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[Title] Splenic diffuse red pulp small B-cell lymphoma: revision of a series of cases reveals characteristic clinico-pathological features.

BACKGROUND: Splenic diffuse red pulp small B-cell lymphoma is an uncommon B-cell lymphoma, now recognized as a provisional entity in the 2008 update of the WHO Classification.

DESIGN AND METHODS: We have retrospectively analyzed the disease features in a highly selected series of 17 patients diagnosed as splenic diffuse red pulp small B-cell lymphoma.

Clinical manifestations were mainly derived from splenomegaly.

All cases showed a purely diffuse pattern of splenic infiltration by monomorphous small cells with small round nuclei and pale cytoplasm.

Peripheral blood cells were small to medium-sized, with clumped chromatin and round nuclear outline and villous cytoplasm.

Neoplastic cells had a CD20(+), CD23(-), bcl6(-), Annexin A1- phenotype, with frequent expression of DBA44+ (15/17) and IgG (10/15).

FCM data had a B-cell phenotype (CD19(+), CD20(+), CD22(+)) with FMC7 (10/11) and CD11c (5/8) expression.

CONCLUSIONS: Our data suggest that splenic diffuse red pulp small B-cell lymphoma is a distinct entity with morphological and immunophenotypical features that differ from those of other splenic lymphomas.

[MeSH-major] Lymphoma, B-Cell / pathology. Splenic Neoplasms / pathology

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(PMID = 20220064.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

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

[Publication-country] Italy

[Other-IDs] NLM/ PMC2895036

   

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[Title] Three-dimensional culturing of the Hodgkin lymphoma cell-line L1236 induces a HL tissue-like gene expression pattern.

To overcome some limitations of in vitro established cell-line tumor models for Hodgkin lymphoma (HL), we explored whether culturing in a three-dimensional (3D) matrix could improve the quality of the model.

The gene expression profile of the 3D-cultured HL derived cell-line L1236 was compared with that of suspension-cultured (2D) L1236, as well as to the gene expression profile found in HL tumor samples.

To validate our results we also included a gene expression data set of laser captured Hodgkin-Reed - Sternberg (H-RS) cells.

We found that the 3D culture affected gene expression of a HL derived cell-line inducing a more tumor-related expression profile.

3D culture affected the expression of 500 genes in L1236, upregulating genes involved in immune response and apoptosis and downregulating genes involved in cell division.

[MeSH-major] Cell Culture Techniques / methods. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Hodgkin Disease / pathology. Reed-Sternberg Cells / pathology

[MeSH-minor] Apoptosis. Biopsy. Cell Line, Tumor. Computational Biology. Humans. Lymph Nodes / pathology. Models, Genetic. Oligonucleotide Array Sequence Analysis. Peptides / chemistry. RNA, Neoplasm / metabolism

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(PMID = 17917972.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Peptides; 0 / RNA, Neoplasm

   

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[Title] [A case of natural killer cell lymphoma with high adenosine deaminase level in pleural effusion].

We finally diagnosed the case as natural killer (NK) cell lymphoma from CT-guided needle biopsy just before death, and necropsy.

In this case, the high level of ADA in the pleural effusion suggested lymphoma.

[MeSH-major] Adenosine Deaminase / metabolism. Killer Cells, Natural. Lymphoma, Non-Hodgkin / diagnosis. Pleural Effusion, Malignant / diagnosis

[MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged. Pleura / pathology

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(PMID = 15997786.001).

[ISSN] 1343-3490

[Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society

[ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi

[Language] jpn

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

[Publication-country] Japan

[Chemical-registry-number] EC 3.5.4.4 / Adenosine Deaminase

   

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[Title] Influence of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone on serologic parameters and clinical course in lymphoma patients with autoimmune diseases.

BACKGROUND: As patients with B-cell lymphomas suffering from an underlying autoimmune condition undergoing therapy with the CD20 antibody rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) offer the unique possibility of monitoring effects of therapy on various rheumatologic parameters, we have evaluated serologic autoimmune markers and the clinical outcome of patients with autoimmune diseases (ADs) who received lymphoma treatment with R-CHOP during the course of their disease.

PATIENTS AND METHODS: We have retrospectively analysed 13 patients with non-Hodgkin's lymphoma who concurrently suffered from ADs and were treated with the R-CHOP regimen.

Ten (77%) patients showed clinical improvement of their autoimmune symptoms, two (15%) reported no difference and one (7%) patient with rheumatoid arthritis-related worsening symptoms during therapy with R-CHOP.

In terms of lymphoma response, 11 patients achieved a complete remission and two a partial remission.

CONCLUSIONS: This analysis indicates that R-CHOP given for lymphoma treatment is also effective for therapy of concurrent rheumatoid diseases.

Both rheumatoid parameters as well as clinical symptoms showed a significant decrease during treatment with this immunochemotherapy.

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[CommentIn] Ann Oncol. 2007 Apr;18(4):615-8 [17355949.001]

(PMID = 17218490.001).

[ISSN] 0923-7534

[Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology

[ISO-abbreviation] Ann. Oncol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9009-79-4 / Rheumatoid Factor; VB0R961HZT / Prednisone

   

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[Title] Diethyl maleate-induced oxidative stress leads to testicular germ cell apoptosis involving Bax and Bcl-2.

Testicular germ cell apoptosis is normally a continuous process throughout life.

However, massive testicular germ cell loss is known to result from a wide variety of cellular stresses including toxicant exposure.

Thus, the present study was aimed to investigate the mechanisms of germ cell loss under stress conditions following diethyl maleate (DEM) exposure.

The germ cell apoptosis was found to be increased as assessed by terminal deoxynucleotidyl transferase (TdT)-mediated deoxy-UTP biotin nick end labeling (TUNEL) staining, evaluation of histoarchitechture of testis, and germ cell numbers.

It was found that the germ cell number was significantly reduced in DEM-treated sections.

RT-PCR was carried out to assess Bax/Bcl-2 mRNA expression levels.

Immunohistochemistry of Bax and Bcl-2 revealed Bax activation.

The prevalence and cellular localization of the above markers in testicular tissues of DEM-treated animals suggest the possible involvement of Bax/Bcl-2 in the male germ cell apoptosis.

[MeSH-major] Apoptosis / drug effects. Maleates / toxicity. Oxidative Stress / drug effects. Spermatozoa / cytology. Spermatozoa / drug effects. Testis / cytology. bcl-2-Associated X Protein / metabolism

[MeSH-minor] Animals. Cell Shape / drug effects. Gene Expression Regulation / drug effects. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Inbred BALB C. RNA, Messenger / genetics. RNA, Messenger / metabolism

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[Copyright] (c) 2008 Wiley Periodicals, Inc.

(PMID = 19110998.001).

[ISSN] 1099-0461

[Journal-full-title] Journal of biochemical and molecular toxicology

[ISO-abbreviation] J. Biochem. Mol. Toxicol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Maleates; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; G81WQB56OL / diethyl maleate

   

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[Title] Dissociation of caspase-mediated events and programmed cell death induced via HLA-DR in follicular lymphoma.

Human leukocyte antigens (HLA) class II antigen-mediated apoptosis has been documented in antigen-presenting cells and B lymphoproliferations.

Characteristics of the apoptosis include rapidity and selectivity for mature cells.

Follicular lymphomas are particularly refractory to apoptosis.

The B-cell lymphoma Ramos shares characteristics of this subgroup and is insensitive to apoptosis via simple HLA-DR engagement.

However, inhibition of caspase activation simply delayed the apoptotic phenotype but neither protected against cell death nor prevented mitochondrial injury.

Finally, blockade of caspase activation in parallel with HLA-DR mAb stimulation could provide a potent autovaccination stimulus by leading to necrotic death of B-cell lymphomas.

[MeSH-major] Apoptosis. Caspase Inhibitors. Caspases / metabolism. HLA-DR Antigens / physiology. Lymphoma, Follicular / genetics. Lymphoma, Follicular / pathology

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(PMID = 16301998.001).

[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 / Antibodies, Monoclonal; 0 / Caspase Inhibitors; 0 / HLA-DR Antigens; EC 3.4.22.- / Caspases

   

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[Title] Direct antilymphoma activity of novel, first-generation "antibody mimics" that bind HLA-DR10-positive non-Hodgkin's lymphoma cells.

A first-generation series of novel small molecules, collectively known as selective high-affinity ligands (SHALs), were designed and synthesized to mimic the binding of Lym-1, a monoclonal antibody (mAb) shown to be an effective cytotoxic and radionuclide carrier molecule for targeting non-Hodgkin's lymphoma (NHL).

Micromolar concentrations of all three SHALs showed binding to Raji, an HLA-DR10-positive human malignant B-cell line but no binding to CEM or Jurkat's, HLA-DR10-negative malignant T-cell lines.

Additionally, the Raji cell membrane distributions of all three SHALs and of Lym-1 were remarkably similar.

Unlike Lym-1, which causes substantial growth inhibition and cell death in NHL cell lines, these SHALs had no direct antilymphoma activity.

In summary, three first-generation SHALs lacked direct antilymphoma activity, although they had selective NHL B-cell binding like Lym-1 mAb.

