH-major]
Basic-Leucine Zipper Transcription Factors / genetics.
Cell
Transformation, Viral / genetics.
Human
T-
lymphotropic virus
1 / genetics.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ genetics. Viral Proteins / genetics.
Virus
Replication / genetics
[MeSH-minor]
Animals.
Cell
Proliferation.
Disease
Models, Animal. Gene Products, tax / deficiency. Gene Products, tax / immunology. Humans. Protein Isoforms / genetics. Protein Isoforms / immunology. RNA, Messenger / genetics. RNA, Messenger / immunology. RNA, Viral / genetics. RNA, Viral / immunology. T-Lymphocytes / immunology. T-Lymphocytes / pathology. T-Lymphocytes / virology
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(PMID = 16917009.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Viral Proteins
[Number-of-references]
102
51.
Ariumi Y, Trono D:
Ataxia-telangiectasia-mutated (ATM) protein can enhance human immunodeficiency virus type 1 replication by stimulating Rev function.
J Virol
; 2006 Mar;80(5):2445-52
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[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Ataxia-telangiectasia-mutated (ATM) protein can enhance
human
immunodeficiency
virus
type 1 replication by stimulating Rev function.
The ataxia-telangiectasia-mutated (ATM) kinase plays a central role in responses to various forms of DNA damage and has been suggested to facilitate
human
immunodeficiency
virus
type 1 (HIV-1) integration.
Notably, ATM overexpression did not stimulate the HIV-1 late gene expression within the context of Rev-independent constructs or the Rex-dependent production of capsid from
human
T-
cell leukemia
virus
type 1 proviral constructs.
[MeSH-major]
Cell
Cycle Proteins / physiology. DNA-Binding Proteins / physiology. Gene Expression Regulation, Viral. Gene Products, rev / physiology. HIV-1 / physiology. Protein-Serine-Threonine Kinases / physiology. Tumor Suppressor Proteins / physiology.
Virus
Replication
[MeSH-minor]
Ataxia Telangiectasia Mutated Proteins. Caffeine.
Cell
Line. Gene Silencing. Genes, Reporter. HIV Core Protein p24 / analysis. Humans. Luciferases / analysis. Luciferases / genetics. rev Gene Products,
Human
Immunodeficiency
Virus
Genetic Alliance.
consumer health - Ataxia
.
Genetic Alliance.
consumer health - Ataxia Telangiectasia
.
Addgene Non-profit plasmid repository.
clones/clone libraries - Get Article's Plasmids - Addgene
(subscription/membership/fee required).
Hazardous Substances Data Bank.
CAFFEINE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
eagle-i research resources.
PMID 16474151 (Special Collections)
.
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(PMID = 16474151.001).
[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 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Gene Products, rev; 0 / HIV Core Protein p24; 0 / Tumor Suppressor Proteins; 0 / rev Gene Products, Human Immunodeficiency Virus; 3G6A5W338E / Caffeine; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
[Other-IDs]
NLM/ PMC1395391
52.
Yoshida M, Satou Y, Yasunaga J, Fujisawa J, Matsuoka M:
Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene.
J Virol
; 2008 Oct;82(19):9359-68
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[Title]
Transcriptional control of spliced and unspliced
human
T-
cell leukemia
virus
type 1 bZIP factor (HBZ) gene.
The
human
T-
cell leukemia
virus
type 1 (
HTLV
-1) basic leucine zipper factor (HBZ) gene is encoded by the minus strand of the
HTLV
-1 provirus and transcribed from the 3' long terminal repeat (LTR).
We compared the functions of the proteins
derived
from the sHBZ and usHBZ transcripts. sHBZ showed a stronger suppression of Tax-mediated transcriptional activation through the 5' LTR than did usHBZ; the level of suppression correlated with the level of protein produced.
The expression of sHBZ had a growth-promoting function in a T-
cell
line, while usHBZ expression did not.
[MeSH-major]
Basic-Leucine Zipper Transcription Factors / chemistry.
Human
T-
lymphotropic virus
1 / genetics. Sp1 Transcription Factor / metabolism. Transcription, Genetic. Viral Proteins / genetics. Viral Proteins / physiology
[MeSH-minor]
Alternative Splicing. Base Sequence.
Cell
Proliferation. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Humans. Molecular Sequence Data. Promoter Regions, Genetic. RNA, Viral / metabolism. Terminal Repeat Sequences
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
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(PMID = 18653454.001).
[ISSN]
1098-5514
[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 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Viral; 0 / Sp1 Transcription Factor; 0 / Viral Proteins
[Other-IDs]
NLM/ PMC2546946
53.
Kress AK, Schneider G, Pichler K, Kalmer M, Fleckenstein B, Grassmann R:
Elevated cyclic AMP levels in T lymphocytes transformed by human T-cell lymphotropic virus type 1.
