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Results: 1 to 10 of 13

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miR-223 regulates cell growth and targets proto-oncogenes in mycosis fungoides/cutaneous T-cell lymphoma.
McGirt LY, Adams CM, Baerenwald DA, Zwerner JP, Zic JA, Eischen CM
(2014) J Invest Dermatol 134: 1101-1107
MeSH Terms: 3' Untranslated Regions, Animals, Biopsy, Cell Line, Tumor, Cell Proliferation, Cell Survival, Disease Progression, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Leukocytes, Mononuclear, Lymphoma, T-Cell, Cutaneous, Mice, MicroRNAs, Mycosis Fungoides, NIH 3T3 Cells, Proto-Oncogenes, Skin
Show Abstract · Added March 5, 2014
The pathogenesis of the cutaneous T-cell lymphoma (CTCL), mycosis fungoides (MF), is unclear. MicroRNA (miRNA) are small noncoding RNAs that target mRNA leading to reduced mRNA translation. Recently, specific miRNA were shown to be altered in CTCL. We detected significantly reduced expression of miR-223 in early-stage MF skin, and further decreased levels of miR-223 in advanced-stage disease. CTCL peripheral blood mononuclear cells and cell lines also had reduced miR-223 as compared with controls. Elevated expression of miR-223 in these cell lines reduced cell growth and clonogenic potential, whereas inhibition of miR-223 increased cell numbers. Investigations into putative miR-223 targets with oncogenic function, including E2F1 and MEF2C, and the predicted miR-223 target, TOX, revealed that all three were targeted by miR-223 in CTCL. E2F1, MEF2C, and TOX proteins were decreased with miR-223 overexpression, whereas miR-223 inhibition led to increased protein levels in CTCL. In addition, we showed that the 3'-UTR of TOX mRNA was a genuine target of miR-223. Therefore, reduced levels of miR-223 in MF/CTCL lead to increased expression of E2F1, MEF2C, and TOX, which likely contributes to the development and/or progression of CTCL. Thus, miR-223 and its targets may be useful for the development of new therapeutics for MF/CTCL.
0 Communities
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18 MeSH Terms
Inhibition of histone deacetylase 3 causes replication stress in cutaneous T cell lymphoma.
Wells CE, Bhaskara S, Stengel KR, Zhao Y, Sirbu B, Chagot B, Cortez D, Khabele D, Chazin WJ, Cooper A, Jacques V, Rusche J, Eischen CM, McGirt LY, Hiebert SW
(2013) PLoS One 8: e68915
MeSH Terms: Antineoplastic Agents, Apoptosis, Cell Line, Tumor, Cell Proliferation, Chromatin, DNA Damage, DNA Replication, Drug Synergism, Histone Deacetylase Inhibitors, Histone Deacetylases, Humans, Lymphoma, T-Cell, Cutaneous, S Phase, Stress, Physiological
Show Abstract · Added September 5, 2013
Given the fundamental roles of histone deacetylases (HDACs) in the regulation of DNA repair, replication, transcription and chromatin structure, it is fitting that therapies targeting HDAC activities are now being explored as anti-cancer agents. In fact, two histone deacetylase inhibitors (HDIs), SAHA and Depsipeptide, are FDA approved for single-agent treatment of refractory cutaneous T cell lymphoma (CTCL). An important target of these HDIs, histone deacetylase 3 (HDAC3), regulates processes such as DNA repair, metabolism, and tumorigenesis through the regulation of chromatin structure and gene expression. Here we show that HDAC3 inhibition using a first in class selective inhibitor, RGFP966, resulted in decreased cell growth in CTCL cell lines due to increased apoptosis that was associated with DNA damage and impaired S phase progression. Through isolation of proteins on nascent DNA (iPOND), we found that HDAC3 was associated with chromatin and is present at and around DNA replication forks. DNA fiber labeling analysis showed that inhibition of HDAC3 resulted in a significant reduction in DNA replication fork velocity within the first hour of drug treatment. These results suggest that selective inhibition of HDAC3 could be useful in treatment of CTCL by disrupting DNA replication of the rapidly cycling tumor cells, ultimately leading to cell death.
2 Communities
5 Members
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14 MeSH Terms
Open-label pilot study of combination therapy with rosiglitazone and bexarotene in the treatment of cutaneous T-cell lymphoma.