Because of their small size, these SHALs have potential as radionuclide carrier substitutes for Lym-1 mAb to target the HLA-DR10 NHL-related cell-surface protein.

[MeSH-major] Antibodies, Monoclonal / chemistry. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Biomimetic Materials / chemistry. Biomimetic Materials / pharmacology. HLA-DR Antigens / metabolism. Lymphoma, Non-Hodgkin / metabolism

[MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Cell Line, Tumor. Cell Survival / drug effects. Enzyme-Linked Immunosorbent Assay. HLA-DR Serological Subtypes. Humans. Ligands. Streptavidin / metabolism

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(PMID = 17257080.001).

[ISSN] 1084-9785

[Journal-full-title] Cancer biotherapy & radiopharmaceuticals

[ISO-abbreviation] Cancer Biother. Radiopharm.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 47829

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / HLA-DR Antigens; 0 / HLA-DR Serological Subtypes; 0 / HLA-DR10 antigen; 0 / Ligands; 0 / Lym-1 monoclonal antibody; 9013-20-1 / Streptavidin

   

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[Title] Immunoreactivity of p53, Mdm2, p21(WAF1/CIP1) Bcl-2, and Bax in soft tissue sarcomas: correlation with histologic grade.

Tumor growth depends on 2 distinctive pathways: cell proliferation and apoptosis.

The p53 pathway is an important regulator of the cell cycle as it triggers growth arrest or leads to apoptosis in response to cellular stress and therefore is commonly targeted during tumorigenesis.

Apoptosis is also controlled by the Bcl-2 family, which includes proapoptotic and antiapoptotic proteins.

Immunohistochemical stains for p21(WAF1/CIP1), p53, Mdm2, Bcl-2, and Bax proteins were carried out on tissue microarrays.

Expression of Bax protein was a common finding in soft tissue sarcoma cases.

Bcl-2 was identified in 59 tumors (38.8%) and was more prevalent in high-grade sarcomas (low grade, 25.9%; intermediate grade, 32.5%; high grade, 55.2%).

The expression of p53, p21(WAF1/CIP1), and Bcl-2 is closely associated with the histologic grade of the tumor, and therefore these proteins may be used as prognostic markers.

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(PMID = 17536310.001).

[ISSN] 1541-2016

[Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM

[ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2

   

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[Title] Histone acetylation and DNA demethylation of B cells result in a Hodgkin-like phenotype.

A unique feature of the tumor cells (Hodgkin/Reed-Sternberg (HRS)) of classical Hodgkin lymphoma (cHL) is the loss of their B-cell phenotype despite their B-cell origin.

Several lines of evidence suggest that epigenomic events, especially promoter DNA methylation, are involved in this silencing of many B-cell-associated genes.

Here, we show that DNA demethylation alone or in conjunction with histone acetylation is not able to reconstitute the B-cell-gene expression program in cultured HRS cells.

Instead, combined DNA demethylation and histone acetylation of B-cell lines induce an almost complete extinction of their B-cell-expression program and a tremendous upregulation of numerous Hodgkin-characteristic genes, including key players such as Id2 known to be involved in the suppression of the B-cell phenotype.

Since the upregulation of Hodgkin-characteristic genes and the extinction of the B-cell-expression program occurred simultaneously, epigenetic changes may also be responsible for the malignant transformation of cHL.

The epigenetic upregulation of Hodgkin-characteristic genes thus plays--in addition to promoter DNA hypermethylation of B-cell-associated genes--a pivotal role for the reprogramming of HRS cells and explains why DNA demethylation alone is unable to reconstitute the B-cell-expression program in HRS cells.

[MeSH-major] B-Lymphocytes / metabolism. DNA Methylation. Histones / metabolism. Hodgkin Disease / pathology

[MeSH-minor] Acetylation. Cell Transformation, Neoplastic. Epigenesis, Genetic. Gene Expression Regulation, Neoplastic. Phenotype

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(PMID = 18256685.001).

[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 / Histones

   

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[Title] Postlymphoproliferative disorder affecting bone after a renal transplantation.

OBJECTIVE: To illustrate a posttransplant lymphoproliferative lymphoma presenting as a solitary osseous lesion situated in the rib.

CLINICAL FEATURES: A 53-year-old man was referred to a surgical department because of persistent local pain over the lower part of his left posterior hemithorax.

The histological study of the surgically removed tissue revealed diffuse infiltration of the marrow by lymphoid-like cells.

There was evidence of interstitial fibrosis, and further immunohistochemical examination showed the presence of B cells in the specimen confirming the diagnosis of B-cell lymphoma.

CONCLUSION: This case report discusses an unusual presentation of a lymphoma induced by immunosuppressive therapy in a patient who had received an organ transplant.

[MeSH-major] Bone Neoplasms / etiology. Immunosuppression / adverse effects. Kidney Transplantation. Lymphoma, B-Cell / etiology. Ribs

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(PMID = 15726037.001).

[ISSN] 1532-6586

[Journal-full-title] Journal of manipulative and physiological therapeutics

[ISO-abbreviation] J Manipulative Physiol Ther

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] Marginal zone B-Cell lymphoma among primary B-Cell lymphoma of Waldeyer's ring: histopathologic and immunohistochemical study of 16 tonsillectomy specimens.

Two subtypes of marginal zone B-cell lymphoma (eg, mucosa-associated lymphoid tissue [MALT] type and splenic type) have been reported in the lymph node.

To determine the presence or absence of marginal zone B-cell lymphoma of MALT type and the splenic type among Waldeyer's ring (WR) lymphomas, 16 tonsillectomy specimens were studied.

Ten cases (63%) were marginal zone B-cell lymphoma.

Among marginal zone B-cell lymphoma, 7 were the MALT type and the remaining 3 cases of marginal zone B-cell lymphoma were the splenic type.

Moreover, 4 cases of 7 MALT-type lymphomas contained numerous large cells (diffuse large B-cell lymphoma arising from a low-grade marginal zone B-cell lymphoma of MALT type).

The low incidence of primary mucosa-associated lymphoid tissue type lymphoma of WR in previous reports may be because it is difficult to correctly identify the characteristic histologic findings of MALT-type lymphoma because of the small biopsy size.

[MeSH-major] Lymphoid Tissue / pathology. Lymphoma, B-Cell, Marginal Zone / pathology. Tonsillar Neoplasms / pathology

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(PMID = 18417673.001).

[ISSN] 1066-8969

[Journal-full-title] International journal of surgical pathology

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

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

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[Title] Primary lymphoma of the bladder: case report.

[MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Cyclophosphamide / administration & dosage. Lymphoma, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Urinary Bladder Neoplasms / drug therapy

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(PMID = 16369978.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Letter

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide

   

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[Title] Distribution of t(14;18)-positive, putative lymphoma precursor cells among B-cell subsets in healthy individuals.

The t(14;18)(q32;q21) is the characteristic chromosomal translocation of follicular lymphoma (FL).

The aim of this study was to determine the immunophenotypic markers of t(14;18)-positive cells in HI and to relate these features to lymphocyte maturation.

B cells from 10 subjects with t(14;18)-positive and three subjects with t(14;18)-negative peripheral blood mononuclear cells (PBMC) were fluorescence-activated cell sorted for antigen-naïve (CD27(-)), immunoglobulin M (IgM) memory (IgM(+)CD27(+)) and switched memory (IgM(-) CD27(+)) cells. t(14;18)-recombinations were detected by quantitative PCR.

Among PBMC-positive subjects, t(14;18)-frequency was significantly higher in IgM memory (median: 380/10(6)) than in antigen-naïve (median: 16/10(6)) or switched memory (median: 5/10(6)) B cells.

All PBMC-negative subjects nevertheless had detectable t(14;18) in sorted B cells; levels were lower than in PBMC-positive subjects, but had the same relative predominance.

These results suggest that t(14;18) is generated during early B-cell development in the bone marrow and that affected cells may mature and expand in germinal centres. t(14;18)-frequency was highest in IgM memory cells, a B-cell subset that shares immunophenotypic similarities with FL.

The significance of these cells as lymphoma precursors or indicators of lymphoma risk remains to be established.

[MeSH-minor] Clone Cells. Gene Frequency. Genes, Immunoglobulin. Genes, bcl-2. Humans. Immunologic Memory. Immunophenotyping. Lymphoma, Non-Hodgkin / immunology. Polymerase Chain Reaction

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(PMID = 17614821.001).

[ISSN] 0007-1048

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Grant] United States / Intramural NIH HHS / /

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

[Publication-country] England

   

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[Title] The spectrum of coincident entities with small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) diagnosed by cytology.

BACKGROUND: The cytologic diagnosis of Small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) often relies on finding a small lymphoid population with the characteristic immunoprofile by ancillary testing.

MATERIALS AND METHODS: We retrospectively reviewed all FNA and TP cytology cases between January 2005 and May 2009 with a diagnosis of SLL/CLL to determine the presence of any coincident process.

Coincident entities were identified in nine cases (31%) and included seven (28%) neoplastic entities (Hodgkin lymphoma [HL], adenocarcinoma, squamous cell carcinoma, seminoma) and two (7%) non-neoplastic entities (infection and immunoglobulin containing cells).

Six cases (21%) suspicious for large cell transformation were also identified.