J Virol
; 2010 Sep;84(17):8732-42
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[Title]
Elevated cyclic AMP levels in T lymphocytes transformed by
human
T-
cell
lymphotropic virus
type 1.
Human
T-
cell
lymphotropic virus
type 1 (
HTLV
-1), the cause of
adult T
-
cell leukemia
/
lymphoma
(
ATLL
), transforms CD4(+) T cells to permanent growth through its transactivator Tax.
HTLV
-1-transformed cells share phenotypic properties with memory and regulatory T cells (T-reg).
This led us to determine cAMP levels in
HTLV
-1-transformed cells.
We found elevated cAMP concentrations as a consistent feature of
all HTLV
-1-transformed
cell
lines, including in vitro-
HTLV
-1-transformed, Tax-transformed, and patient-
derived
cells.
We found specific downregulation of the cAMP-degrading phosphodiesterase 3B (PDE3B) in
HTLV
-1-transformed cells, which was independent of Tax in transient expression experiments.
Overexpression of PDE3B led to a decrease of cAMP in
HTLV
-1-transformed cells.
Decreased expression of PDE3B was
associated
with inhibitory histone modifications at the PDE3B promoter and the PDE3B locus.
This shows that
HTLV
-1-transformed cells assume biological features of long-lived T-
cell
populations that potentially contribute to viral persistence.
[MeSH-major]
Cell
Transformation, Viral. Cyclic AMP / metabolism.
HTLV
-I Infections / metabolism.
Human
T-
lymphotropic virus
1 / physiology.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ metabolism
[MeSH-minor]
Cell
Line, Transformed. Cells, Cultured. Cyclic Nucleotide Phosphodiesterases, Type 3 / genetics. Cyclic Nucleotide Phosphodiesterases, Type 3 / metabolism. Gene Products, tax / genetics. Gene Products, tax / metabolism. Humans. T-Lymphocytes / metabolism. T-Lymphocytes / virology
SciCrunch.
ArrayExpress: Data: Microarray
.
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[ISSN]
1098-5514
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE17718
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Gene Products, tax; 0 / tax protein, Human T-lymphotrophic virus 1; E0399OZS9N / Cyclic AMP; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 3; EC 3.1.4.17 / PDE3B protein, human
[Other-IDs]
NLM/ PMC2918996
54.
Klabusay M, Pevná M, Kissová J, Doubek M, Heidekerová M, Mayer J, Vorlícek J:
[Rare diagnosis of CD4+56+ leukemia from dendritic cells type DC2].
Cas Lek Cesk
; 2008;147(10):511-5
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[Title]
[Rare
diagnosis
of CD4+56+
leukemia
from dendritic cells type DC2].
CD4+56+ hematodermic neoplasm or
leukemia
from early plasmocytoid dendritic cells type DC2 was recognized by WHO-EORTC classification of cutaneous
lymphomas
as a separate entity related to the plasmacytoid precursor dendritic
cell
(pDC).
This
diagnosis
is based on expression of CD4 and CD56 antigens and absence of B, T or myeloid lineage markers.
Immunohistochemistry and flow cytometry are the only methods, which allow identification of this
disease
, either in isolated skin lesions or in a leukemic form.
Although the co-expression of CD4 and CD56 is rare and the number of described cases is low, this group bears similar characteristics in
a clinical
course of
disease
.
It is a very aggressive
leukemia
/
lymphoma
, usually with primary skin involvement, in half of the cases infiltrating bone marrow or lymph nodes.
Despite high rate of initial response to treatment, early and widespread relapses occur and patients die of
disease
progression.
Although the physiological counterpart of tumour cells was identified, the origin of the
disease
is still discussed because of aberrant expression of
cell
markers.
However, this aggressive
disease
requires radical approach with intensive chemotherapy regimens, prophylaxis of CNS involvement and early indication of allogeneic bone marrow transplantation.
[MeSH-major]
Antigens, CD4 / analysis. Antigens, CD56 / analysis. Dendritic Cells / immunology.
Leukemia
/
diagnosis
. Skin Neoplasms /
diagnosis
[MeSH-minor]
Adult
. Aged. Female. Humans. Male
MedlinePlus Health Information.
consumer health - Leukemia
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
COS Scholar Universe.
author profiles
.
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(PMID = 19177732.001).
[ISSN]
0008-7335
[Journal-full-title]
Casopís lékar̆ů c̆eských
[ISO-abbreviation]
Cas. Lek. Cesk.
[Language]
cze
[Publication-type]
Case Reports; English Abstract; Journal Article; Review
[Publication-country]
Czech Republic
[Chemical-registry-number]
0 / Antigens, CD4; 0 / Antigens, CD56
[Number-of-references]
26
55.
Kameda T, Shide K, Shimoda HK, Hidaka T, Kubuki Y, Katayose K, Taniguchi Y, Sekine M, Kamiunntenn A, Maeda K, Nagata K, Matsunaga T, Shimoda K:
Absence of gain-of-function JAK1 and JAK3 mutations in adult T cell leukemia/lymphoma.