Sepmeyer JA, Greer JP, Koyama T, Zic JA
(2007) J Am Acad Dermatol 56: 584-7
MeSH Terms: Aged, Anticarcinogenic Agents, Bexarotene, Biopsy, Needle, Dose-Response Relationship, Drug, Drug Administration Schedule, Drug Therapy, Combination, Female, Follow-Up Studies, Humans, Immunohistochemistry, Lymphoma, T-Cell, Cutaneous, Male, Maximum Tolerated Dose, Middle Aged, Neoplasm Staging, Pilot Projects, Risk Assessment, Rosiglitazone, Single-Blind Method, Survival Analysis, Tetrahydronaphthalenes, Thiazolidinediones, Treatment Outcome
Show Abstract · Added March 20, 2014
Four patients with stable or progressive cutaneous T-cell lymphoma treated with oral bexarotene received oral rosiglitazone. After 16 weeks of combination therapy, skin score decreased in two patients. Pruritus was alleviated in 3 of 4 patients, whereas quality of life was unchanged. Adverse events included hyperlipidemia, anemia, neutropenia, and lymphopenia.
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1 Members
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24 MeSH Terms
Non-Hodgkin's lymphoma involving the liver: clinical and therapeutic considerations.
Salmon JS, Thompson MA, Arildsen RC, Greer JP
(2006) Clin Lymphoma Myeloma 6: 273-80
MeSH Terms: Hepatitis C, Humans, Liver Failure, Liver Neoplasms, Lymphoma, T-Cell, Splenic Neoplasms
Show Abstract · Added June 26, 2014
Primary hepatic non-Hodgkin's lymphoma (NHL) is a rare disease that presents unique diagnostic and therapeutic challenges. Secondary liver involvement by lymphoma is common and can complicate treatment decisions. A review of the published case reports and the few larger series suggests that primary hepatic NHL represents a heterogeneous mixture of disparate diseases rather than a single entity. Presentations vary from the incidental discovery of hepatic abnormalities in an otherwise asymptomatic patient to that of fulminant hepatic failure with rapid progression of encephalopathy to coma and death. The clinical, laboratory, and radiographic characteristics are nonspecific, which means the diagnosis is often not suspected until histopathologic examination of liver tissue. There appears to be a strong association between primary hepatic NHL and the hepatitis C virus. Hepatosplenic T-cell lymphoma has attained its own status as a unique disease, whereas case reports suggest that the spectrum of hepatic lymphoma includes many histologies. Involvement of the liver by lymphoma can compound the difficulty of pursuing aggressive chemotherapy in patients who have a life-threatening illness and impaired metabolism of the most effective drugs. Therapy should be tailored to the individual clinical situation, with consideration of the underlying histology and degree of hepatic insufficiency.
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6 MeSH Terms
Inhibition of antitumor immunity by invariant natural killer T cells in a T-cell lymphoma model in vivo.
Renukaradhya GJ, Sriram V, Du W, Gervay-Hague J, Van Kaer L, Brutkiewicz RR
(2006) Int J Cancer 118: 3045-53
MeSH Terms: Animals, Antigens, CD1, Antigens, CD1d, Cell Line, Tumor, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Female, Flow Cytometry, Granulocyte-Macrophage Colony-Stimulating Factor, Interferon-gamma, Interleukin-13, Killer Cells, Natural, Lymphocyte Activation, Lymphoma, T-Cell, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Time Factors
Show Abstract · Added December 10, 2013
We have investigated the role of the host's CD1d-dependent innate antitumor immune response in a murine T-cell lymphoma model in vivo. We found that C57BL/6 wildtype (WT) mice inoculated with RMA/S cells transfected with murine CD1d1 died at the same rate as mice inoculated with vector-transfected cells. In contrast, natural killer T (NKT) cell-deficient CD1d or Jalpha18 knockout mice inoculated with CD1d-transfected RMA/S cells survived significantly longer than mice inoculated with vector-transfected RMA/S cells, implicating the involvement of invariant NKT (iNKT) cells in inhibiting antitumor activity in vivo. In contrast to the mutant mice, which produced more of the proinflammatory cytokines IFN-gamma and GM-CSF, WT mice produced significantly elevated amounts of IL-13. Antitumor activity in the knockout mice was not due to the development of CD1d-specific cytotoxic T lymphocytes or circulating antibodies. However, iNKT cell numbers were elevated in tumor-bearing mice. Thus, iNKT cells may be playing a negative role in the host's antitumor immune response against T-cell lymphomas in a CD1d-dependent manner.
Copyright 2006 Wiley-Liss, Inc.
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19 MeSH Terms
Allogeneic bone marrow transplantation for chemotherapy-refractory hepatosplenic gammadelta T-cell lymphoma: case report and review of the literature.