CONCLUSION: In our review of SLL/CLL, coincident entities were present in 31% of the cases and included a spectrum of non-neoplastic and neoplastic processes.

FC was the most frequently utilized ancillary test, but IHC provided important information by excluding a mantle cell lymphoma or confirming a coincident process.

Thus, cytomorphologic evaluation in these patients is important due to the high risk of a coincident process that may not be apparent by FC alone and may require clinical management.

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(PMID = 20976208.001).

[ISSN] 1742-6413

[Journal-full-title] CytoJournal

[ISO-abbreviation] Cytojournal

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Other-IDs] NLM/ PMC2955352

[Keywords] NOTNLM ; Chronic lymphocytic leukemia / SLL/CLL / cytopathology / small lymphocytic lymphoma

   

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[Title] Clinical development of radioimmunotherapy for B-cell non-Hodgkin's lymphoma.

Over the past several decades, several biomolecules have been investigated for their ability to deliver radiation to cancer cells, but antibodies have been the carriers of choice in systemic targeted radionuclide therapy (STaRT).

Food and Drug Administration for the treatment of patients with relapsed or refractory B-cell non-Hodgkin's lymphoma (NHL), and clinical trials have shown that they are effective as monotherapies in the salvage setting, producing response rates that are often higher and durations of response that are often longer than those with chemotherapy.

Escalated doses of these agents can be supported with stem cell transplantation and can produce high rates of complete response and greater survival in patients with relapsed NHL.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Lymphoma, B-Cell / radiotherapy. Radioimmunotherapy / methods

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(PMID = 16979433.001).

[ISSN] 0360-3016

[Journal-full-title] International journal of radiation oncology, biology, physics

[ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / Iodine Radioisotopes; 0 / Yttrium Radioisotopes; 0 / ibritumomab tiuxetan; 0 / iodine-131 anti-B1 antibody

[Number-of-references] 45

   

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[Title] Bcl2/bcl-xL inhibitor engenders apoptosis and increases chemosensitivity in mesothelioma.

Mesothelioma is a neoplasm of the pleura that is currently incurable by conventional therapies.

Previously, we demonstrated that mesothelioma overexpresses BCL-X(L), an anti-apoptotic member of the BCL-2 family.

In addition, we have shown that down regulation of BCL-X(L) using a BCL-X(L) antisense oligonucleotide engenders mesothelioma apoptotic cell death in vitro and in vivo.

The purpose of this study is to evaluate the efficacy of bcl2/bcl-x(L) inhibitor, 2-methoxy antimycin A3, in inducing apoptosis and increasing chemo-sensitivity in vitro and in vivo.

Several bcl-x(L) high-expression tumor cell lines and one normal human cell line were exposed to 2-methoxy antimycin A3.

2-methoxy antimycin A3 demonstrated significant growth inhibition only in these tumor cell lines, with little effect on normal human cells.

Treatment with 2-methoxy antimycin A3 alone resulted in a dramatic increase in the induction of apoptosis in the cancer cells.

Notably, treatment with 2-methoxy antimycin A3 does not alter BCL-2 family protein expression.

Together, these findings indicate that exposure of cancer cells to small molecule Bcl-2/x(L) inhibitors such as 2-methoxy antimycin A3 alone, or in the combination with other chemotherapeutics, may represent a novel therapeutic strategy in treatment of cancer, especially mesothelioma.

[MeSH-major] Antimycin A / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Genes, bcl-2 / drug effects. Mesothelioma / drug therapy. Pleural Neoplasms / drug therapy. bcl-X Protein / drug effects

[MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Humans. In Vitro Techniques

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[CommentIn] Cancer Biol Ther. 2007 Mar;6(3):465-6 [17471026.001]

(PMID = 17224645.001).

[ISSN] 1538-4047

[Journal-full-title] Cancer biology & therapy

[ISO-abbreviation] Cancer Biol. Ther.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / bcl-X Protein; 642-15-9 / Antimycin A

   

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[Title] [Expression of p53, Ki-67, bcl-2, c-erb-2, estrogen, and progesterone receptors in endometrial cancer].

[Transliterated title] Exprese p53, Ki-67, bcl-2, c-erb-2, estrogenového, a progesteronového receptoru v endometriálním karcinomu.

OBJECTIVE: To assess the immunohistochemical expression of p53, bcl-2, c-erb-2, Ki-67, estrogen and progesterone receptors in endometrial cancer patients.

METHODS: We studied 103 cases of primary untreated endometrial carcinoma in which the p53, bcl-2, c-erb-2, Ki-67, estrogen and progesterone receptor antigens were investigated by an immunohistochemical method.

We evaluated the correlations among the immunohistochemical staining assessed by histoscore, and the age, grading, depth of invasion, stage of the neoplasia and extrauterine disease.

p53, bcl-2, c-erb-2, Ki-67, estrogen and progesterone receptors were positive in 49 (48%), 81 (79%).

There was no clear association between immunohistochemical parameters and the age of patients. p53 and Ki-67 overexpression was found to be related to poor grade of differentiation, deeper myometrial invasion, advanced stage of neoplasia and extrauterine spread of disease.

Immunostaining for bcl-2 correlated inversely with FIGO stage, while c-erb-2 was overexpressed in tumors with deeper myometrial invasion.

Estrogen and progesterone receptor positive tumors showed a statistically significant association with clinicopathological parameters of better clinical outcome.

CONCLUSION: The overexpression of p53 and Ki-67 seems to indicate more malignant phenotype, while bcl-2 and c-erb-2 may have a limited role in the identification of high-risk tumors.

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(PMID = 18711961.001).

[ISSN] 1210-7832

[Journal-full-title] Ceska gynekologie

[ISO-abbreviation] Ceska Gynekol

[Language] CZE

[Publication-type] English Abstract; Journal Article

[Publication-country] Czech Republic

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, ErbB-2

   

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[Title] Bcl-2 expression and p38MAPK activity in cells infected with influenza A virus: impact on virally induced apoptosis and viral replication.

Previous reports have shown that various steps in the influenza A virus life cycle are impaired in cells expressing the antiapoptotic protein Bcl-2 (Bcl-2(+) cells).

We demonstrated a direct link between Bcl-2 and the reduced nuclear export of viral ribonucleoprotein (vRNP) complexes in these cells.

However, despite its negative impact on viral replication, Bcl-2 did not prevent host cells from undergoing virally triggered apoptosis.

In infected Bcl-2(+) cells, activated p38MAPK was found predominantly in the cytoplasm, colocalized with Bcl-2, and both Bcl-2 phosphorylation and virally induced apoptosis were diminished by specific inhibition of p38MAPK activity.

In contrast, in Bcl-2-negative (Bcl-2(-)) cells, which are fully permissive to viral infection, p38MAPK activity was predominantly nuclear, and its inhibition decreased vRNP traffic, phosphorylation of viral nucleoprotein, and virus titers in cell supernatants, suggesting that this kinase also contributes to the regulation of vRNP export and viral replication.

This could explain why in Bcl-2(+) cells, where p38MAPK is active in the cytoplasm, phosphorylating Bcl-2, influenza viral replication is substantially reduced, whereas apoptosis proceeds at rates similar to those observed in Bcl-2(-) cells.

Our findings suggest that the impact of p38MAPK on the influenza virus life cycle and the apoptotic response of host cells to infection depends on whether or not the cells express Bcl-2, highlighting the possibility that the pathological effects of the virus are partly determined by the cell type it targets.

[MeSH-major] Influenza A Virus, H1N1 Subtype / physiology. Kidney / physiology. Proto-Oncogene Proteins c-bcl-2 / genetics. p38 Mitogen-Activated Protein Kinases / metabolism

[MeSH-minor] Animals. Apoptosis. Cell Line. DNA Primers. Dogs. Down-Regulation. Humans. Life Cycle Stages. Plasmids. Polymerase Chain Reaction. RNA, Small Interfering / genetics. Transfection. Virus Replication

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(PMID = 19336399.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA Primers; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases

[Other-IDs] NLM/ PMC2708894

   

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[Title] CD14 and CD169 expression in human lymph nodes and spleen: specific expansion of CD14+CD169- monocyte-derived cells in diffuse large B-cell lymphomas.

The mononuclear phagocyte system of human lymphoid tissue comprises macrophages and dendritic cells (DCs).

The heterogeneity of the non-DC mononuclear phagocyte population in human lymphoid tissue has been little addressed.

Here, we studied the expression of 2 monocyte-derived markers, CD14 and CD169 (sialoadhesin), in reactive human lymphoid tissue as well as in a series of 51 B-cell lymphomas by immunohistochemistry on paraffin-embedded tissue.

We confirmed that lymph node sinusoidal monocyte-derived cells were the only population staining for CD169.

Although most sinusoidal histiocytes also expressed CD14, monocyte-derived cells with phagocytosis such as erythrophagocytosis, anthracosis, or tingible bodies macrophage lacked CD14 and CD169.

Among B-cell lymphomas, splenic marginal zone lymphoma was the only one associated with an expansion of the CD14(+)CD169(+) cells in the cords.

With respect to nodal B-cell lymphomas, CD14(+) cells were rare among B-chronic lymphocytic leukemia, follicular lymphoma (FL), mantle cell lymphoma (MCL).