Int J Hematol
; 2010 Sep;92(2):320-5
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[Title]
Absence of gain-of-function JAK1 and JAK3 mutations in
adult T cell leukemia
/
lymphoma
.
Somatic JAK1 mutations are found in 18% of
adult
precursor T
acute
lymphoblastic
leukemias
and somatic JAK3 mutations are found in 3.3% of cutaneous
T cell lymphomas
.
Adult T cell leukemia
/
lymphoma
(
ATLL
) is a type of
T cell
neoplasm, and activation of JAK/STAT pathways is sometimes observed in them.
We investigated JAK1 and JAK3 mutations in 20
ATLL
patients.
JAK1 and JAK3 mutations are unlikely involved in the leukemogenesis of
ATLL
.
[MeSH-major]
Janus Kinase 1 / genetics. Janus Kinase 3 / genetics.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ genetics
[MeSH-minor]
Adult
.
Cell
Differentiation.
Cell
Proliferation. DNA Mutational Analysis. Humans. Japan. Polymorphism, Single Nucleotide
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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J Immunol. 2007 Mar 1;178(5):2623-9
[
17312100.001
]
(PMID = 20697856.001).
[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3
56.
Oschlies I, Klapper W, Zimmermann M, Krams M, Wacker HH, Burkhardt B, Harder L, Siebert R, Reiter A, Parwaresch R:
Diffuse large B-cell lymphoma in pediatric patients belongs predominantly to the germinal-center type B-cell lymphomas: a clinicopathologic analysis of cases included in the German BFM (Berlin-Frankfurt-Munster) Multicenter Trial.
Blood
; 2006 May 15;107(10):4047-52
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[Title]
Diffuse large B-
cell
lymphoma
in pediatric patients belongs predominantly to the germinal-center type B-
cell lymphomas
: a clinicopathologic analysis of cases included in the German BFM (Berlin-Frankfurt-Munster) Multicenter Trial.
Diffuse large B-
cell
lymphoma
(DLBCL) in adults is a heterogeneous
disease
.
Biologic subgroups of DLBCL with a favorable prognosis (germinal center B-
cell
-like, GCB) and with a poor prognosis (activated B-
cell
-like, ABC) have been defined by gene expression profiling and can be distinguished by immunohistochemistry.
In contrast to their
adult
counterparts, children with DLBCL have an excellent prognosis.
We analyzed 63 cases of DLBCL in pediatric patients by immunohistochemistry and fluorescence in situ hybridization (FISH) and found a striking predominance of a GCB subtype, which might explain the good
clinical
outcome in these
lymphomas
.
Interestingly, FISH applied to 50 of these cases, as well as conventional cytogenetics available in 3 cases, revealed absence of the translocation t(14;18) involving the BCL2 gene, which is present in about 15% of
adult
GCB subtype DLBCL.
Our data indicate that pediatric DLBCL differs from
adult
DLBCL and might comprise a biologically unique subgroup of DLBCL from which important insights into the pathogenesis and biology of this
disease
might be gained.
[MeSH-major]
Chromosomes,
Human
, Pair 14. Chromosomes,
Human
, Pair 18.
Leukemia
, Lymphoid / classification.
Lymphoma
, B-
Cell
/ classification. Translocation, Genetic
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.
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.
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(PMID = 16424389.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
57.
Masutani H, Ueda S, Yodoi J:
The thioredoxin system in retroviral infection and apoptosis.
Cell Death Differ
; 2005 Aug;12 Suppl 1:991-8
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Human
thioredoxin (TRX) was first identified in
human
T-
cell leukemia
virus
type I (
HTLV
-I)-
positive
T-
cell
lines and is
associated
with the pathophysiology of retroviral infections.
Thioredoxin binding protein-2/vitamin D(3) upregulated protein 1 is a growth suppressor and its expression is suppressed in
HTLV
-I-transformed cells.
Studies of these molecules of the TRX system provide novel insights into the apoptosis
associated
with retroviral diseases.
[MeSH-minor]
Animals. Glutathione / metabolism. HIV Infections / metabolism.
HTLV
-I Infections / metabolism. Humans. MAP Kinase Kinase Kinase 5 / metabolism. Membrane Proteins / metabolism. Peroxidases / metabolism. Peroxiredoxins
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(PMID = 15818395.001).
[ISSN]
1350-9047
[Journal-full-title]
Cell death and differentiation
[ISO-abbreviation]
Cell Death Differ.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Membrane Proteins; 52500-60-4 / Thioredoxins; EC 1.11.1.- / Peroxidases; EC 1.11.1.15 / Peroxiredoxins; EC 2.7.11.25 / MAP Kinase Kinase Kinase 5; GAN16C9B8O / Glutathione
[Number-of-references]
93
58.
Mukherjee S, Negi VS, Keitany G, Tanaka Y, Orth K:
In vitro activation of the IkappaB kinase complex by human T-cell leukemia virus type-1 Tax.