Domm JA, Thompson M, Kuttesch JF, Acra S, Frangoul H
(2005) J Pediatr Hematol Oncol 27: 607-10
MeSH Terms: Antineoplastic Combined Chemotherapy Protocols, Bone Marrow Transplantation, Child, Combined Modality Therapy, Drug Resistance, Neoplasm, Female, Flow Cytometry, Humans, Liver Neoplasms, Lymphoma, T-Cell, Receptors, Antigen, T-Cell, gamma-delta, Splenic Neoplasms, Transplantation, Homologous, Whole-Body Irradiation
Show Abstract · Added March 27, 2014
Hepatosplenic gammadelta T-cell lymphoma is an uncommon pediatric disease and is associated with an aggressive and often fatal course. The authors describe the case of an 8-year-old girl who presented with transaminitis and hepatosplenomegaly. Liver biopsy and peripheral blood flow cytometry were diagnostic of hepatosplenic gammadelta T-cell lymphoma. She was treated with multi-agent chemotherapy with cyclophosphamide, vincristine, prednisone, doxorubicin, and high-dose methotrexate but failed to achieve durable remission. She underwent an allogeneic bone marrow transplant from her HLA-identical brother with a preparative regimen including total body irradiation and cyclophosphamide. She is currently alive and has remained in remission for 30 months after transplantation. The authors also review the literature for similar pediatric cases.
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14 MeSH Terms
Histology impacts the outcome of peripheral T-cell lymphomas after high dose chemotherapy and stem cell transplant.
Jagasia M, Morgan D, Goodman S, Hamilton K, Kinney M, Shyr Y, Stein R, Zic J, Greer J
(2004) Leuk Lymphoma 45: 2261-7
MeSH Terms: Adult, Anaplastic Lymphoma Kinase, Disease-Free Survival, Female, Humans, Lymphoma, B-Cell, Lymphoma, Large-Cell, Anaplastic, Lymphoma, T-Cell, Peripheral, Male, Middle Aged, Prognosis, Protein-Tyrosine Kinases, Receptor Protein-Tyrosine Kinases, Recurrence, Stem Cell Transplantation, Time Factors, Treatment Outcome
Show Abstract · Added March 5, 2014
The role of high dose chemotherapy (HDC) and stem cell transplant (SCT) in peripheral T-cell lymphoma (PTCL) was studied in 28 patients, from 1988 to 2002. The aim was to determine if subsets recognized by the REAL/WHO classification have different prognoses. Outcome was compared to 86 patients with diffuse large B-cell lymphoma (DLBCL) transplanted during 1986-2000. The 3-year overall survival (OS) and event free survival (EFS) were 69% and 50%. Patients with anaplastic large cell lymphoma (ALCL) had a better 3-year OS compared to those with non-ALCL histology (86% vs. 47%, P=0.0122). Anaplastic lymphoma kinase (ALK)- positive ALCL patients had a superior EFS compared to ALK-negative ALCL (100% vs. 0; P=0.0228). Patients with cutaneous ALCL (ALK-negative) relapsed, but had an indolent course after SCT. Low International Prognostic Index score at relapse predicted for a better 3-year OS (85% vs. 34%, P=0.0238). When compared to DLBCL, patients with ALCL had a superior OS (86% vs. 36%, P=0.0034) and patients with non-ALCL had a comparable OS. ALCL histology confers better survival compared to non-ALCL and DLBCL histologies. ALK-positive ALCL is associated with the best EFS after relapse with HDC and SCT. The timing of SCT for non-ALCL histology remains to be determined.
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17 MeSH Terms
Peripheral T-cell lymphomas: clinical features and prognostic factors of 92 cases defined by the revised European American lymphoma classification.
Arrowsmith ER, Macon WR, Kinney MC, Stein RS, Goodman SA, Morgan DS, Flexner JM, Cousar JB, Jagasia MH, McCurley TL, Greer JP
(2003) Leuk Lymphoma 44: 241-9
MeSH Terms: Adolescent, Adult, Aged, Aged, 80 and over, Child, Female, Humans, Immunoblastic Lymphadenopathy, Lymphoma, Large B-Cell, Diffuse, Lymphoma, T-Cell, Peripheral, Male, Middle Aged, Prognosis, Retrospective Studies, Survival Analysis, Survival Rate, Treatment Outcome
Show Abstract · Added March 5, 2014
The purpose of this study was to better define the clinical features and natural history of peripheral T-cell lymphomas (PTCL) entities included in the Revised European American lymphoma (REAL) classification. Cases of PTCL were retrieved from the records of the Department of Pathology and classified according to the REAL classification. In addition, cases of anaplastic large cell lymphoma (ALCL) were divided into classical, small cell, and primary cutaneous subtypes, and immunostaining for the anaplastic large-cell kinase (ALK) protein was performed on all cases of ALCL. Clinical features, response to therapy and survival were abstracted. Ninety-two cases of PTCL with adequate clinical information were retrieved. There were 40 cases of ALCL (30 classical, 7 small cell variant, 3 primary cutaneous), 28 PTCL, unspecified, 13 angioimmunoblastic T-cell lymphoma and 11 with other entities. The patients had a median age of 48 years with a range of 6-84 and had an estimated overall survival (OS) of 49% and progression-free survival (PFS) of 22% at 5 years. The International Prognostic Index (IPI) was a significant prognostic factor for both progression-free and OS. Histology was a significant predictor of PFS with anaplastic large cell having the best prognosis. ALK expression was not associated with an improved progression-free or overall-survival in patients with systemic T-cell ALCL. In conclusion, the REAL classification describes distinct PTCL entities. The IPI is the most important predictor of progression-free and OS in patients with PTCL. ALK expression may not provide prognostic information for systemic ALCL.