However, strikingly, we found a strong expansion of CD14(+)CD169(-) cells in numerous diffuse large B-cell lymphomas (DLBCLs), except in cases associated with numerous mitoses, apoptotic bodies, and tingible bodies macrophages.

When cultivated in granulocyte/macrophage colony stimulating factor/interleukin 4, DLBCL purified CD14(+) cells differentiate into plasmacytoid cells, expressing DC-specific intercellular adhesion molecule 3-grabbing nonintegrin, suggesting dendritic cell differentiation potential.

[MeSH-major] Antigens, CD14 / metabolism. Lymph Nodes / metabolism. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Membrane Glycoproteins / metabolism. Monocytes / metabolism. Receptors, Immunologic / metabolism. Spleen / metabolism

[MeSH-minor] Biomarkers, Tumor / metabolism. Cell Separation. Dendritic Cells / metabolism. Dendritic Cells / pathology. Flow Cytometry. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Lymphadenitis / metabolism. Lymphadenitis / pathology. Sialic Acid Binding Ig-like Lectin 1

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(PMID = 16360418.001).

[ISSN] 0046-8177

[Journal-full-title] Human pathology

[ISO-abbreviation] Hum. Pathol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD14; 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic; 0 / SIGLEC1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 1

   

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[Title] Efficient tumor cell lysis mediated by a Bcl-X(L) specific T cell clone isolated from a breast cancer patient.

Based on the detection of spontaneous immune responses in cancer patients with cancer of different origin, Bcl-X(L) was recently described as a highly interesting tumor antigen recognized by CD8 positive cytotoxic T lymphocytes.

To further characterize Bcl-X(L) as a tumor antigen we isolated and expanded Bcl-X(L) specific T cells from the peripheral blood of a breast cancer patient hosting a strong Bcl-X(L) specific T cell response.

We describe that HLA-A2 restricted Bcl-X(L) specific T cell clones very efficiently lyse peptide pulsed T2 cells.

Furthermore, tumor cell lines of different origin, i.e., breast cancer, colon cancer, and melanoma, are efficiently lysed in an HLA-dependent manner.

Finally, ex vivo-isolated leukemia cells, but not non-malignant B and T cells are killed by Bcl-X(L) specific T cells.

Our data underline Bcl-X(L) as an universal tumor antigen widely applicable in specific anticancer immunotherapy.

[MeSH-major] Antigens, Neoplasm / immunology. Breast Neoplasms / immunology. Neoplasms / immunology. T-Lymphocytes, Cytotoxic / immunology. bcl-X Protein / immunology

[MeSH-minor] Clone Cells. Cytotoxicity, Immunologic. Female. Flow Cytometry. HLA-A2 Antigen. Humans. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 16850344.001).

[ISSN] 0340-7004

[Journal-full-title] Cancer immunology, immunotherapy : CII

[ISO-abbreviation] Cancer Immunol. Immunother.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HLA-A2 Antigen; 0 / bcl-X Protein

   

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[Title] Requirement for JNK-dependent upregulation of BimL in anti-IgM-induced apoptosis in murine B lymphoma cell lines WEHI-231 and CH31.

The cross-linking of B cell receptor (BCR) undergoes growth arrest, accompanied by apoptosis, in the CH31 and WEHI-231 B lymphoma cells, a model representing primary immature B cells.

In unstimulated cells, BimL protein was complexed with Bcl-x(L) and changed the partner to associate with Bax on the mitochondrial membrane after ligation of BCR, leading to initiation of apoptotic processes.

Retroviral transduction of BimL into WEHI-231 cells overexpressing dominant-negative form of JNK1 (dnJNK1) resulted in a comparable level of apoptotic cells to control cells, whereas the BimL-mediated apoptosis was partially prevented by Bcl-x(L).

[MeSH-major] Apoptosis Regulatory Proteins / genetics. JNK Mitogen-Activated Protein Kinases / metabolism. Lymphoma, B-Cell / metabolism. Membrane Proteins / genetics. Proto-Oncogene Proteins / genetics

[MeSH-minor] Animals. Antibodies, Anti-Idiotypic / administration & dosage. Apoptosis / immunology. Base Sequence. Biological Transport, Active. Cell Line, Tumor. DNA Primers / genetics. Immunoglobulin M. Mice. Protein Isoforms / genetics. Protein Isoforms / metabolism. Receptors, Antigen, B-Cell / metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transduction, Genetic. Up-Regulation. bcl-2-Associated X Protein / metabolism. bcl-X Protein / metabolism

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(PMID = 17007835.001).

[ISSN] 0014-4827

[Journal-full-title] Experimental cell research

[ISO-abbreviation] Exp. Cell Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Apoptosis Regulatory Proteins; 0 / Bax protein, mouse; 0 / Bcl-2-like protein 11; 0 / Bcl2l1 protein, mouse; 0 / DNA Primers; 0 / Immunoglobulin M; 0 / Membrane Proteins; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Receptors, Antigen, B-Cell; 0 / Recombinant Proteins; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases

   

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[Title] New insights into the molecular biology and targeted therapy of cutaneous T-cell lymphomas.

Cutaneous T-cell lymphoma is an extra-nodal non-Hodgkin lymphoma of mature T cells.

These tumor cells home to and persist in the skin,producing a broad spectrum of clinical entities.

Recent results of basic research on tumor biology and tumor immunology as well as molecular genetics of cutaneous T-cell lymphoma have fostered the development of new therapeutic approaches.

Several clinical trials testing these targeted therapies have shown encouraging results.

This article provides an overview of recent research developments and therapeutic strategies for cutaneous T-cell lymphoma.

[MeSH-major] Antineoplastic Agents / administration & dosage. Drug Delivery Systems / trends. Genetic Therapy / trends. Lymphoma, T-Cell / drug therapy. Lymphoma, T-Cell / physiopathology. Skin Neoplasms / drug therapy. Skin Neoplasms / physiopathology

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(PMID = 16686607.001).

[ISSN] 1610-0379

[Journal-full-title] Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG

[ISO-abbreviation] J Dtsch Dermatol Ges

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 90

   

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[Title] Peripheral blood complete remission after splenic irradiation in mantle-cell lymphoma with 11q22-23 deletion and ATM inactivation.

Mantle Cell Lymphoma (MCL) is a well-known histological and clinical subtype of B-cell non-Hodgkin's Lymphomas.

It is usually characterized by an aggressive disease course, presenting with advanced stage disease at diagnosis and with low response rates to therapy.

We herein report a case of MCL with splenomegaly and peripheral blood involvement as main clinical features.

Mainly advocated mechanisms responsible for this phenomenon are considered direct radiation-induced apoptotic cell death, immune modulation via proportional changes of lymphocyte subsets due to known differences in intrinsic radiosensitivity and a radiation-induced cytokine release.

The peculiar intrinsic radiosensitivity pattern of lymphoid cells could probably be explained by well-defined individual genetic and molecular features.

In this context, among NHLs, MCL subtype has the highest rate of ATM (Ataxia Teleangiectasia Mutated) inactivation.

While the ATM gene is thought to play a key-role in detecting radiation-induced DNA damage (especially Double Strand Breaks), recent in vitro data support the hypothesis that ATM loss may actually contribute to the radiosensitivity of MCL cells.

[MeSH-major] Cell Cycle Proteins / genetics. Chromosome Deletion. Chromosomes, Human, Pair 11. DNA-Binding Proteins / genetics. Lymphoma, Mantle-Cell / genetics. Lymphoma, Mantle-Cell / radiotherapy. Protein-Serine-Threonine Kinases / genetics. Spleen / radiation effects. Tumor Suppressor Proteins / genetics

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(PMID = 16956411.001).

[ISSN] 1748-717X

[Journal-full-title] Radiation oncology (London, England)

[ISO-abbreviation] Radiat Oncol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; 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/ PMC1569379

[General-notes] NLM/ Original DateCompleted: 20070726

   

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[Title] Plasmablastic lymphoma: Cytologic findings in 5 cases with unusual presentation.

BACKGROUND: Plasmablastic lymphoma (PBL) is a rare form of non-Hodgkin lymphoma that was once believed to occur primarily in the oral cavity of human immunodeficiency virus-positive individuals.

The presence of the following was evaluated: cellularity, plasmablastic cells, background necrosis (BN), single-cell necrosis (SCN), lymphoglandular bodies (LGB), tingible-body macrophages (TBM), 3-dimensional clusters/sheets, and cytoplasmic vacuoles.

Two patients had the acquired immunodeficiency syndrome and 3 had second non-PBL related malignancies including endometrial carcinoma, lung adenocarcinoma, and small lymphocytic lymphoma.

The most common cytologic features were hypercellularity (80%), plasmablastic cells (73%), SCN (73%), BN (87%), and LGB (66%).

These include hypercellular specimens with abundant plasmablastic cells, LGB, SCN, and BN.

However, although these findings may suggest PBL, a definitive diagnosis requires adjunctive studies including immunohistochemistry and flow cytometry.

[MeSH-major] Lymphoma, Non-Hodgkin / metabolism. Lymphoma, Non-Hodgkin / pathology

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[Copyright] (c) 2008 American Cancer Society.