J Biol Chem
; 2008 May 30;283(22):15127-33
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[Title]
In vitro activation of the IkappaB kinase complex by
human
T-
cell leukemia
virus
type-1 Tax.
Human
T-
cell leukemia
virus
type-I expresses Tax, a 40-kDa oncoprotein that activates IkappaB kinase (IKK), resulting in constitutive activation of NFkappaB.
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.
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[Cites]
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Cell. 2000 Oct 13;103(2):351-61
[
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]
(PMID = 18223255.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01 AI 056404; United States / NIDDK NIH HHS / DK / R21 DK 072134
[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 / Bacterial Proteins; 0 / Gene Products, tax; 0 / HSP90 Heat-Shock Proteins; 0 / Multiprotein Complexes; 0 / NF-kappa B; 0 / Recombinant Proteins; 0 / YopP protein, Yersinia; EC 2.7.11.10 / I-kappa B Kinase; EC 3.1.3.16 / Phosphoprotein Phosphatases
[Other-IDs]
NLM/ PMC2397464
59.
Chiba K, Hashino S, Izumiyama K, Toyoshima N, Suzuki S, Kurosawa M, Asaka M:
Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with adult T cell leukemia.
Int J Lab Hematol
; 2009 Jun;31(3):368-71
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[Title]
Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with
adult T cell leukemia
.
A 37-year-old woman was diagnosed as having chronic
adult T
-
cell leukemia
(
ATL
) of the skin by a skin biopsy and
human
T-
cell leukemia
virus
type-1 serology at our hospital in August 1992.
The skin lesions of
ATL
were improved by treatment with psoralen ultraviolet ray A.
[MeSH-major]
Chemokines / blood. Interleukin-6 / blood.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ blood.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ complications. Osteolysis / blood. Osteolysis / etiology
[MeSH-minor]
Adult
. Chronic
Disease
. Fatal Outcome. Female. Humans
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.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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.
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(PMID = 18177436.001).
[ISSN]
1751-553X
[Journal-full-title]
International journal of laboratory hematology
[ISO-abbreviation]
Int J Lab Hematol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Chemokines; 0 / Interleukin-6
60.
Fan J, Ma G, Nosaka K, Tanabe J, Satou Y, Koito A, Wain-Hobson S, Vartanian JP, Matsuoka M:
APOBEC3G generates nonsense mutations in human T-cell leukemia virus type 1 proviral genomes in vivo.
J Virol
; 2010 Jul;84(14):7278-87
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[Title]
APOBEC3G generates nonsense mutations in
human
T-
cell leukemia
virus
type 1 proviral genomes in vivo.
Human
T-
cell leukemia
virus
type 1 (
HTLV
-1) induces
cell
proliferation after infection, leading to efficient transmission by
cell
-to-
cell
contact.
After a long latent period, a fraction of carriers develop
adult T
-
cell leukemia
(
ATL
).
Genetic changes in the tax gene in
ATL
cells were reported in about 10% of
ATL
cases.
To determine genetic changes that may occur throughout the provirus, we determined the entire sequence of the
HTLV
-1 provirus in 60
ATL
cases.
Abortive genetic changes, including deletions, insertions, and nonsense mutations, were frequent in all viral genes except the HBZ gene, which is transcribed from the minus strand of the
virus
.
G-to-A base substitutions were the most frequent mutations in
ATL
cells.
The sequence context of G-to-A mutations was in accordance with the preferred target sequence of
human
APOBEC3G (hA3G).
The target sequences of hA3G were less frequent in the plus strand of the HBZ coding region than in other coding regions of the
HTLV
-1 provirus.
HTLV
-1-infected cells likely take advantage of hA3G to escape from the host immune system by losing expression of viral proteins.
[MeSH-major]
Cytidine Deaminase / metabolism. Genome, Viral.
HTLV
-I Infections / virology.
Human
T-
lymphotropic virus
1 / genetics.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ virology. Mutation. Proviruses / genetics
[MeSH-minor]
Base Sequence.
Cell
Line. Genes, Reporter. Genetic Variation. Genetic Vectors. Humans. Molecular Sequence Data. Mutagenesis
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(PMID = 20463074.001).
[ISSN]
1098-5514
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / APOBEC3G protein, human; EC 3.5.4.5 / Cytidine Deaminase
[Other-IDs]
NLM/ PMC2898234
61.
Lang P, Schumm M, Greil J, Bader P, Klingebiel T, Müller I, Feuchtinger T, Pfeiffer M, Schlegel PG, Niethammer D, Handgretinger R:
A comparison between three graft manipulation methods for haploidentical stem cell transplantation in pediatric patients: preliminary results of a pilot study.
Klin Padiatr
; 2005 Nov-Dec;217(6):334-8
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[Title]
A comparison between three graft manipulation methods for haploidentical stem
cell
transplantation in pediatric patients: preliminary results of a pilot study.