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17 MeSH Terms
Negative regulation of Wee1 expression and Cdc2 phosphorylation during p53-mediated growth arrest and apoptosis.
Leach SD, Scatena CD, Keefer CJ, Goodman HA, Song SY, Yang L, Pietenpol JA
(1998) Cancer Res 58: 3231-6
MeSH Terms: Animals, Antineoplastic Agents, Apoptosis, Blotting, Western, CDC2 Protein Kinase, Cell Cycle Proteins, Cell Division, Cyclin B, Cyclin B1, Down-Regulation, Embryo, Mammalian, Enzyme Activation, Fibroblasts, G2 Phase, Lymphoma, T-Cell, Mice, Nocodazole, Nuclear Proteins, Phosphorylation, Protein Conformation, Protein-Tyrosine Kinases, Rats, Transformation, Genetic, Tumor Cells, Cultured, Tumor Suppressor Protein p53
Show Abstract · Added February 15, 2016
The G2 cell cycle checkpoint protects cells from potentially lethal mitotic entry after DNA damage. This checkpoint involves inhibitory phosphorylation of Cdc2 at the tyrosine-15 (Y15) position, mediated in part by the Wee1 protein kinase. Recent evidence suggests that p53 may accelerate mitotic entry after DNA damage and that the override of the G2 checkpoint may play a role in the induction of apoptosis by p53. To determine the biochemical mechanism by which p53 inactivates the G2 checkpoint, the effects of p53 activation on Wee1 expression, Cdc2-Y15 phosphorylation, and cyclin B1-associated Cdc2 kinase activity were examined. Under conditions of either growth arrest or apoptosis, p53 activation resulted in the down-regulation of Wee1 expression and dephosphorylation of Cdc2. A parallel increase in cyclin B1/Cdc2 kinase activity was observed during p53-mediated apoptosis. Negative regulation of the Wee1 expression and Cdc2 phosphorylation by p53 was also evident in thymus tissue from p53+/+ mice but not from p53-/- mice. Inactivation of the G2 checkpoint may contribute to the tumor suppressor activity of p53.
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25 MeSH Terms
Rejection of allogeneic and syngeneic but not MHC class I-deficient tumor grafts by MHC class I-deficient mice.
Freland S, Chambers BJ, Andersson M, Van Kaer L, Ljunggren HG
(1998) J Immunol 160: 572-9
MeSH Terms: ATP Binding Cassette Transporter, Subfamily B, Member 2, ATP-Binding Cassette Transporters, Animals, Graft Rejection, Histocompatibility Antigens Class I, Lymphoma, T-Cell, Mast-Cell Sarcoma, Mice, Mice, Inbred C57BL, Mice, Knockout, Neoplasm Transplantation, Sarcoma, Experimental, Species Specificity, Transplantation, Homologous, Transplantation, Isogeneic, Tumor Cells, Cultured, beta 2-Microglobulin
Show Abstract · Added December 10, 2013
The ability of TAP1-/-, beta2m-/-, and TAP1/beta2m-/- mice to mount rejection responses against allogeneic, syngeneic, and MHC class I-deficient tumor grafts was examined. The results demonstrate a potent ability of TAP1-/- and beta2m-/- as well as TAP1/beta2m-/- mice to reject allogeneic tumors. In contrast to published data, rejection of syngeneic MHC class I-expressing tumors was also observed. This response was specific for the MHC class I-deficient mice, since wild-type mice did not reject syngeneic MHC class I-positive tumors under identical experimental conditions. The rejection response of syngeneic tumors required preimmunization of the mice and was MHC class I specific at the level of priming as well as at the level of the tumor target. Finally, MHC class I-deficient tumor grafts were accepted in MHC class I-deficient mice while similar grafts were rejected in wild-type mice. In summary, while MHC class I-deficient mice have retained a capacity to reject allogeneic tumors. they have gained an ability to reject syngeneic MHC class I-positive tumors and lost the ability to reject MHC class I-negative tumors. The present results are discussed in relation to the role of MHC class I molecules in selecting functional CD8+ T and NK cell repertoires, and the development of cell-mediated immunity.
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17 MeSH Terms