(PMID = 18683216.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] Stem cell transplantation in childhood non-Hodgkin's lymphomas.

Despite the high cure rates achieved with intensified primary therapies for childhood non-Hodgkin's lymphomas (NHL), the prognosis for children with relapsed or refractory disease is poor.

Dose intensification followed by stem cell transplantation has been used in these circumstances and may provide a curative treatment option for these patients, but the number of children treated using this approach is relatively small and its effectiveness has been difficult to judge.

We summarize the current experience for stem cell transplantation in childhood NHL and offer our recommendations.

[MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, Non-Hodgkin / therapy

[MeSH-minor] Child. Clinical Trials as Topic. Humans. Lymphoma, B-Cell / therapy. Lymphoma, Large-Cell, Anaplastic / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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(PMID = 20661786.001).

[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

   

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[Title] Association of VEGF genetic polymorphisms with the clinical characteristics of non-Hodgkin's lymphoma.

We investigated the possible associations of two polymorphisms (-2578C/A and +936C/T) in the VEGF gene with the clinicopathologic parameters for patients with non-Hodgkin's lymphoma (NHL).

RESULTS: The -2578A allele was significantly associated with less frequent clinical staging III, IV and bone marrow involvement (The odds ratio (OR) 0.59; 95% confidence interval (CI) 0.43-0.82; and OR 0.66; 95% CI 0.48-0.91, respectively).

The TT genotype of the +936C/T polymorphism was significantly associated with less frequent T cell histological type, clinical staging III, IV and bone marrow involvement (OR 0.25; 95% CI 0.07-0.89; OR 0.37; 95% CI 0.15-0.89; and OR 0.31; 95% CI 0.10-0.96, respectively).

The +936 T allele was marginally associated with less frequent bone marrow involvement and with Clinical staging III, IV (OR 0.71; 95% CI 0.49-1.01; and OR 0.70; 95% CI 0.49-1.00, respectively).

None of the evaluated genotypes of -2578C/A was significantly associated with the gender, age, tumor size, B symptoms and immunohistological subtype.

[MeSH-major] Lymphoma, Non-Hodgkin / genetics. Vascular Endothelial Growth Factor A / genetics

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Genotype. Humans. Male. Middle Aged. Neoplasm Staging. Polymorphism, Genetic

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(PMID = 19649652.001).

[ISSN] 1432-1335

[Journal-full-title] Journal of cancer research and clinical oncology

[ISO-abbreviation] J. Cancer Res. Clin. Oncol.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A

   

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CpG 7909, acting through the TLR9 receptor present in B cells and plasmacytoid dendritic cells, stimulates human B-cell proliferation, enhances antigen-specific antibody production and induces interferon-alpha production, interleukin-10 secretion and natural killer cell activity.

In 2002, GlaxoSmithKline (GSK) was granted a worldwide, non-exclusive licence to Coley's CpG immunostimulatory oligonucleotides, including CpG 7909 [VaxImmune], for their use as adjuvants for cancer vaccines.

A phase I/II trial in patients with NHL has also been conducted in 24 patients with relapsed or refractory disease at the University of Iowa.

These trials are evaluating CpG 7909 in combination with chemotherapy versus chemotherapy alone as a first-line treatment for patients with advanced (stage IIIb or IV) non-small-cell lung cancer (NSCLC).

[MeSH-major] Lymphoma, Non-Hodgkin / drug therapy. Oligodeoxyribonucleotides / administration & dosage. Oligodeoxyribonucleotides / adverse effects

[MeSH-minor] Adjuvants, Immunologic / administration & dosage. Adjuvants, Immunologic / adverse effects. Anthrax Vaccines / administration & dosage. Anthrax Vaccines / adverse effects. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Clinical Trials, Phase I as Topic. Humans. Rituximab. Toll-Like Receptor 9 / agonists

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(PMID = 16922592.001).

[ISSN] 1174-5886

[Journal-full-title] Drugs in R&D

[ISO-abbreviation] Drugs R D

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] New Zealand

[Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Anthrax Vaccines; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Oligodeoxyribonucleotides; 0 / ProMune; 0 / TLR9 protein, human; 0 / Toll-Like Receptor 9; 4F4X42SYQ6 / Rituximab

[Number-of-references] 14

   

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[Title] Regression of large B-cell non-Hodgkin's lymphoma of stomach with HAART: case report and review.

[MeSH-major] Antiretroviral Therapy, Highly Active. Lymphoma, AIDS-Related / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Stomach Neoplasms / drug therapy

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(PMID = 16886274.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

   

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OBJECTIVE: It has been reported that high-dose cytarabine (HD-AraC) was very effective for childhood hematological malignancies, especially for improving the long-term survival of high-risk acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), and T-cell lymphoid malignancies (T-ALL, T-cell non-Hodgkin's lymphoma).

METHODS: The drug levels of Ara-C in plasma and cerebrospinal fluid were detected with HPLC while HD-AraC was used, the expression of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) mRNA in human leukemia cell lines and the bone marrow cells were investigated in 48 cases of childhood hematological malignancies with RT-PCR methods, and the relationship between the expression of these enzymes mRNA and the outcome of the patients was analyzed. RESULTS:.

There were no significant differences in expressions of dCK in T-ALL and B lineage ALL. (3) In vitro study found that the expressions of dCK and CDA mRNA did not change in leukemia cell lines incubated at different doses and times of Ara-C.

[MeSH-minor] Child. Cytidine Deaminase / genetics. Deoxycytidine Kinase / genetics. Gene Expression. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / genetics. Lymphoma, Non-Hodgkin / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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(PMID = 19099730.001).

[ISSN] 0578-1310

[Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics

[ISO-abbreviation] Zhonghua Er Ke Za Zhi

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.5.4.5 / Cytidine Deaminase

   

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[Title] [A case of secondary non-Hodgkin's lymphoma of the colon after the treatment for Hodgkin's disease].

[MeSH-major] Colonic Neoplasms / etiology. Hodgkin Disease / therapy. Lymphoma, Non-Hodgkin / etiology. Neoplasms, Second Primary / etiology

[MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Female. Humans. Peripheral Blood Stem Cell Transplantation. Prednisone / administration & dosage. Procarbazine / administration & dosage. Radiotherapy Dosage. Remission Induction. Vincristine / administration & dosage

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(PMID = 15682817.001).

[ISSN] 0446-6586

[Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology

[ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi

[Language] jpn

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; COPP protocol

   

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[Title] B cell lymphomas express CX3CR1 a non-B cell lineage adhesion molecule.

To study the differential expression of cell membrane-bound receptors and their potential role in growth and/or survival of the tumor cells, highly purified follicular lymphoma cells were analyzed, using gene expression analysis, and compared to non-malignant B cell populations.

Filtering the genome for overexpressed genes coding for cell membrane-bound proteins/receptors resulted in a hit list of 27 identified genes.

Among these, we have focused on the aberrant over expression of CX3CR1, in different types of B cell lymphoma, as compared to non-malignant B cells.

We show that CX3CR1, which normally is not expressed on B cells, is expressed both at the mRNA and protein level in several subtypes of lymphoma.

CX3CR1 has also shown to be involved in the homing to specific tissues that express the ligand, CX3CL1, in breast and prostate cancer and may thus be involved in dissemination of lymphoma.

[MeSH-major] B-Lymphocytes / immunology. Lymphoma, Follicular / immunology. Lymphoma, Mantle-Cell / immunology. Palatine Tonsil / immunology. Receptors, Chemokine / analysis

[MeSH-minor] Cell Separation. Flow Cytometry. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis

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(PMID = 18060687.001).

[ISSN] 0304-3835

[Journal-full-title] Cancer letters

[ISO-abbreviation] Cancer Lett.

[Language] eng

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

[Publication-country] Ireland

[Chemical-registry-number] 0 / CX3CR1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Chemokine

   

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[Title] Bcl-2 inhibitors potentiate the cytotoxic effects of radiation in Bcl-2 overexpressing radioresistant tumor cells.

PURPOSE: Bcl-2, an inhibitor of apoptosis frequently shows elevated expression in human tumors, thus resulting in resistance to radiation therapy.

Therefore, inhibiting Bcl-2 function may enhance the radiosensitivity of tumor cells.

Tetrocarcin A (TC-A) and bcl-2 antisense oligonucleotides exhibit antitumor activity by inhibiting Bcl-2 function and transcription, respectively.

We investigated whether these antitumor agents would enhance the cytotoxic effects of radiation in tumor cells overexpressing Bcl-2.

METHODS AND MATERIALS: We used HeLa/bcl-2 cells, a stable Bcl-2-expressing cell line derived from wild-type HeLa (HeLa/wt) cells.

Cells were incubated with TC-A and bcl-2 antisense oligonucleotides for 24 h after irradiation, and cell viability was then determined.

Apoptotic cells were quantified by flow cytometric assay.

RESULTS: The HeLa/bcl-2 cells were more resistant to radiation than HeLa/wt cells.

At concentrations that are not inherently cytotoxic, both TC-A and bcl-2 antisense oligonucleotides increased the cytotoxic effects of radiation in HeLa/bcl-2 cells, but not in HeLa/wt cells.

However, in HeLa/bcl-2 cells, additional treatment with TC-A in combination with radiation did not significantly increase apoptosis.