Transplantation of hematopoietic stem cells from mismatched related donors makes a potential donor available for every child in need of stem
cell
transplantation.
Here, we compare three different graft manipulation methods in patients with
leukemias
and
lymphomas
:
positive
selection of stem cells with either CD34 (n = 39) or CD133-coated magnetic microbeads (n = 14) and a new strategy which depletes T- and B-cells through the use of CD3- and CD19-coated microbeads (n = 11).
Indirect depletion of T-cells by
positive
selection resulted in 1 x 10 (4) (median) residual CD3 (+)-cells/kg (0.7-3 x 10 (4)).
Primary engraftment of the stem
cell
products was comparable after CD34- and CD133-selection (85 and 72 %).
Since effector
cell
with potential antileukemic activity are cotransfused, such grafts may be suited in particular for patients with insufficient remission.
[MeSH-major]
Haploidy. Hematopoietic Stem
Cell
Transplantation / methods.
Leukemia
/ therapy.
Lymphoma
/ therapy
[MeSH-minor]
Adolescent.
Adult
. Antigens, CD / immunology. Antigens, CD19 / immunology. Antigens, CD3 / immunology. Antigens, CD34 / immunology.
Cell
Count. Child. Child, Preschool. Female. Glycoproteins / immunology. Humans. Infant. Lymphocyte Depletion. Male. Microspheres. Peptides / immunology. Pilot Projects. Survival Rate
Genetic Alliance.
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.
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.
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.
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.
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(PMID = 16307419.001).
[ISSN]
0300-8630
[Journal-full-title]
Klinische Pädiatrie
[ISO-abbreviation]
Klin Padiatr
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Glycoproteins; 0 / Peptides
62.
Mizobe T, Tsukada J, Higashi T, Mouri F, Matsuura A, Tanikawa R, Minami Y, Yoshida Y, Tanaka Y:
Constitutive association of MyD88 to IRAK in HTLV-I-transformed T cells.
Exp Hematol
; 2007 Dec;35(12):1812-22
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[Title]
Constitutive association of MyD88 to IRAK in
HTLV
-I-transformed T cells.
OBJECTIVE: Constitutive activation of nuclear factor (NF)-kappaB is a common feature of
human
T-
cell leukemia
virus
type I (
HTLV
-I)-transformed T cells.
Inhibition of NF-kappaB activity reduces
cell
growth and induces apoptosis of
HTLV
-I-transformed T cells, suggesting a central role of NF-kappaB in their proliferation and survival.
In this study, we investigated whether MyD88, an adaptor protein of Toll-like receptor (TLR) signaling, contributes to constitutive NF-kappaB activation in
HTLV
-I-transformed T cells.
MATERIALS AND METHODS: Activation status of MyD88 and interleukin (IL)-1R-
associated
kinase 1 (IRAK1) in
HTLV
-I-transformed
human
T cells, MT2, MT4, and HUT102 was examined by using Western blot and immunoprecipitation.
An expression vector encoding a dominant negative MyD88 with a deletion of its death domain (MyD88dn) was transfected into MT2 cells to evaluate roles of MyD88 in spontaneous activation of cytokine gene promoters and transcription factors, proliferation, and apoptosis in
HTLV
-I-transformed T cells.
RESULTS: Constitutive association of MyD88 with IRAK1 was observed in all three of
HTLV
-I-transformed T cells, but not in
HTLV
-I-negative T cells, such as Jurkat, HUT78, and MOLT4.
HTLV
-I Tax enhanced TLR expression and synergistically activated NF-kappaB with wild-type MyD88.
CONCLUSION: Our results show a novel pathway in NF-kappaB activation in
HTLV
-I-transformed T cells and further demonstrate a critical role of MyD88 in their dysregulated gene activation, survival, and proliferation.
[MeSH-major]
Human
T-
lymphotropic virus
1 / physiology. Interleukin-1 Receptor-
Associated
Kinases / metabolism. Myeloid Differentiation Factor 88 / metabolism
[MeSH-minor]
Base Sequence.
Cell
Line, Transformed.
Cell
Transformation, Viral. DNA Primers. Humans. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / metabolism
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(PMID = 17920759.001).
[ISSN]
0301-472X
[Journal-full-title]
Experimental hematology
[ISO-abbreviation]
Exp. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / DNA Primers; 0 / MYD88 protein, human; 0 / Myeloid Differentiation Factor 88; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
63.
Yamazaki T, Sawada U, Kura Y, Ito T, Takeuchi J, Hatta Y, Aikawa S, Takei K, Ishizuka H, Saiki M, Uenogawa K:
Treatment of high-risk peripheral T-cell lymphomas other than anaplastic large-cell lymphoma with a dose-intensified CHOP regimen followed by high-dose chemotherapy. A single institution study.