CONCLUSIONS: The present results suggest that TC-A and bcl-2 antisense oligonucleotides reduce radioresistance of tumor cells overexpressing Bcl-2.

Therefore, a combination of radiotherapy and Bcl-2 inhibitors may prove to be a useful therapeutic approach for treating tumors that overexpress Bcl-2.

[MeSH-major] Aminoglycosides / pharmacology. Apoptosis. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Radiation Tolerance / drug effects. Radiation-Sensitizing Agents / pharmacology

[MeSH-minor] Analysis of Variance. Cell Survival / drug effects. Cell Survival / radiation effects. HeLa Cells / drug effects. HeLa Cells / metabolism. HeLa Cells / radiation effects. Humans. RNA, Messenger / antagonists & inhibitors. Tumor Stem Cell Assay

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(PMID = 15667975.001).

[ISSN] 0360-3016

[Journal-full-title] International journal of radiation oncology, biology, physics

[ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Aminoglycosides; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Radiation-Sensitizing Agents; 73666-84-9 / tetrocarcin A

   

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[Title] Personalized immunotherapy for the treatment of non-Hodgkin's lymphoma: a promising approach.

In patients with B-cell lymphomas, particularly indolent lymphoma, the use of passive immunotherapy, such as the anti-CD20 monoclonal antibody rituximab, has made an impressive impact on patient outcome.

Personalized immunotherapy, a method that triggers the immune system to mount a response against tumor cells, has shown promising results in early clinical trials in hematologic malignancies.

Currently, 3 large phase III studies are evaluating the efficacy and safety of personalized immunotherapy in patients with follicular lymphoma.

It is hoped that the results of these studies will lead to the incorporation of this promising approach into the standard treatment of patients with lymphoma.

[MeSH-major] Cancer Vaccines. Hodgkin Disease / immunology. Immunotherapy / methods

[MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Combined Modality Therapy. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Humans

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(PMID = 16447298.001).

[ISSN] 0278-0232

[Journal-full-title] Hematological oncology

[ISO-abbreviation] Hematol Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor

[Number-of-references] 64

   

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[Title] Vaccinia virus anti-apoptotic F1L is a novel Bcl-2-like domain-swapped dimer that binds a highly selective subset of BH3-containing death ligands.

Some viruses express proteins homologous in sequence and function to mammalian pro-survival Bcl-2 proteins.

Anti-apoptotic F1L expressed by vaccinia virus is essential for survival of infected cells, but it bears no discernable sequence homology to proteins other than its immediate orthologues in related pox viruses.

Here we report that the crystal structure of F1L reveals a Bcl-2-like fold with an unusual N-terminal extension.

Structural comparison of F1L with other Bcl-2 family members reveals a novel sequence signature that redefines the BH4 domain as a structural motif present in both pro- and anti-apoptotic Bcl-2 members, including viral Bcl-2-like proteins.

[MeSH-major] Protein Structure, Quaternary. Protein Structure, Tertiary. Proto-Oncogene Proteins c-bcl-2 / chemistry. Viral Proteins / chemistry. Viral Proteins / metabolism

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(PMID = 18551131.001).

[ISSN] 1350-9047

[Journal-full-title] Cell death and differentiation

[ISO-abbreviation] Cell Death Differ.

[Language] eng

[Databank-accession-numbers] PDB/ 2VTY

[Grant] United States / NCI NIH HHS / CA / CA43540; United States / NCI NIH HHS / CA / CA80188

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

[Publication-country] England

[Chemical-registry-number] 0 / F1L protein, vaccinia virus; 0 / Ligands; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Proteins; 0 / Viral Proteins

   

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Overexpression of antiapoptotic members of the Bcl-2 family is observed in approximately 80% of B-cell lymphomas, contributing to intrinsic and acquired drug resistance.

ABT-737 is a BH3-only mimetic and potent inhibitor of the antiapoptotic Bcl-2 family members Bcl-2, Bcl-X(L), and Bcl-w.

In vitro, ABT-737 exhibited concentration-dependent cytotoxicity against a broad panel of lymphoma cell lines including mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL).

ABT-737 showed synergism when combined with the proteasome inhibitors bortezomib or carfilzomib in select lymphoma cell lines and induced potent mitochondrial membrane depolarization and apoptosis when combined with either.

ABT-737 plus bortezomib also induced significant apoptosis in primary samples of MCL, DLBCL, and chronic lymphocytic leukemia (CLL) but no significant cytotoxic effect was observed in peripheral blood mononuclear cells from healthy donors.

Collectively, these data suggest that ABT-737 alone or in combination with a proteasome inhibitor represents a novel and potentially important platform for the treatment of B-cell malignancies.

[MeSH-major] Antineoplastic Agents / pharmacology. Biphenyl Compounds / pharmacology. Enzyme Inhibitors / pharmacology. Lymphoma / enzymology. Lymphoma / pathology. Molecular Mimicry / drug effects. Nitrophenols / pharmacology. Proteasome Inhibitors. Sulfonamides / pharmacology

[MeSH-minor] Animals. Boronic Acids / pharmacology. Bortezomib. Cell Death / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm / drug effects. Drug Synergism. Health. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukocytes, Mononuclear / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / pathology. Membrane Potential, Mitochondrial / drug effects. Mice. Microscopy, Confocal. Piperazines / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Pyrazines / pharmacology. Tissue Donors. Xenograft Model Antitumor Assays

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(PMID = 18591385.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / ABT-737; 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Nitrophenols; 0 / Piperazines; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Sulfonamides; 69G8BD63PP / Bortezomib

   

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[Title] Aberrant somatic hypermutations in thyroid lymphomas.

To determine a possible role of aberrant somatic hypermutation (ASHM) in the pathogenesis of thyroid lymphoma (TL), mutational status of genes affected by ASHM, including c-MYC, PIM-1, PAX-5 and RhoH/TTF, was analyzed.

Tumor specimens from 33 patients with thyroid B-cell lymphoma and 14 with chronic lymphocytic thyroiditis (CLTH), an autoimmune thyroiditis known to provide a basis for TL development, was examined.

Occurrence of ASHM in PIM-1, RhoH/TTF, and c-MYC was a constant finding in follicular lymphoma (FL) (all of 11 cases) but not so frequent in diffuse large B-cell lymphoma (DLBCL) (4 (33.3%) of 12 cases) and Marginal zone B-cell lymphoma (MZBCL) (1 (10.0%) of 10 cases).

[MeSH-major] Lymphoma, Non-Hodgkin / genetics. Mutation. Thyroid Neoplasms / genetics

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(PMID = 19019431.001).

[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

   

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[Title] Expression of a soluble decoy receptor 3 in patients with diffuse large B-cell lymphoma predicts clinical outcome.

It is regarded as a decoy receptor released from tumor cells to escape host immune response by neutralizing the cytotoxic and immunomodulatory effects of FasL, LIGHT and TL1A.

Overexpression of DcR3 has been observed in several human malignancies; however, only limited information exists on the role of DcR3 in non-Hodgkin lymphoma especially for B-cell origin.

In the current study, the expression profile of DcR3 was analyzed by RT-PCR and immunohistochemistry (IHC) in a set of lymphoma cell lines including T-cell and B-cell lymphomas.

The result demonstrated that overexpression of DcR3 was detected in most T-cell lymphoma cells, which was consistent with previous reports.

Interestingly, overexpression of DcR3 was also detected both in the B-cell lymphoma cell lines and diffuse large B cell lymphoma (DLBCL) patients.

An in vitro study showed that neutralization of DcR3 increased the percentage of doxorubicin-mediated apoptosis in two B-cell lymphoma cell lines, which indicated the possibility of DcR3 mediated chemo-resistance in B-cell lymphomas.

We suggest that overexpression of DcR3 is associated with a worse prognosis in DLBCL and the possible mechanism may act through the increase of chemo-resistance of lymphoma cells.

[MeSH-major] Biomarkers, Tumor / analysis. Drug Resistance, Neoplasm / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Receptors, Tumor Necrosis Factor, Member 6b / biosynthesis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Gene Expression. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Lymphoma, T-Cell / metabolism. Lymphoma, T-Cell / mortality. Lymphoma, T-Cell / pathology. Male. Middle Aged. Prednisone / therapeutic use. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Vincristine / therapeutic use

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(PMID = 18695885.001).

[ISSN] 1019-6439

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

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

[Publication-country] Greece

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / TNFRSF6B protein, human; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol

   

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[Title] Blood viscosity in patients with diffuse large B cell non-Hodgkin's lymphoma.

The aim of the study was to evaluate blood viscosity as possible marker of disease progression in patients with newly diagnosed non-Hodgkin's lymphoma (NHL).

[MeSH-major] Blood Viscosity. Lymphoma, B-Cell / blood. Lymphoma, Large B-Cell, Diffuse / blood

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(PMID = 17285120.001).

[ISSN] 1812-9269

[Journal-full-title] Experimental oncology

[ISO-abbreviation] Exp. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Ukraine

   

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[Title] [Autologous hematopoietic stem cell transplantation for aggressive B-cell non-Hodgkin's lymphoma].

To evaluate the results of high-dose chemotherapy (HDT) and autologous hematopoietic stem cell transplantation (ASCT) in patients with diffuse B-cell aggressive non-Hodgkin's lymphoma(NHL).

The 5-year probability of disease-free survival for patients in the low-risk group and in the high-risk group was 68.8% and 60.0%,respectively (p = 0.9 6).

[MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, B-Cell / therapy. Lymphoma, Large B-Cell, Diffuse / therapy. Transplantation, Autologous

[MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Disease-Free Survival. Drug Administration Schedule. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Nitrosourea Compounds / administration & dosage. Remission Induction. Treatment Outcome

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(PMID = 16352929.001).

[ISSN] 0385-0684

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

[ISO-abbreviation] Gan To Kagaku Ryoho

[Language] jpn

[Publication-type] English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Nitrosourea Compounds; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin; RYH2T97J77 / ranimustine

   

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[Title] Notch-regulation upon Dll4-stimulation of TGFb-induced apoptosis and gene expression in human B-cell non-Hodgkin lymphomas.

Notch-signalling has been implicated as a pathogenetic factor and a therapeutical target in T-cell leukaemias and in some lymphomas of B-cell origin.

Our aim was to investigate the role of Notch-signalling in apoptosis regulation in human non-Hodgkin B-cell lymphoma (B-NHL) cell lines and in primary chronic lymhocytic leukaemia (CLL) cells using Delta-like 4 (Dll4) ligand mediated Notch activation and gamma-secretase inhibitor (GSI) mediated Notch inhibition in vitro.

Modulation of Notch-signalling by itself did not change the rate of apoptosis in B-NHL cell lines and in CLL cells.

TGFb-induced apoptosis was decreased - but not completely abolished - by GSI in TGFb-sensitive cell lines, but resistance to the apoptotic effects of TGFb were not reversed by Notch activation or inhibition.

We identified Hairy/Enhancer of Split (HES)-1 as a TGFb target gene in selected - TGFb-sensitive - B-NHL cell lines.

[MeSH-major] Apoptosis / drug effects. Intercellular Signaling Peptides and Proteins / pharmacology. Lymphoma, B-Cell / pathology. Receptors, Notch / physiology. Transforming Growth Factor beta / pharmacology

[MeSH-minor] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Line, Tumor. Dipeptides / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Homeodomain Proteins / genetics. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Repressor Proteins / genetics. Signal Transduction

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(PMID = 20017807.001).

[ISSN] 1365-3083

[Journal-full-title] Scandinavian journal of immunology

[ISO-abbreviation] Scand. J. Immunol.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DLL4 protein, human; 0 / Dipeptides; 0 / HEY2 protein, human; 0 / Homeodomain Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / N-(N-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester; 0 / Receptors, Notch; 0 / Repressor Proteins; 0 / Transforming Growth Factor beta; 149348-15-2 / HES1 protein, human; EC 3.4.- / Amyloid Precursor Protein Secretases

   

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[Title] [Primary intraocular B-cell lymphoma: case report].

[Transliterated title] Linfoma intra-ocular primário de células tipo B: relato de caso.

Ocular non-Hodgkin's lymphoma is a rare condition that can involve the retina, the vitreous and the optic nerve.

It can occur alone or can be associated with lymphoma of the central nervous system and a frequent manifestation is a posterior uveitis of difficult treatment.

This kind of ocular tumor is difficult and a challenge to diagnosis.

We describe a case of non-Hodgkin's intraocular B-cell lymphoma in a 47-year-old woman who had a posterior uveitis as the first manifestation.

We emphasize the importance of a careful investigation and of the general clinical examination since this is the most common type in the eye.

We expect to call the attention to this disease that many times appears in an unspecific form with unspecific symptoms.

[MeSH-major] Eye Neoplasms / diagnosis. Lymphoma, B-Cell / diagnosis

[MeSH-minor] Female. Humans. Lymphoma, Non-Hodgkin / diagnosis. Middle Aged. Uveitis / diagnosis

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(PMID = 17906772.001).

[ISSN] 0004-2749

[Journal-full-title] Arquivos brasileiros de oftalmologia

[ISO-abbreviation] Arq Bras Oftalmol

[Language] por

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

[Publication-country] Brazil

   

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[Title] Translocation (18;22)(q21;q11) in B-cell lymphomas: a report of 4 cases and review of the literature.

Follicular lymphomas characteristically carry t(14;18)(q32;q21) which results in IGH-BCL-2 fusion.

Variant translocations that juxtapose the BCL-2 gene with the immunoglobulin kappa (2p11) and lambda (22q11) light chain genes are rare.

We report 4 cases of B-cell lymphoma/leukemia associated with t(18;22)(q21;q11).

Three cases were classified as chronic lymphocytic leukemia, and one as follicular lymphoma based on morphology and immunophenotype.

Fluorescence in situ hybridization analysis was performed on all 4 cases using a BCL-2 breakapart probe.

The BCL-2 gene was rearranged in all cases.

These cases illustrate that t(18;22)(q21;q11) is more commonly observed in chronic lymphocytic leukemia and may represent either an initial or secondary genetic event.

[MeSH-major] Chromosomes, Human, Pair 18. Chromosomes, Human, Pair 22. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, B-Cell / genetics

[MeSH-minor] Aged. Fatal Outcome. Female. Gene Rearrangement, B-Lymphocyte. Genes, bcl-2. Humans. Male. Middle Aged. Translocation, Genetic

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(PMID = 18656237.001).

[ISSN] 1532-8392

[Journal-full-title] Human pathology

[ISO-abbreviation] Hum. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 25

   

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[Title] A complete response with rituximab in metastatic diffuse large B-cell lymphoma of the testis: case report.

Primary testicular lymphoma is an uncommon testicular tumour.

We present a case of a primary non-Hodgkin lymphoma of the testis, describing its clinical and pathological features and discussing our treatment strategy.

Light microscopy demonstrated the classic appearance of a diffuse large B-cell lymphoma.

The immunohistochemical study showed tumour cells intensively positive for CD45, Ki67 and CD20.

No evidence of extra-testicular involvement by lymphoma was found.

At 6 months, a TC-PET showed a clinical relapse in lung and abdominal lymphonodes, while clinical examination demonstrated a single, indolent and erythematous nodule in the left foot.

The histologic analysis confirmed diagnosis of CD-20 positive B-cell lymphoma.

After 3 months a complete response was observed in all sites of disease.

The patient was free from disease at 12 months follow-up.

[MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Lymphoma, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Testicular Neoplasms / drug therapy

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(PMID = 17624254.001).

[ISSN] 0394-6320

[Journal-full-title] International journal of immunopathology and pharmacology

[ISO-abbreviation] Int J Immunopathol Pharmacol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab

   

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[Title] Clinical, laboratory, and histopathologic features of equine lymphoma.

Clinical, laboratory and tissue findings from 37 horses with lymphoma were investigated.

Tumor cell morphology was heterogeneous in 17 tumors, and 8 tumors had marked histiocytic and multinucleated giant cell infiltrates.

Extensive necrosis or focal fibrosis was present in 22 and 4 lymphomas, respectively.

Staining of tumor sections with antibodies against CD3 and CD79alpha molecules resulted in classification of T-cell (n = 26) or B-cell (n = 7) origin.

Most T-cell tumors comprised small to medium CD3(+) lymphocytes, whereas 5 of 7 B-cell tumors were infiltrated by numerous small T lymphocytes and classified as T-cell-rich B-cell lymphoma.

Fresh tumor cells from 6 horses bound antibodies reactive with equine CD4, CD5, CD8, CD21, or major histocompatibility class II molecules, confirming T-cell (n = 5) or B-cell origin (n = 1).

These findings suggest that T-cell lymphoma is more common than B-cell lymphoma in horses and that inflammation, possibly from tumor cytokine production, is frequent.

[MeSH-major] Horse Diseases / pathology. Lymphoma / veterinary

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(PMID = 17099148.001).

[ISSN] 0300-9858

[Journal-full-title] Veterinary pathology

[ISO-abbreviation] Vet. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Non-Hodgkin lymphoma (NHL) subtypes defined by common translocations: utility of fluorescence in situ hybridization (FISH) in a case-control study.

We used fluorescence in situ hybridization (FISH) assays to identify t(14;18) translocations in archival paraffin-embedded tumor sections from non-Hodgkin lymphoma (NHL) cases enrolled in a population-based study. t(14;18) was identified in 54% of 152 cases, including 39% of diffuse large cell lymphomas (26 of 66 cases) and 84% of follicular lymphomas (36 of 43 cases).

Eighty-seven percent of t(14;18)-positive cases and 57% of t(14;18)-negative cases expressed bcl-2.

FISH assays detected twice as many t(14;18)-positive follicular lymphomas as PCR assays.

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[Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.

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(PMID = 19505720.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] ENG

[Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NCI NIH HHS / CA / R21 CA107966-01; United States / NICHD NIH HHS / HD / R24 HD050924; United States / NCI NIH HHS / CA / R03 CA71617-01; United States / NIEHS NIH HHS / ES / P30ES10126; United States / NCI NIH HHS / CA / CA107966-01

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

[Publication-country] England

[Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2

[Other-IDs] NLM/ NIHMS157999; NLM/ PMC2815151

   

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[Title] A novel Bcl-2-like inhibitor of apoptosis is encoded by the parapoxvirus ORF virus.