Acta Haematol
; 2006;116(2):90-5
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[Title]
Treatment of high-risk peripheral T-
cell lymphomas
other than anaplastic large-
cell
lymphoma
with a dose-intensified CHOP regimen followed by high-dose chemotherapy. A single institution study.
We investigated the efficacy of a dose-intensified double-CHOP regimen followed by high-dose chemotherapy with or without peripheral blood stem
cell
transplantation (PBSCT) in 11 patients with four types of peripheral T-
cell
lymphoma
(PTCL).
Three of the 4 patients with unspecified PTCL (PTCLu) achieved complete response (CR); 1 patient relapsed and 1 died of secondary
leukemia
after consolidation therapy.
All angioimmunoblastic T-
cell
lymphoma
(AILT) and subcutaneous panniculitis-like T-
cell
lymphoma
(SPTCL) patients achieved CR; 5 of 6 have remained
disease
free for more than 3 years.
The patient with hepatosplenic
lymphoma
did not achieve CR even after PBSCT and underwent allogenic bone marrow transplantation (allo-BMT).
However, allo-BMT should be considered for high-risk of PTCLu and hepatosplenic T-
cell
lymphoma
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Lymphoma
, T-
Cell
/ drug therapy
[MeSH-minor]
Adolescent.
Adult
. Aged. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Retrospective Studies. Vincristine / administration & dosage
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.
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CYCLOPHOSPHAMIDE
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PREDNISOLONE
.
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VINCRISTINE
.
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(PMID = 16914902.001).
[ISSN]
0001-5792
[Journal-full-title]
Acta haematologica
[ISO-abbreviation]
Acta Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VAP-cyclo protocol
64.
Park CW, Kim A, Cha SW, Jung SH, Yang HW, Lee YJ, Lee HIe, Kim SH, Kim YH:
A case of phlegmonous gastritis associated with marked gastric distension.
Gut Liver
; 2010 Sep;4(3):415-8
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[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
65.
Arisawa K, Soda M, Ono M, Uemura H, Hiyoshi M, Suyama A:
Trends of incidence rate of adult T-cell leukemia/lymphoma in an HTLV-1 endemic area in Japan.
Int J Cancer
; 2009 Aug 1;125(3):737-8
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[Title]
Trends of incidence rate of
adult T
-
cell leukemia
/
lymphoma
in an
HTLV
-1 endemic area in Japan.
[MeSH-major]
Endemic Diseases.
HTLV
-I Infections / epidemiology.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ epidemiology
[MeSH-minor]
Adult
. Age Distribution. Aged. Aged, 80 and over. Female. Humans. Incidence. Japan / epidemiology. Male. Middle Aged. Odds Ratio. Registries. Risk Assessment. Risk Factors. Time Factors
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(PMID = 19437534.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Comparative Study; Letter
[Publication-country]
United States
66.
Venkitaraman R, Sagar TG, George MK:
Adult T-cell lymphoma with HTLV-I and HTLV-II infection.
South Med J
; 2007 Nov;100(11):1178-9
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[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
67.
Miyagi T, Nagasaki A, Taira T, Shinhama A, Suzuki M, Ohshima K, Takasu N:
Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature.
Leuk Lymphoma
; 2009 Feb;50(2):187-95
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[Title]
Extranodal
adult T
-
cell leukemia
/
lymphoma
of the head and neck: a clinicopathological study of nine cases and a review of the literature.
Extranodal
adult T
-
cell leukemia
/
lymphoma
(
ATLL
) of the head and neck is a rare
disease
.
We studied the clinicopathological features of nine patients with
ATLL
involving extranodal head and neck sites and conducted a literature review.
Histopathology included diffuse pleomorphic-type (with angiocentric features), Hodgkin-like and anaplastic large
cell
-type.
Five patients with localised
disease
showed prolonged survival regardless of unfavourable histology and/or aberrant provirus status, including integration of multiple copies or defective provirus.
Patients with localised
disease
documented in the literature, including our study series, had a reduced frequency of elevated lactate dehydrogenase, no hypercalcemia and longer survival.
ATLL
should be included in the differential
diagnosis
of extranodal head and neck
lymphoma
.
Localised extranodal
ATLL
of the head and neck may exhibit indolent
clinical
behaviours.
[MeSH-major]
Head and Neck Neoplasms / pathology.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ pathology
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed
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[CommentIn]
Leuk Lymphoma. 2009 Feb;50(2):148-9
[
19235009.001
]
[CommentIn]
Leuk Lymphoma. 2009 Feb;50(2):150-1
[
19235010.001
]
(PMID = 19197730.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
England
[Number-of-references]
50
68.
Janik JE, Morris JC:
Survivin(g) adult T-cell leukemia/lymphoma.
Oncology (Williston Park)
; 2009 Dec;23(14):1256, 1261, 1266
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[Title]
Survivin(g)
adult T
-
cell leukemia
/
lymphoma
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / genetics. Hematopoietic Stem
Cell
Transplantation.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ drug therapy.
Leukemia
-
Lymphoma
,
Adult T
-
Cell
/ therapy. Microtubule-
Associated
Proteins / genetics
[MeSH-minor]
Adult
. Female. Gene Expression Profiling. Humans. Inhibitor of Apoptosis Proteins. Male. Transplantation, Homologous
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[CommentOn]
Oncology (Williston Park). 2009 Dec;23(14):1250-6
[
20120837.001
]
(PMID = 20120838.001).
[ISSN]
0890-9091
[Journal-full-title]
Oncology (Williston Park, N.Y.)
[ISO-abbreviation]
Oncology (Williston Park, N.Y.)
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Comment; Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins
69.
Boström H, Leuchowius KJ, Hallböök H, Nordgren A, Thörn I, Thorselius M, Rosenquist R, Söderberg O, Sundström C:
U-2973, a novel B-cell line established from a patient with a mature B-cell leukemia displaying concurrent t(14;18) and MYC translocation to a non-IG gene partner.
Eur J Haematol
; 2008 Sep;81(3):218-25
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[Title]
U-2973, a novel B-
cell
line established from a patient with a mature B-
cell leukemia
displaying concurrent t(14;18) and MYC translocation to a non-IG gene partner.
B-
cell lymphomas
/
leukemias
with simultaneous t(14;18)(q32;q21) and MYC rearrangements have recently been shown to constitute a separate diagnostic entity, presenting with a rapid
clinical
course and a very poor prognosis.
We describe the establishment of an Epstein-Barr
virus
negative
cell
line, designated U-2973, from a male patient with
a de
novo aggressive B-
cell
lymphoma
/
leukemia
and very high peripheral blast
cell
count.
Flow cytometry of bone marrow cells and U-2973 displayed a mature B-
cell
phenotype, and immunostaining showed expression of MYC and BCL2.
[MeSH-major]
Cell
Line. Chromosomes,
Human
, Pair 14 / genetics. Chromosomes,
Human
, Pair 18 / genetics.
Leukemia
, B-
Cell
/ genetics.
Lymphoma
, B-
Cell
/ genetics. Proto-Oncogene Proteins c-myc / genetics. Translocation, Genetic
[MeSH-minor]
Adult
. Base Sequence. Bone Marrow Cells / pathology. Chromosome Aberrations. Chromosomes,
Human
, Pair 12 / genetics. Cytogenetic Analysis. Flow Cytometry / methods. Genes, Immunoglobulin / genetics. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukocyte Count. Male. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis / methods. Phenotype. Polymorphism, Single Nucleotide / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics
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(PMID = 18510704.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc
70.
Nascimento MC, Primo J, Bittencourt A, Siqueira I, de Fátima Oliveira M, Meyer R, Schriefer A, Santos SB, Carvalho EM:
Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis.
Clin Exp Immunol
; 2009 Jun;156(3):455-62
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[Title]
Infective dermatitis has similar immunological features to
human
T
lymphotropic virus
-type 1-
associated
myelopathy/tropical spastic paraparesis.
Human
T
lymphotropic virus
-type 1 (
HTLV
-1) is the causal agent of the
HTLV
-1-
associated
myelopathy/tropical spastic paraparesis (HAM/TSP),
adult T cell
leukaemia
/
lymphoma
and infective dermatitis
associated
with
HTLV
-1 (IDH).
Over-production of proinflammatory cytokines and an increase in
HTLV
-1 proviral load are features of HAM/TSP, but the immunological basis of IDH has not been established.
In this study we determined the immune response in patients with IDH measuring interleukin (IL)-4, IL-5, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels as well as the
HTLV
-1 proviral load.
HTLV
-1 carriers and patients with HAM/TSP served as controls.
TNF-alpha and IFN-gamma levels were higher in IDH than in
HTLV
-1 carriers.
There was a tendency for higher IL-4 mRNA expression and immunoglobulin E (IgE) levels in IDH than in
HTLV
-1 carriers, but the difference did not reach statistical significance.
The
HTLV
-1 proviral load was significantly higher in IDH patients than in
HTLV
-1 carriers.
IDH is characterized by an exaggerated Th1 immune response and high
HTLV
-1 proviral load.
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(PMID = 19438598.001).
[ISSN]
1365-2249
[Journal-full-title]
Clinical and experimental immunology
[ISO-abbreviation]
Clin. Exp. Immunol.
[Language]
ENG
[Grant]
United States / FIC NIH HHS / TW / D43 TW007127; United States / FIC NIH HHS / TW / TW007127-05; United States / FIC NIH HHS / TW / D43 TW007127-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cytokines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 37341-29-0 / Immunoglobulin E; 82115-62-6 / Interferon-gamma
[Other-IDs]
NLM/ PMC2691974
71.
Mizuguchi M, Asao H, Hara T, Higuchi M, Fujii M, Nakamura M:
Transcriptional activation of the interleukin-21 gene and its receptor gene by human T-cell leukemia virus type 1 Tax in human T-cells.
J Biol Chem
; 2009 Sep 18;284(38):25501-11
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[Title]
Transcriptional activation of the interleukin-21 gene and its receptor gene by
human
T-
cell leukemia
virus
type 1 Tax in
human
T-cells.
At the incipient stages of the development of
adult T
-
cell leukemia
, T-cells infected with
human
T-
cell leukemia
virus
type 1 (
HTLV
-1) suffer disregulation in
cell
growth caused by aberrant expression of host genes by the
HTLV
-1 transactivator protein Tax (Tax1).
Tax1-mediated growth promotion is thought to result from, at least in part, up-regulation of genes for growth factors and their receptors that induce T-
cell
growth.
In the present study, we demonstrate that Tax1 transactivates the interleukin-21 (IL-21) and its receptor (IL-21R) genes in
human
T-cells.
Chromatin immunoprecipitation assay and gel mobility shift assay exhibited that the IL-21 promoter elements bound transcription factors AP-1 and NF-kappaB, and the IL-21R promoter elements were
associated
with AP-1 and interferon regulatory factor.
The related
virus HTLV
-2 with Tax2 similar to Tax1 is known not to be pathogenic.
The study suggests insights into cytokine-dependent aberrant growth of
HTLV
-1-infected T-cells and the molecular basis of different pathogenicity between
HTLV
-1 and
HTLV
-2.
[MeSH-major]
CD4-
Positive
T-Lymphocytes / metabolism. Gene Products, tax / metabolism.
Human
T-
lymphotropic virus
1 / metabolism. Interleukin-21 Receptor alpha Subunit / biosynthesis. Interleukins / biosynthesis. Response Elements. Transcriptional Activation
[MeSH-minor]
Adenoviridae.
HTLV
-I Infections / genetics.
HTLV
-I Infections / metabolism.
Human
T-
lymphotropic virus
2 / genetics.
Human
T-
lymphotropic virus
2 / metabolism.
Human
T-
lymphotropic virus
2 / pathogenicity. Humans. Jurkat Cells. NF-kappa B / genetics. NF-kappa B / metabolism. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism. Transduction, Genetic
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[Cites]
Lancet. 1986 May 3;1(8488):1031-2
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2871307.001
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(PMID = 19617351.001).
[ISSN]
1083-351X
[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 / Gene Products, tax; 0 / IL21R protein, human; 0 / Interleukin-21 Receptor alpha Subunit; 0 / Interleukins; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 0 / interleukin-21; 0 / tax protein, Human T-lymphotrophic virus 1; 0 / tax protein, Human T-lymphotrophic virus 2
[Other-IDs]
NLM/ PMC2757951
72.
Silveira-Lacerda Ede P, Vilanova-Costa CA, Hamaguchi A, Pavanin LA, Goulart LR, Homsi-Brandenburgo MI, Dos Santos WB, Soares AM, Nomizo A:
The ruthenium complex cis-(dichloro)tetraammineruthenium(III) chloride presents selective cytotoxicity against murine B cell lymphoma (A-20), murine ascitic sarcoma 180 (S-180), human breast adenocarcinoma (SK-BR-3), and human T cell leukemia (Jurkat) tumor cell lines.
Biol Trace Elem Res
; 2010 Jun;135(1-3):98-111
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[Title]
The ruthenium complex cis-(dichloro)tetraammineruthenium(III) chloride presents selective cytotoxicity against murine B
cell
lymphoma
(A-20), murine ascitic sarcoma 180 (S-180),
human
breast adenocarcinoma (SK-BR-3), and
human
T cell leukemia
(Jurkat) tumor
cell
lines.
The aim of present study was to verify the in vitro antitumor activity of a ruthenium complex, cis-(dichloro)tetraammineruthenium(III) chloride (cis-[RuCl(2)(NH(3))(4)]
Cl
) toward different tumor
cell
lines.
The antitumor studies showed that ruthenium(III) complex presents a relevant cytotoxic activity against murine B
cell
lymphoma
(A-20), murine ascitic sarcoma 180 (S-180),
human
breast adenocarcinoma (SK-BR-3), and
human
T cell leukemia
(Jurkat)
cell
lines and a very low cytotoxicity toward
human
peripheral blood mononuclear cells.
The cytotoxic activity of a high concentration (2 mg mL(-1)) of cis-[RuCl(2)(NH(3))(4)]
Cl
toward Jurkat cells correlated with an increased number of annexin V-
positive
cells and also the presence of DNA fragmentation, suggesting that this compound induces apoptosis in tumor cells.
Thus, a mechanistic understanding of how metal complexes achieve their activities is crucial to their
clinical
success and to the rational design of new compounds with improved potency.
[MeSH-minor]
Animals. Breast Neoplasms / drug therapy.
Cell
Cycle / drug effects.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Cytotoxicity, Immunologic / drug effects.