Apoptotic cell death forms part of the host defense against virus infection.

We tested orf virus, a member of the poxvirus family, for the ability to inhibit apoptosis and found that orf virus-infected cells were fully resistant to UV-induced changes in cell morphology, caspase activation, and DNA fragmentation.

These features are comparable to the antiapoptotic properties of the mitochondrial regulator Bcl-2.

Furthermore, bioinformatic analyses revealed sequence and secondary-structure similarities to Bcl-2 family members, including characteristic residues of all four Bcl-2 homology domains.

Consistent with this, the viral protein inhibited the UV-induced activation of the proapoptotic Bcl-2 family members Bax and Bak.

ORFV125 is the first parapoxvirus apoptosis inhibitor to be identified, and we propose that it is a new antiapoptotic member of the Bcl-2 family.

[MeSH-minor] Apoptosis. Caspases / metabolism. DNA Fragmentation / radiation effects. Enzyme Activation / genetics. Enzyme Activation / radiation effects. HeLa Cells. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. Mitochondria / metabolism. Protein Structure, Secondary. Protein Structure, Tertiary. Ultraviolet Rays. bcl-2 Homologous Antagonist-Killer Protein / genetics. bcl-2 Homologous Antagonist-Killer Protein / metabolism. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism

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(PMID = 17475653.001).

[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 / Inhibitor of Apoptosis Proteins; 0 / Viral Proteins; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases

[Other-IDs] NLM/ PMC1933275

   

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[Title] Efficacy and safety of tositumomab and iodine-131 tositumomab (Bexxar) in B-cell lymphoma, progressive after rituximab.

PURPOSE: To determine overall response (OR) and complete response (CR) rates, response duration, progression-free (PFS) and overall survival and safety with the tositumomab and iodine-131 tositumomab ((131)I tositumomab) therapeutic regimen in patients with indolent, follicular large-cell, or transformed B-cell lymphoma, progressive after rituximab.

CONCLUSION: (131)I tositumomab is effective in CD20-positive lymphoma progressive after rituximab, with a 65% OR rate and median PFS of 24.5 months for responders.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Lymphoma, B-Cell / radiotherapy. Radioimmunotherapy

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(PMID = 15613695.001).

[ISSN] 0732-183X

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / iodine-131 anti-B1 antibody; 4F4X42SYQ6 / Rituximab

   

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[Title] CD4-negative variant of CD4+/CD56+ hematodermic neoplasm: description of three cases.

BACKGROUND: CD4+/CD56+ hematodermic neoplasm (HN) (blastic natural killer (NK)-cell lymphoma) is a rare entity characterized by dense, monomorphous infiltrates of medium-sized cells with blastic appearance and a characteristic immunophenotype (positivity for CD4, CD56 and CD123).

The term 'CD4+/CD56+ hematodermic neoplasm' adopted in the World Health Organization-European Organization for Research and Treatment of Cancer classification of cutaneous lymphomas may be misleading and should probably be revised in the light of all data published in the literature.

[MeSH-major] Antigens, CD4 / metabolism. Antigens, CD56 / metabolism. Killer Cells, Natural / pathology. Lymphoma, Non-Hodgkin / pathology. Skin Neoplasms / pathology

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(PMID = 18494823.001).

[ISSN] 1600-0560

[Journal-full-title] Journal of cutaneous pathology

[ISO-abbreviation] J. Cutan. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Denmark

[Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor

   

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[Title] EBV-induced human CD8(+) NKT cells synergise CD4(+) NKT cells suppressing EBV-associated tumours upon induction of Th1-bias.

CD8(+) natural killer T (NKT) cells from EBV-associated tumour patients are quantitatively and functionally impaired.

EBV-induced CD8(+) NKT cells drive syngeneic T cells into a Th1-bias response to suppress EBV-associated malignancies.

IL-4-biased CD4(+) NKT cells do not affect either syngeneic T cell cytotoxicity or Th cytokine secretion.

Circulating mDC1 cells from patients with EBV-associated malignancies impair the production of IFN-gamma by CD8(+) NKT cells.

In this study, we have established a human-thymus-SCID chimaera model to further investigate the underlying mechanism of EBV-induced CD8(+) NKT cells in suppressing EBV-associated malignancies.

In the human-thymus-SCID chimera, EBV-induced CD8(+) NKT cells suppress EBV-associated malignancies in a manner dependent on the Th1-bias response and syngeneic CD3(+) T cells.

However, adoptive transfer with CD4(+) NKT cells alone inhibits T cell immunity.

Interestingly, CD4(+) NKT cells themselves secrete high levels of IL-2, enhancing the persistence of adoptively transferred CD8(+) NKT cells and T cells, thereby leading to a more pronounced T cell anti-tumour response in chimaeras co-transferred with CD4(+) and CD8(+) NKT cells.

Thus, immune reconstitution with EBV-induced CD4(+) and CD8(+) NKT cells synergistically enhances T cell tumour immunity, providing a potential prophylactic and therapeutic treatment for EBV-associated malignancies.

[MeSH-major] Antigens, CD8 / immunology. Cytotoxicity, Immunologic. Epstein-Barr Virus Infections / immunology. Herpesvirus 4, Human / immunology. Hodgkin Disease / immunology. Hodgkin Disease / therapy. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / therapy. Nasopharyngeal Neoplasms / immunology. Nasopharyngeal Neoplasms / therapy. Natural Killer T-Cells / immunology. Th1 Cells / immunology

[MeSH-minor] Adoptive Transfer. Animals. Antigens, CD4 / immunology. Cell Line, Tumor. Chimera. Humans. Interferon-gamma / metabolism. Interleukin-2 / metabolism. Interleukin-4 / immunology. Lymphocyte Activation. Mice. Mice, SCID. T-Lymphocyte Subsets / immunology. T-Lymphocyte Subsets / metabolism

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[ErratumIn] Cell Mol Immunol. 2011 Jul;8(4):368

(PMID = 19887050.001).

[ISSN] 2042-0226

[Journal-full-title] Cellular & molecular immunology

[ISO-abbreviation] Cell. Mol. Immunol.

[Language] eng

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

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Interleukin-2; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma

[Other-IDs] NLM/ PMC4003220

   

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[Title] Primary uterine lymphoma: report of 2 cases and review of literature.

Primary uterine non-Hodgkin's lymphoma is a rare malignancy.

We here describe 2 patients who presented with cervical growth, stage IE, diffuse large B cell histology.

They achieved complete clinical and radiological response.

[MeSH-major] Lymphoma, Non-Hodgkin / drug therapy. Uterine Neoplasms / drug therapy

[MeSH-minor] Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Humans. Middle Aged. Neoplasm Staging. Prednisone / therapeutic use. Radiotherapy Dosage. Vincristine / therapeutic use

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(PMID = 16813759.001).

[ISSN] 1097-6868

[Journal-full-title] American journal of obstetrics and gynecology

[ISO-abbreviation] Am. J. Obstet. Gynecol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol

[Number-of-references] 30

   

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[Title] Hepatitis C virus productive infection in mononuclear cells from patients with cryoglobulinaemia.

HCV minus strand RNA, the viral replicative intermediate, was searched for by a polyA(+) tract strand-specific Tth-based reverse transcriptase-polymerase chain reaction (RT-PCR) in lymphoid cells of 46 patients with acute and chronic infection.

The HCV replicating form in lymphoid cells was associated strictly with mixed cryoglobulinaemia (MCG), in that it was found in six of 13 (46%) MCG patients, including two with B cell non-Hodgkin's lymphoma (NHL).

These results emphasize the direct role of the virus in the pathogenesis of MCG and support the contention that HCV is not specifically lymphotropic, its entry and replication in lymphoid cells being determined largely by selective interactions.

[MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow Cells / virology. Female. Hepatitis C, Chronic / complications. Humans. Lymphoma, B-Cell / virology. Male. Middle Aged. RNA, Viral / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Virus Replication

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(PMID = 17223964.001).

[ISSN] 0009-9104

[Journal-full-title] Clinical and experimental immunology

[ISO-abbreviation] Clin. Exp. Immunol.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Viral

[Other-IDs] NLM/ PMC1810461

   

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[Title] Dose-escalated CHOEP for the treatment of young patients with aggressive non-Hodgkin's lymphoma: I. A randomized dose escalation and feasibility study with bi- and tri-weekly regimens.

BACKGROUND: To determine the maximum tolerated dose of a bi- and tri-weekly combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone plus etoposide (CHOEP) regimen without stem-cell support.

PATIENTS AND METHODS: Randomized phase I/II multicenter four-level (cyclophosphamide: 1000-1200-1400-1600 mg/m2; doxorubicin: 55-60-65-70 mg/m2; etoposide: 375-450-525-600 mg/m2) dose escalation study with CHOEP-14 and CHOEP-21 in young patients (18-60 years) with newly diagnosed aggressive non-Hodgkin's lymphoma.

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(PMID = 18212092.001).

[ISSN] 1569-8041

[Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology

[ISO-abbreviation] Ann. Oncol.

[Language] ENG

[Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone