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1. Villela L, García M, Caballero R, Borbolla-Escoboza JR, Bolaños-Meade J: Rapid complete response using intrathecal rituximab in a patient with leptomeningeal lymphomatosis due to mantle cell lymphoma. Anticancer Drugs; 2008 Oct;19(9):917-20
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  • [Title] Rapid complete response using intrathecal rituximab in a patient with leptomeningeal lymphomatosis due to mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) is a B-cell lymphoid tumor that expresses CD20 and is associated with a poor prognosis.
  • The patient was treated with intrathecal rituximab (IT-R) 25 mg every third day for five doses with clearance of tumor after the third dose.
  • Systemic therapy consisted of R-HyperCVAD alternating with rituximab, high-dose methotrexate, and cytarabine every 21 days, with IT-R on day 1 of each chemotherapy cycle.
  • The patient was consolidated with an autologous stem cell transplant and remains in remission 23 months later.
  • The use of IT-R and conventional intrathecal chemotherapy in MCLs is discussed here.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Meningeal Neoplasms / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Injections, Spinal. Male. Middle Aged. Rituximab

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  • (PMID = 18766006.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
  • [Other-IDs] NLM/ NIHMS737074; NLM/ PMC4703051
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2. Loomis R, Carbone R, Reiss M, Lacy J: Bcl-2 antisense (G3139, Genasense) enhances the in vitro and in vivo response of Epstein-Barr virus-associated lymphoproliferative disease to rituximab. Clin Cancer Res; 2003 May;9(5):1931-9
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  • These studies showed that G3139 treatment decreased Bcl-2 protein levels in association with antiproliferative and proapoptotic effects in lymphoblastoid cell lines (LCLs) in vitro.
  • In vivo, although G3139 treatment completely abrogated EBV(+) lymphoid tumor engraftment in the human/SCID model of PTLD, antisense treatment alone was not curative in animals with established tumors.
  • Because the humanized anti-CD20 antibody, rituximab, has antitumor activity in patients with PTLD and stimulates apoptosis in some lymphoid cell lines, we sought to determine whether Bcl-2 antisense treatment potentiates the antitumor effects of rituximab in EBV-associated lymphoproliferative disease in vitro and in vivo.
  • Flow cytometric terminal deoxynucleotidyltransferase-mediated nick end labeling assays confirmed that G3139 treatment enhanced the apoptotic response of LCLs to rituximab, and this interaction was oligonucleotide sequence dependent.
  • To test the in vivo efficacy of G3139 and rituximab in the human/SCID model of PTLD, we used a delayed treatment schedule that permitted detection of enhanced antitumor activity of combination therapy.
  • Although G3139 or rituximab treatment significantly prolonged survival compared with untreated controls, 89% of animals in the monotherapy arms died with disseminated tumors.
  • In contrast, 79% of animals in the combined G3139 and rituximab arm remained tumor free for the duration of follow-up (>160 days) with no evidence of tumors at the time of sacrifice, indicating that G3139 in combination with rituximab was curative therapy in the majority of tumor-bearing animals.
  • This is the first report of G3139 potentiating the antitumor activity of an antibody-based therapy both in vitro and in vivo.
  • Bcl-2 antisense oligonucleotide therapy in combination with rituximab may represent a promising nontoxic and effective targeted therapy for EBV-associated lymphoproliferative diseases such as PTLD and ARL.
  • Furthermore, this approach may have broader applications to other Bcl-2- and CD20-expressing lymphoid malignancies.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoproliferative Disorders / therapy. Thionucleotides / pharmacology
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Murine-Derived. Apoptosis / drug effects. Cell Division / drug effects. Combined Modality Therapy. Epstein-Barr Virus Infections / complications. Epstein-Barr Virus Infections / genetics. Epstein-Barr Virus Infections / therapy. Female. Herpesvirus 4, Human. Humans. In Vitro Techniques. Mice. Mice, SCID. Oligonucleotides, Antisense / genetics. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Rituximab. Survival Rate

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  • (PMID = 12738752.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 67396
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Thionucleotides; 4F4X42SYQ6 / Rituximab; 85J5ZP6YSL / oblimersen
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3. Weston VJ, Oldreive CE, Skowronska A, Oscier DG, Pratt G, Dyer MJ, Smith G, Powell JE, Rudzki Z, Kearns P, Moss PA, Taylor AM, Stankovic T: The PARP inhibitor olaparib induces significant killing of ATM-deficient lymphoid tumor cells in vitro and in vivo. Blood; 2010 Nov 25;116(22):4578-87
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  • [Title] The PARP inhibitor olaparib induces significant killing of ATM-deficient lymphoid tumor cells in vitro and in vivo.
  • The Ataxia Telangiectasia Mutated (ATM) gene is frequently inactivated in lymphoid malignancies such as chronic lymphocytic leukemia (CLL), T-prolymphocytic leukemia (T-PLL), and mantle cell lymphoma (MCL) and is associated with defective apoptosis in response to alkylating agents and purine analogues.
  • Poly (ADP-ribose) polymerase (PARP) inhibition that imposes the requirement for DNA double strand break repair should selectively sensitize ATM-deficient tumor cells to killing.
  • We investigated in vitro sensitivity to the poly (ADP-ribose) polymerase inhibitor olaparib (AZD2281) of 5 ATM mutant lymphoblastoid cell lines (LCL), an ATM mutant MCL cell line, an ATM knockdown PGA CLL cell line, and 9 ATM-deficient primary CLLs induced to cycle and observed differential killing compared with ATM wildtype counterparts.
  • Pharmacologic inhibition of ATM and ATM knockdown confirmed the effect was ATM-dependent and mediated through mitotic catastrophe independently of apoptosis.
  • A nonobese diabetic/severe combined immunodeficient (NOD/SCID) murine xenograft model of an ATM mutant MCL cell line demonstrated significantly reduced tumor load and an increased survival of animals after olaparib treatment in vivo.
  • Addition of olaparib sensitized ATM null tumor cells to DNA-damaging agents.
  • We suggest that olaparib would be an appropriate agent for treating refractory ATM mutant lymphoid tumors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Phthalazines / therapeutic use. Piperazines / therapeutic use. Poly(ADP-ribose) Polymerase Inhibitors. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Ataxia Telangiectasia Mutated Proteins. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. DNA Damage / drug effects. Gene Knockdown Techniques. Humans. Mice. Mice, SCID. Mutation

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  • (PMID = 20739657.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G9901249; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Phthalazines; 0 / Piperazines; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 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 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; WOH1JD9AR8 / olaparib
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4. Jares P, Campo E: Advances in the understanding of mantle cell lymphoma. Br J Haematol; 2008 Jun;142(2):149-65
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  • [Title] Advances in the understanding of mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) is a well-defined lymphoid neoplasm characterized by a proliferation of mature B lymphocytes expressing CD5 that may show a spectrum of morphological and phenotypic features broader than initially described.
  • Although some patients may follow an indolent clinical evolution, in most of them the tumour has an aggressive behaviour with poor response to conventional chemotherapy.
  • In addition to this translocation, MCL may carry a high number of secondary chromosomal and molecular alterations that target regulatory elements of the cell cycle machinery and senescence (BMI1/INK4/ARF/CDK4/RB1), DNA damage response pathways (ATM/CHK2/p53), and cell survival signals.
  • The knowledge of these mechanisms and their influence on the behaviour of the tumour are facilitating the development of prognostic models with a more precise prediction of the clinical evolution of the patients.
  • This information coupled with the availability of a new generation of innovative drugs targeting basic molecular process of the tumour cells, should facilitate the design of new therapeutic protocols able to overcome the resistance of this aggressive lymphoma to conventional treatments and improve the life expectancy of the patients.
  • [MeSH-major] Cell Cycle / genetics. Cyclin D1 / genetics. DNA Damage / genetics. Lymphoma, Mantle-Cell / physiopathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Humans. Immunotherapy. Translocation, Genetic


5. Chestovich PJ, Schiller G, Sasu S, Hiatt JR: Duodenal lymphoma: a rare and morbid tumor. Am Surg; 2007 Oct;73(10):1057-62
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  • [Title] Duodenal lymphoma: a rare and morbid tumor.
  • We conducted a retrospective tumor registry review of a 36-year experience in a university center and identified 10 patients with duodenal lymphoma (five localized, five disseminated).
  • Histologic types included diffuse large B-cell in four patients, mucosa-associated lymphoid tumor in three, and Hodgkin, follicular, and unclassified (one each).
  • Treatments included chemotherapy in four patients, radiation therapy (RT) in two patients, Helicobacter pylori treatment in two, and observation in one.
  • Surgical patients were younger and had more advanced lesions and less favorable cell types.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Female. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / surgery. Lymphoma, B-Cell, Marginal Zone / drug therapy. Male. Middle Aged. Prognosis. Retrospective Studies

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  • (PMID = 17983081.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 43
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6. Murase T, Inagaki H, Takagi N, Okabe M, Eimoto T: Nasal NK-cell lymphoma followed by relapse in the uterine cervix. Leuk Lymphoma; 2002 Jan;43(1):203-6
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  • [Title] Nasal NK-cell lymphoma followed by relapse in the uterine cervix.
  • We report a case of nasal natural killer (NK)-cell lymphoma in a 51-year-old Japanese woman who showed a later relapse in the uterine cervix.
  • The nasal NK-cell lymphoma regressed after local radiation therapy.
  • Six months after the diagnosis while the patient was being treated with chemotherapy for a subclinical tumor, a mass lesion of the uterine cervix was noticed by follow-up computed tomography.
  • Giemsa-stained vaginal smear showed lymphoid tumor cells with large azurophilic granules, leading to a rapid diagnosis of cervical involvement by NK-cell lymphoma.
  • The chemotherapy regimens were immediately changed, but the patient died 2 months after the relapse with an overall survival of 8 months.
  • This case may be of value in elucidating the biological behavior and natural history of NK-cell lymphoma.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoma, T-Cell / pathology. Nose Neoplasms / pathology. Uterine Cervical Neoplasms / pathology
  • [MeSH-minor] Fatal Outcome. Female. Humans. Immunohistochemistry. Middle Aged. Neoplasm Invasiveness / pathology. Recurrence


7. Shiratori S, Kondo T, Kubota K, Wakasa K, Ibata M, Shono Y, Takahata M, Shigematu A, Kato N, Ota S, Tanaka J, Matsuno Y, Asaka M, Imamura M: [Loss of CD20 expression following rituximab-combined chemotherapy in CD20-positive and CyclinD1-positive multiple myeloma]. Rinsho Ketsueki; 2008 Nov;49(11):1536-40
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  • [Title] [Loss of CD20 expression following rituximab-combined chemotherapy in CD20-positive and CyclinD1-positive multiple myeloma].
  • The use of rituximab (RIT) in the treatment of CD20-positive MM has been reported, however its effectiveness is still not well established.
  • We encountered a case of CD20-positive/CyclinD1-positive MM; interestingly, CD20 expression could not be detected in MM cells following RIT-combined chemotherapy, while it gradually recovered when RIT therapy was discontinued.
  • This is the first report in which the transition of CD20 expression was accurately analyzed by flow cytometry and immunohistochemical staining before, during and after RIT treatment.
  • Consequently, this case provides insight regarding the mechanism through which CD20 expression is lost following RIT therapy for CD20-positive lymphoid neoplasm, as well as the efficacy of RIT in CD20-positive MM.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD20 / analysis. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / analysis. Cyclin D1 / analysis. Multiple Myeloma / drug therapy. Multiple Myeloma / genetics
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Female. Gene Expression. Humans. Middle Aged. Rituximab. Treatment Outcome

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  • (PMID = 19047784.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / CCND1 protein, human; 136601-57-5 / Cyclin D1; 4F4X42SYQ6 / Rituximab
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8. Pui CH, Schrappe M, Ribeiro RC, Niemeyer CM: Childhood and adolescent lymphoid and myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2004;:118-45
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  • [Title] Childhood and adolescent lymphoid and myeloid leukemia.
  • Remarkable progress has been made in the past decade in the treatment and in the understanding of the biology of childhood lymphoid and myeloid leukemias.
  • With contemporary improved risk assessment, chemotherapy, hematopoietic stem cell transplantation and supportive care, approximately 80% of children with newly diagnosed acute lymphoblastic leukemia and 50% of those with myeloid neoplasm can be cured to date.
  • Ching-Hon Pui describes certain clinical and biologic features that still have prognostic and therapeutic relevance in the context of contemporary treatment programs.
  • He emphasizes that treatment failure in some patients is not due to intrinsic drug resistance of leukemic cells but is rather caused by suboptimal drug dosing due to host compliance, pharmacodynamics, and pharmacogenetics.
  • Finally, he contends that with optimal risk-directed systemic and intrathecal therapy, cranial irradiation may be omitted in all patients, regardless of the presenting features.
  • Martin Schrappe performs detailed analyses of the prognostic impact of presenting age, leukocyte count, sex, immunophenotype, genetic abnormality, early treatment response, and in vitro drug sensitivity/resistance in childhood acute lymphoblastic leukemia, based on the large database of the Berlin-Frankfurt-Münster consortium.
  • He also succinctly summarizes the important treatment components resulting in the improved outcome of children and young adolescents with this disease.
  • He describes the treatment approach that led to the improved outcome of adolescent patients, a finding that may be applied to young adults in the second and third decade of life.
  • Finally, he believes that treatment reduction under well-controlled clinical trials is feasible in a subgroup of patients with excellent early treatment response as evidenced by minimal residual disease measurement during induction and consolidation therapy.
  • Raul Ribeiro describes distinct morphologic and genetic subtypes of acute myeloid leukemia.
  • He then describes the principles of treatment as well as the efficacy and toxicity of various forms of postremission therapy, emphasizing the need of tailoring therapy to both the disease and the age of the patient.
  • She then describes the various treatment approaches for both juvenile myelomonocytic leukemia and myelodysplastic syndromes in the US and Europe, emphasizing the differences between childhood and adult cases for the latter group of diseases.
  • She also raises some controversial issues regarding treatment that will require well-controlled international clinical trials to address.

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  • (PMID = 15561680.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-36401; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / CA-71907; United States / NCI NIH HHS / CA / CA-71970; United States / NCI NIH HHS / CA / CA-78224; United States / NCI NIH HHS / CA / CA20180; United States / NIGMS NIH HHS / GM / GM-61374; United States / NIGMS NIH HHS / GM / GM-61393
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 157
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9. Miles RR, Afify Z, Yaish H, Perkins SL: CD56-negative extranodal nasal type NK/T-cell lymphoma. Pediatr Blood Cancer; 2010 Jul 15;55(1):186-9
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  • [Title] CD56-negative extranodal nasal type NK/T-cell lymphoma.
  • Extranodal natural killer (NK)/T-cell lymphoma, nasal type, is a rare lymphoma that occurs predominantly in Asian adults.
  • In this report, we describe the clinical and pathologic features of an unusual aggressive lymphoid neoplasm in a child and review the literature on NK/T-cell lymphoma in children.
  • Biopsy demonstrated neoplastic lymphoid cells that expressed CD3, CD8, TIA-1, and EBV-encoded RNA without CD56.
  • The patient failed multiagent chemotherapy and died of therapy-related complications.
  • This case represents an extranodal NK/T-cell lymphoma, nasal type, with an unusual lack of CD56.
  • [MeSH-major] Lymphoma, Extranodal NK-T-Cell / drug therapy
  • [MeSH-minor] Antigens, CD56 / biosynthesis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child, Preschool. Fatal Outcome. Humans. Male

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  • (PMID = 20486184.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56
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10. D'Costa S, Slobod KS, Hurwitz JL: Do the immunosuppressive drugs used as treatment for graft-versus-host disease directly inhibit lymphoid tumor cell growth? Leuk Lymphoma; 2003 Jan;44(1):139-42
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  • [Title] Do the immunosuppressive drugs used as treatment for graft-versus-host disease directly inhibit lymphoid tumor cell growth?
  • Hematopoietic stem cell transplantation (HSCT) is a curative treatment for certain leukemias and lymphomas that prove resistant to standard chemotherapy.
  • The immunosuppressive drugs prednisone and cyclosporin A (CsA) are routinely used during HSCT to prevent or treat graft-versus-host disease (GVHD) or to inhibit antibody-mediated inflammation.
  • However, little is known about the direct impact of prednisone and CsA on the growth of malignant lymphoid cells in the setting of HSCT.
  • To address this issue, we measured tumor cell growth in vitro and in vivo after treatment with prednisone and CsA, used separately, together, and in combination with irradiation.
  • Our results showed that: (i) combinations of CsA and prednisone inhibited the growth of a variety of lymphoid tumors in vitro, particularly in combination with irradiation, and (ii) tumor size was significantly reduced in a mouse B-lymphoid tumor model following CsA or CsA plus prednisone treatments, with or without HSCT.
  • [MeSH-major] Graft vs Host Disease / drug therapy. Immunosuppressive Agents / pharmacology. Lymphoma / pathology. Lymphoma / therapy
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Division / drug effects. Cell Division / radiation effects. Cyclosporine / pharmacology. Cyclosporine / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Hematopoietic Stem Cell Transplantation / methods. Humans. Mice. Mice, SCID. Prednisone / pharmacology. Prednisone / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 12691154.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30-CA21765; United States / NCI NIH HHS / CA / R01-CA57419
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; VB0R961HZT / Prednisone
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11. Aref S, El-Sherbiny M, Mabed M, Menessy A, El-Refaei M: Urokinase plasminogen activator receptor and soluble matrix metalloproteinase-9 in acute myeloid leukemia patients: a possible relation to disease invasion. Hematology; 2003 Dec;8(6):385-91
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  • Extracellular proteolytic enzymes of the urokinase-type plasminogen activator (uPA) and metalloproteinase (MMP) family play a crucial role in the matrix degradation and tissue remodeling process characteristic of malignant disorders.
  • Although the biological significance of MMP-9 and soluble urokinase receptor in growth and progression of lymphoid neoplasm is understood, its clinical significance in acute myeloid leukemia (AML) has not been fully elucidated.
  • In this study, we determined the levels of soluble urokinase-type plasminogen activator receptor (suPAR), cellular uPAR and sMMP-9 in 43 newly diagnosed AML patients at diagnosis, before chemotherapy, and also studied 10 normal subjects served as a control group.
  • After chemotherapy suPAR and MMP-9 were determined at remission and relapse.
  • The levels of suPAR, cellular PAR were significantly higher (P= 0.001, 0.001) and MMP-9 was significantly lower (P=0.001) in AML patients at diagnosis as compared to controls. suPAR and MMP-9 levels were significantly lower in AML patients who achieved complete remission (CR) as compared to those who did not (P= 0.001 for both).
  • Levels of suPAR and MMP-9 were significantly correlated to peripheral blood blast cells (r= 0.88, P= 0.001; r= 0.65, P= 0.001, respectively) and blast cell distribution ratio (BCDR, r= 0.84, P= 0.001; r=65, P= 0.001, respectively).
  • suPAR, cellular PAR and MMP-9 were significantly higher in patients with extramedullary infiltration as compared with those without (P= 0.001, 0.001, <0.05).
  • In conclusion, MMP-9 and su PAR levels might be used as a marker for disease activity and may contribute to blast cell dissemination.
  • MMP-9 and suPAR may be target molecules in the strategy of treatment of AML.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Matrix Metalloproteinase 9 / metabolism. Receptors, Urokinase Plasminogen Activator / metabolism
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Female. Humans. Immunophenotyping. Male. Middle Aged. Neoplasm Invasiveness. Signal Transduction

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  • (PMID = 14668033.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Urokinase Plasminogen Activator; EC 3.4.24.35 / MMP9 protein, human; EC 3.4.24.35 / Matrix Metalloproteinase 9
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12. Al-Saleh N, Itty P, Kukawski P, Al-Khaldi K: Solitary intra-abdominal Castleman's disease, hyaline vascular type: case report. Gulf J Oncolog; 2010 Jan;(7):53-6
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  • [Title] Solitary intra-abdominal Castleman's disease, hyaline vascular type: case report.
  • CASE PRESENTATION AND INTERVENTION: A 20 year old gentleman who presented with a recurrent intra-abdominal retroperitoneal mass.
  • Previous biopsies obtained from a laparotomy showed Castleman disease- vascular hyaline type.
  • Patient did not respond to chemotherapy and the mass was gradually increasing in size.
  • CONCLUSION: Castleman's disease is a fairly rare benign tumor of lymphoid origin.
  • [MeSH-major] Abdominal Neoplasms / pathology. Giant Lymph Node Hyperplasia / pathology. Hyalin / metabolism. Lymph Nodes / pathology. Plasma Cells / pathology. Retroperitoneal Neoplasms / pathology
  • [MeSH-minor] Adult. Humans. Male. Tomography, X-Ray Computed. Young Adult

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  • (PMID = 20164010.001).
  • [ISSN] 2078-2101
  • [Journal-full-title] The Gulf journal of oncology
  • [ISO-abbreviation] Gulf J Oncolog
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Kuwait
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13. Yoo J, Choi HS, Choi CH, Chung Y, Kim BH, Cho H: Synthesis and evaluation of antitumor activity of novel 2-[Nmethyl-N-(4-methyl-1,3-benzothiazol-2-yl)aminomethyl]-5,8-diacyloxy-1,4-naphthoquinones. Arch Pharm Res; 2008 Feb;31(2):142-7
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  • Increasing the size of the acyl group (compounds 7-9) up to propyl increased the antitumor activity (T/C value), whereas the cytotoxicity of these compounds was comparable against L1210 (lymphocytic leukemia) and P388 (lymphoid neoplasm) cancer cells.
  • The most potent compound of this series was 2-[N-methyl-N-(4-methyl-1,3-benzothiazol-2-yl)aminomethyl]-5,8-dipropylcarbonyloxy-1,4-naphthoquinone (compound 9) with a T/C (%) value of 354.
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor. Leukemia L1210 / drug therapy. Leukemia P388 / drug therapy. Male. Mice. Mice, Inbred ICR. Neoplasm Transplantation. Sarcoma 180 / drug therapy. Structure-Activity Relationship. Tetrazolium Salts. Thiazoles

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  • (PMID = 18365681.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Naphthoquinones; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue
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14. Jia L, Wei W, Cao J, Xu H, Miao X, Zhang J: Silencing CD147 inhibits tumor progression and increases chemosensitivity in murine lymphoid neoplasm P388D1 cells. Ann Hematol; 2009 Aug;88(8):753-60
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  • [Title] Silencing CD147 inhibits tumor progression and increases chemosensitivity in murine lymphoid neoplasm P388D1 cells.
  • Overexpression of extracellular matrix metalloproteinase inducer (EMMPRIN or CD147), a member glycoprotein enriched on the surface of many malignant tumor cells, promotes tumor progression and confers resistance to some chemotherapeutic drugs.
  • To investigate the possible role of CD147 in the macrophage-like lymphoid neoplasm P388D1 cells progression, we used RNA interference approach to silence CD147 expression.
  • Furthermore, the down-regulation of CD147 expression sensitized cells to be more sensitive to chemotherapeutic drugs.
  • Treatment of tumor cells with U-0126, an inhibitor of mitogen-activated protein kinase/Erk, also down-regulated the expression of MMP11.
  • Our current results indicate that the expression of CD147 functionally mediates tumor progression and is a potential target for therapeutic anti-cancer drugs.
  • [MeSH-major] Antigens, CD147 / genetics. Drug Resistance, Neoplasm / drug effects. Gene Silencing. Lymphoma / drug therapy. RNA, Small Interfering / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Disease Progression. Lymph Nodes / pathology. Matrix Metalloproteinase Inhibitors. Mice. Mice, Inbred DBA. Neoplasm Metastasis / drug therapy. Neoplasm Transplantation

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  • (PMID = 19125248.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bsg protein, mouse; 0 / Matrix Metalloproteinase Inhibitors; 0 / RNA, Small Interfering; 136894-56-9 / Antigens, CD147
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15. Portlock CS, Hamlin P, Noy A, Chey W, Gaydos CA, Palomba L, Schwartz I, Corcoran S, Rosenzweig L, Walker D, Papanicolaou G, Markowitz A: Infectious disease associations in advanced stage, indolent lymphoma (follicular and nonfollicular): developing a lymphoma prevention strategy. Ann Oncol; 2008 Feb;19(2):254-8
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  • BACKGROUND: Eradication of Helicobacter pylori in gastric mucosa-associated lymphoid tumor can result in lymphoma remission.
  • MATERIALS AND METHODS: Stool H. pylori, hepatitis C and Borrelia serologies, Borrelia and Chlamydia fixed tissue PCR, Chlamydia peripheral blood mononuclear cell PCR and hydrogen breath test for small bowel bacterial overgrowth (SBBO) were obtained.
  • Lymphoma responses to antimicrobial therapy: H. pylori [one complete response (CR), 24+ months; one transient near CR]; hepatitis C [two CRs, 18+ and 30+ months; one partial response (PR) but hepatitis C virus persistent]; SBBO (one PR, 30+ months).
  • Patients with associated infections, but without lymphoma CR, have required lymphoma treatment sooner than those without initial infections (treatment-free survival at 23.4 months median follow-up, 40.5% versus 74.7%, P = 0.01), indicating a different biology.
  • The identification and treatment of associated infections may be a first step towards developing a lymphoma prevention strategy.


16. Zabala M, Lasarte JJ, Perret C, Sola J, Berraondo P, Alfaro M, Larrea E, Prieto J, Kramer MG: Induction of immunosuppressive molecules and regulatory T cells counteracts the antitumor effect of interleukin-12-based gene therapy in a transgenic mouse model of liver cancer. J Hepatol; 2007 Dec;47(6):807-15
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  • [Title] Induction of immunosuppressive molecules and regulatory T cells counteracts the antitumor effect of interleukin-12-based gene therapy in a transgenic mouse model of liver cancer.
  • BACKGROUND/AIMS: Hepatocellular carcinoma (HCC) often lacks curative treatment; therefore new efficient therapies are needed.
  • In this work we aimed at evaluating the antitumor effect of interleukin-12 (IL-12)-based gene therapy on HCC occurring spontaneously in mice.
  • RESULTS: Dox administration increased serum IL-12 and IFN-gamma and induced tumor lymphocytic infiltration in all treated mice which was accompanied by tumor stabilization or regression in 40% of animals.
  • The antitumor effect did not correlate with levels of IL-12 or IFN-gamma nor with the intensity of tumor mononuclear infiltration.
  • However, tumors from non-responder mice showed more abundance of Foxp3+ regulatory T cells and higher expression of the immunosuppressive molecules PD-1, PD-L1, VEGF, CTLA-4, IDO, and IL-10 than those that responded to therapy.
  • CONCLUSIONS: Although long-term induction of IL-12 expression in the liver can inhibit HCC growth, the efficacy of the treatment appears to be limited by the activation of immunosuppressive mechanisms.
  • [MeSH-major] Genetic Therapy / methods. Interleukin-12 / administration & dosage. Liver Neoplasms / therapy
  • [MeSH-minor] Animals. Chemotaxis, Leukocyte. Doxycycline / pharmacology. Gene Expression Regulation / drug effects. Immunologic Factors / genetics. Interferon-gamma / blood. Lymphocytes. Mice. Mice, Transgenic. Plasmids. T-Lymphocytes, Regulatory. Treatment Outcome. Tumor Burden

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  • (PMID = 17935823.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunologic Factors; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma; N12000U13O / Doxycycline
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17. Pérez-Galán P, Roué G, López-Guerra M, Nguyen M, Villamor N, Montserrat E, Shore GC, Campo E, Colomer D: BCL-2 phosphorylation modulates sensitivity to the BH3 mimetic GX15-070 (Obatoclax) and reduces its synergistic interaction with bortezomib in chronic lymphocytic leukemia cells. Leukemia; 2008 Sep;22(9):1712-20
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  • [Title] BCL-2 phosphorylation modulates sensitivity to the BH3 mimetic GX15-070 (Obatoclax) and reduces its synergistic interaction with bortezomib in chronic lymphocytic leukemia cells.
  • Chronic lymphocytic leukemia (CLL) is a B-cell lymphoid neoplasm with deregulated apoptosis and overexpression of several antiapoptotic BCL-2 proteins.
  • CLL cells showed lower sensitivity to GX15-070 than primary mantle cell lymphoma (MCL) ones, in correlation with higher levels of phosphorylated BCL-2 at serine 70 residue (pBCL-2(Ser70)) in CLL cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Boronic Acids / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Proto-Oncogene Proteins c-bcl-2 / metabolism. Pyrazines / pharmacology. Pyrroles / pharmacology
  • [MeSH-minor] Apoptosis. Bortezomib. Drug Synergism. Humans. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Mitochondria / metabolism. Phosphorylation. Protease Inhibitors / pharmacology. Tumor Cells, Cultured

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  • (PMID = 18596739.001).
  • [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 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Pyrroles; 0 / obatoclax; 69G8BD63PP / Bortezomib
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18. Re M, Di Massimo U, Romeo R, Mallardi V: Burkitt-like lymphoma of the sphenoid sinus: case report. Acta Otorhinolaryngol Ital; 2004 Feb;24(1):30-2

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  • Burkitt's lymphoma is a malignant endemic neoplasia with a mandibular localization, described for the first time in 1958, in African children.
  • The World Health Organization classification recognises several variants of Burkitt's lymphoma; all are highly malignant B cell lymphomas.
  • This subtype includes those cases diagnosed as "Burkitt-like" lymphoma in the REAL (Revised European-American Classification of Lymphoid Neoplasm).
  • The therapeutic protocol is similar to that used for classic Burkitt's lymphoma, with chemotherapy being standard treatment.
  • Prognosis is extremely poor, with a mean survival of < 1 year.
  • The extremely rare localisation of this histological variant of Burkitt's lymphoma is stressed as well as the extremely aggressive nature of the neoplasm.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diagnosis, Differential. Humans. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 15270431.001).
  • [ISSN] 0392-100X
  • [Journal-full-title] Acta otorhinolaryngologica Italica : organo ufficiale della Società italiana di otorinolaringologia e chirurgia cervico-facciale
  • [ISO-abbreviation] Acta Otorhinolaryngol Ital
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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19. Cahill RA, McGreal G, Neary P, Redmond HP: Synchronous high-risk melanoma and lymphoid neoplasia. Melanoma Res; 2001 Oct;11(5):517-22
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  • [Title] Synchronous high-risk melanoma and lymphoid neoplasia.
  • Large population-based studies have shown a significant association between melanoma and lymphoid neoplasia, particularly non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukaemia (CLL), that is independent of any treatment received for the initial tumour.
  • This study examines the presentation, diagnosis, treatment and progress of three patients who developed advanced melanoma concurrently with a lymphoid neoplasm (one NHL, two CLLs), in order to illustrate their association, discuss common aetiological factors and examine possible therapeutic options.
  • As it is the melanoma rather than the lymphoid neoplasm that represents the bigger threat to overall survival, initial treatment should be targeted towards this cancer.
  • However, because of the interplay between the diseases and the possible side-effects of the various treatments, the choice of adjuvant therapy requires careful consideration.
  • Immunosuppression associated with chemotherapy may permit a more aggressive course for the melanoma, while locoregional radiotherapy is contraindicated following lymph node dissections.
  • As immunotherapy is of benefit in the treatment of melanoma and has also been recently shown to be effective in the management of lymphoid neoplasia, we instituted interferon-alpha as adjuvant therapy for these patients, thereby utilizing a single agent to treat the dual pathologies.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell. Lymphoma, Non-Hodgkin. Melanoma. Neoplasms, Multiple Primary
  • [MeSH-minor] Aged. Aged, 80 and over. Chemotherapy, Adjuvant / methods. Disease Susceptibility. Environment. Female. Humans. Incidence. Interferon-alpha / therapeutic use. Lymph Nodes / pathology. Male. Middle Aged. Radiotherapy / contraindications. Risk Factors. Ultraviolet Rays / adverse effects

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  • (PMID = 11595890.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha
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20. Yan Z, Yang B, Wang QS, Wang LL, Han XP, Ren F, Yu L: [Clinical pathological features of the 8p11 myeloproliferative syndrome]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1321-6
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  • This study was aimed to investigate the clinico-pathological features, diagnosis and treatment of the 8p11 (eight p11) myeloproliferative syndrome (EMS).
  • The cell immunophenotypes were analysed by flow cytometry.
  • The results indicated that EMS was a relatively rare disease characterized by the occurrence of a bcr/abl-negative myeloproliferative disorder and a T-cell lymphoblastic lymphoma (T-LBL).
  • Bone marrow examination showed myeloid hyperplasia or myeloproliferative neoplasm, often accompanied by eosinophilia.
  • At the molecular level, all cases carried a chromosomal abnormality involving the fibroblast growth factor receptor 1 (FGFR1) at chromosome 8p11.
  • Majority of patients terminate in acute myeloid leukemia which is resistant to conventional chemotherapy.
  • Currently, the only curative option appears to be allogeneic hematopoietic stem cell transplantation.
  • In conclusion, EMS is myeloid and lymphoid neoplasm, associates with FGFR1 rearrangements.

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  • (PMID = 21129285.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
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21. Papadopoulos N, Kotini A, Cheva A, Jivannakis T, Manavis J, Alexiadis G, Lambropoulou M, Vavetsis S, Tamiolakis D: Gains and losses of CD8, CD20 and CD56 expression in tumor stroma-infiltrating lymphocytes compared with tumor-associated lymphocytes from ascitic fluid and lymphocytes from tumor draining lymph nodes in serous papillary ovarian carcinoma patients. Eur J Gynaecol Oncol; 2002;23(6):533-6
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  • [Title] Gains and losses of CD8, CD20 and CD56 expression in tumor stroma-infiltrating lymphocytes compared with tumor-associated lymphocytes from ascitic fluid and lymphocytes from tumor draining lymph nodes in serous papillary ovarian carcinoma patients.
  • Serous papillary ovarian cancer (SPC) is a highly aggressive tumor.
  • About two-thirds of women have advanced disease at the time of diagnosis.
  • Although many women with disseminated disease respond at first to combinations of surgery and chemotherapy, nearly 90% of tumors recur and women die of disease.
  • Update progress in our knowledge of tumor-associated antigens and insight into mechanisms involved in immune-mediated recognition of these antigens, have provided a strong starting point for using the immune system as a model for novel therapy.
  • In this study we determined the immunological profile of tumor-infiltrating lymphocytes (TILs), tumor-associated lymphocytes (TALs) in ascitic fluids, and lymphocytes from tumor draining regional lymph nodes (LNs) in SPC patients by CD20 (L26), CD8, and CD56 immunostaining.
  • TILs were infiltrating tumor stroma.
  • No significant difference was detected in TILs, TALs and LNs in the expression of the B-cell marker CD20.
  • In contrast, CD8 (T-cytotoxic) and CD56 (natural killer cell, NK) markers were dominant in LNs and TALs, but not in TILs.
  • We conclude that SPC tumor lymphocytic infiltrate demonstrates a deplete T cytotoxic (CD8+) and NK cell (CD56+) immunophenotypic profile.
  • [MeSH-major] Cystadenocarcinoma, Papillary / immunology. Lymphocytes, Tumor-Infiltrating / immunology. Ovarian Neoplasms / immunology
  • [MeSH-minor] Antigens, CD / metabolism. Antigens, CD20 / metabolism. Antigens, CD56 / metabolism. Antigens, Differentiation, T-Lymphocyte / metabolism. Ascites / pathology. Female. Gene Expression Regulation, Neoplastic. Humans. Immunophenotyping. Lymph Nodes / cytology. Neoplasm Metastasis. Peritoneum / pathology

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  • (PMID = 12556098.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD20; 0 / Antigens, CD56; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / CD6 antigen
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22. Zeng Y, Ni X, Meng WT, Wen Q, Jia YQ: [Inhibitive effect of artesunate on human lymphoblastic leukemia/lymphoma cells]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2009 Nov;40(6):1038-43
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  • OBJECTIVE: To test the effect of Artesunate (ART) on the proliferation of Raji cells, Jurkat cells and acute lymphoblastic leukemia (ALL) primary cells; to determine the synergistic antiproliferation effect between ART and Vincristine (VCR) or Cytarabine(Ara-C) on Raji and Jurkat cells; and to explore the mechanism of ART induced apoptosis of tumor cells in vitro.
  • Colorimetric method was used to measure the activities of caspase-3 in those tumor cells.
  • CONCLUSION: ART alone or combined with chemotherapy drugs could inhibit the proliferation of B/T lymphocytic tumor cell lines as well ALL primary cells in vitro, probably through the mechanism of apoptosis, which suggest that ART is likely to be a potential drug in the treatment of leukemia/lymphoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Artemisinins / pharmacology. Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Blood-Brain Barrier / drug effects. Cell Line, Tumor. Cytarabine / pharmacology. Drug Synergism. Humans. Jurkat Cells

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  • (PMID = 20067115.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Artemisinins; 04079A1RDZ / Cytarabine; 60W3249T9M / artesunate
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23. Meneses A, Verastegui E, Barrera JL, de la Garza J, Hadden JW: Lymph node histology in head and neck cancer: impact of immunotherapy with IRX-2. Int Immunopharmacol; 2003 Aug;3(8):1083-91
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  • PATIENTS: Thirty patients with advanced squamous cell carcinoma of the head and neck (H and N SCC) and 10 non-cancer controls.
  • Clinical responses were assessed at surgery, and the specimen and a sample of lymph node were analyzed with respect to changes in morphology and lymphoid and inflammatory infiltration (T and B lymphocytes, plasma cells, macrophages, granulocytes, and giant cells).
  • Lymph node histology of the 10 H and N SCC controls showed, compared to non-cancer controls, reduced size, decreased T cell area and density and increased sinus histiocytosis.
  • The lymph nodes of IRX-2-treated H and N SCC patients showed increased size (over both control groups), increased T cell area and density and decreased follicles and sinus histiocytosis.
  • The T cell and/or B cell areas of LN of IRX-2-treated patients showed a high correlation with T and/or B cell infiltration into these tumors (p<0.001).
  • CONCLUSION: The lymph nodes of patients with H and N SCC are distinguished by T cell depletion and sinus histiocytosis (SH).
  • Immunotherapy reverses these changes and induces nodal expansion and lymphoid infiltration into the tumor that correlates with LN changes.
  • The correlation of nodal expansion with tumor lymphoid infiltration and regression implies an effective immunization to host tumor antigens occurring at the level of the regional lymph node.
  • The reversal of sinus histiocytosis, by IRX-2 treatment, in association with nodal expansion suggests that tumor antigen processing via dendritic cells is defective in cancer-bearing patients and that it is corrected by the treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Head and Neck Neoplasms / drug therapy. Lymph Nodes / pathology. Neoplasms, Squamous Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant / methods. Cyclophosphamide / administration & dosage. Cytokines / administration & dosage. Female. Humans. Immunotherapy / methods. Indomethacin / administration & dosage. Male. Middle Aged. Zinc / administration & dosage

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  • (PMID = 12860165.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / IRX 2; 8N3DW7272P / Cyclophosphamide; J41CSQ7QDS / Zinc; XXE1CET956 / Indomethacin
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24. Ren S, Zhang Y, Wang Y, Lui Y, Wei W, Huang X, Mao W, Zuo Y: Targeting P2X₇ receptor inhibits the metastasis of murine P388D1 lymphoid neoplasm cells to lymph nodes. Cell Biol Int; 2010 Dec;34(12):1205-11
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  • [Title] Targeting P2X₇ receptor inhibits the metastasis of murine P388D1 lymphoid neoplasm cells to lymph nodes.
  • The P2X₇R (P2X₇ receptor) is an ATP-gated cation channel expressed in normal cells that participates in both cell proliferation and apoptosis.
  • Here, we have confirmed P2X₇R expression on murine P388D1 lymphoid neoplasm cells.
  • These results indicate that inhibition of the expression and function of P2X₇R attenuates the metastatic ability of murine lymphoid neoplasm cell line P388D1, which represents a new potential target for anti-metastatic therapy.
  • [MeSH-major] Lymphoma / pathology. Lymphoma / prevention & control. Purinergic P2X Receptor Antagonists / therapeutic use
  • [MeSH-minor] 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / analogs & derivatives. 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / pharmacology. 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / therapeutic use. Animals. Cell Line, Tumor. Lymph Nodes / drug effects. Lymph Nodes / pathology. Lymphatic Metastasis. Lymphocytes / drug effects. Lymphocytes / pathology. Mice. Mice, Inbred DBA. Molecular Targeted Therapy. Neoplasm Transplantation. RNA, Small Interfering / pharmacology. RNA, Small Interfering / therapeutic use. Receptors, Purinergic P2X7 / genetics. Receptors, Purinergic P2X7 / metabolism. Receptors, Purinergic P2X7 / physiology

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  • (PMID = 20722629.001).
  • [ISSN] 1095-8355
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Purinergic P2X Receptor Antagonists; 0 / RNA, Small Interfering; 0 / Receptors, Purinergic P2X7; 127191-97-3 / KN 62; 84477-87-2 / 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
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25. Lee WY, Lim DS, Ko SH, Park YJ, Ryu KS, Ahn MY, Kim YR, Lee DW, Cho CW: Photoactivation of pheophorbide a induces a mitochondrial-mediated apoptosis in Jurkat leukaemia cells. J Photochem Photobiol B; 2004 Sep 8;75(3):119-26

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The mechanism of cell death by pheophorbide a (Pba) which has been established to be a potential photosensitizer was examined in experimental photodynamic therapy (PDT) on Jurkat cells, a human lymphoid tumor cell line.
  • Taken together, it was concluded that the mode of Jurkat cell death by Pba/PDT is an apoptosis, which is initiated by mitochondrial cytochrome c release and caspase-3-pathways.
  • [MeSH-minor] Caspase 3. Caspase Inhibitors. Caspases / physiology. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Humans. Jurkat Cells. Light

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  • (PMID = 15341925.001).
  • [ISSN] 1011-1344
  • [Journal-full-title] Journal of photochemistry and photobiology. B, Biology
  • [ISO-abbreviation] J. Photochem. Photobiol. B, Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Radiation-Sensitizing Agents; 1406-65-1 / Chlorophyll; 15664-29-6 / pheophorbide a; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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26. Nelson BP, Nalesnik MA, Bahler DW, Locker J, Fung JJ, Swerdlow SH: Epstein-Barr virus-negative post-transplant lymphoproliferative disorders: a distinct entity? Am J Surg Pathol; 2000 Mar;24(3):375-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The morphologic, immunophenotypic, genotypic, and clinical features of the EBV-negative PTLDs were reviewed, and selected features were compared with EBV-positive cases.
  • Of the EBV-negative PTLDs, 67% were of monomorphic type (M-PTLD) compared with 42% of EBV-positive cases (p <0.05).
  • The other EBV-negative PTLDs were of infectious mononucleosis-like, plasma cell-rich (n = 2), small B-cell lymphoid neoplasm, large granular lymphocyte disorder (n = 4) and polymorphic (P) types.
  • B-cell clonality was established in 14 specimens and T-cell clonality was established in three (two patients).
  • Ten patients were alive at 3 to 63 months (only three patients received chemotherapy).
  • Seven patients, all with M-PTLDs, are dead at 0.3 to 6 months.

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  • (PMID = 10716151.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
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27. Sokol JA, Landau L, Lauer SA: Rituximab immunotherapy for ocular adnexal lymphoma: clinicopathologic correlation with 5-year follow-up. Ophthal Plast Reconstr Surg; 2009 Jul-Aug;25(4):322-4
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  • Two patients with primary ocular adnexal mucosa-associated lymphoid tumor lymphoma were treated with rituximab immunotherapy.
  • Biopsies were performed 6 months after treatment.
  • Rituximab immunotherapy is an alternative to regional radiotherapy for ocular adnexal mucosa-associated lymphoid tumor lymphoma.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Conjunctival Neoplasms / drug therapy. Eyelid Neoplasms / drug therapy. Immunotherapy / methods. Lymphoma, B-Cell, Marginal Zone / drug therapy

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  • (PMID = 19617799.001).
  • [ISSN] 1537-2677
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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28. Chen TY, Chen JS, Su WC, Wu MS, Tsao CJ: Expression of DNA repair gene Ku80 in lymphoid neoplasm. Eur J Haematol; 2005 Jun;74(6):481-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of DNA repair gene Ku80 in lymphoid neoplasm.
  • Ku80 is a putative tumor suppressor gene that might play an important role in drug resistance.
  • Our aim was to determine the role of Ku80 in lymphoid malignancy.
  • RESULTS: No mutation or Ku80 variant at the RNA level was seen in any patient samples or in the Raji or CCRF-CEM cell lines.
  • In Ku80 expression, 8.8-, 1.9-, and 6.2-fold mean increases were seen in adult, pediatric ALL, and chronic lymphoid malignancies compared with the control.
  • The amount of Ku80 expression in ALL was moderately correlated with peripheral white blood cell counts, but not with Ki67 labeling index.
  • High Ku80 expressers (higher than the mean of all patients with ALL) tended to respond poorly to therapy: Only 22% of high Ku80 expressers achieved durable complete remission compared to 62% of low expressers.
  • [MeSH-major] Antigens, Nuclear / biosynthesis. DNA Repair / genetics. DNA-Binding Proteins / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Child. Child, Preschool. Humans. Infant. Ki-67 Antigen / biosynthesis. Ki-67 Antigen / genetics. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Prognosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 15876251.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Ku autoantigen; 0 / RNA, Messenger
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29. Lin JT, Wu MS, Wang WS, Yen CC, Chiou TJ, Liu JH, Yang MH, Chao TC, Chou SC, Chen PM: All-trans retinoid acid increases Notch1 transcript expression in acute promyelocytic leukemia. Adv Ther; 2003 Nov-Dec;20(6):337-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The effect of all-trans retinoid acid (ATRA) on the expression of Notch1 gene by real-time reverse transcriptase polymerase chain reaction (RT-PCR) in acute promyelocytic leukemia cells (APL), NB4, and HL-60 lacking t(15;17) was studied.
  • As Notch1 gene is involved in the differentiation and leukemogenesis in lymphoid neoplasm, observations suggest that Notch1 is involved in ATRA-modulated differentiation process in APL.
  • [MeSH-major] Genetic Predisposition to Disease. Leukemia, Promyelocytic, Acute / genetics. Receptors, Cell Surface / genetics. Transcription Factors. Tretinoin / pharmacology
  • [MeSH-minor] Base Sequence. Cell Division / drug effects. Cell Division / physiology. Female. Gene Expression Regulation, Neoplastic. HL-60 Cells / drug effects. HL-60 Cells / physiology. Humans. Male. Molecular Sequence Data. Neoplasm Proteins / genetics. Receptor, Notch1. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity

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  • (PMID = 15058751.001).
  • [ISSN] 0741-238X
  • [Journal-full-title] Advances in therapy
  • [ISO-abbreviation] Adv Ther
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Receptor, Notch1; 0 / Receptors, Cell Surface; 0 / Transcription Factors; 5688UTC01R / Tretinoin
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30. D'Costa SS, Hurwitz JL: Phytohemagglutinin inhibits lymphoid tumor growth in vitro and in vivo. Leuk Lymphoma; 2003 Oct;44(10):1785-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phytohemagglutinin inhibits lymphoid tumor growth in vitro and in vivo.
  • Viable treatment options for relapsed disease are few, encouraging the development of novel therapies.
  • In the present paper, we describe phytohemagglutinin (PHA), a standard T cell mitogen, as an inhibitor of both T- and B-cell tumors.
  • In vitro studies show that PHA can inhibit incorporation of 3H-thymidine and mediate apoptosis of B- and T-cell tumor lines.
  • The inhibitory effects are enhanced when PHA is used in conjunction with the cell cycle directed drug 5-fluorouracil (5-FU).
  • Phytohemagglutinin treatments can also impede tumor growth in mice while showing no toxic side effects in this animal model.
  • [MeSH-major] Apoptosis / drug effects. Cell Cycle / drug effects. Lymphoma, B-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Phytohemagglutinins / therapeutic use
  • [MeSH-minor] Animals. Annexin A5 / metabolism. Antimetabolites, Antineoplastic / therapeutic use. Drug Combinations. Drug Synergism. Fluorouracil / therapeutic use. In Vitro Techniques. Male. Mice. Mice, SCID. Thymidine / metabolism. Tumor Cells, Cultured

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  • (PMID = 14692534.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30-CA21765; United States / NCI NIH HHS / CA / R01-CA57419
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0 / Phytohemagglutinins; U3P01618RT / Fluorouracil; VC2W18DGKR / Thymidine
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31. Ylikangas P, Mononen I: Serious neutropenia in ALL patients treated with L-asparaginase may be avoided by therapeutic monitoring of the enzyme activity in the circulation. Ther Drug Monit; 2002 Aug;24(4):502-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serious neutropenia in ALL patients treated with L-asparaginase may be avoided by therapeutic monitoring of the enzyme activity in the circulation.
  • L-Asparagine is an essential amino acid for many lymphoid tumor cells and L-asparaginase catalyzes its conversion to L-aspartic acid and ammonia.
  • The dosage of this highly toxic drug is individualized based on the body surface area of the patient, but monitoring of L-asparaginase activity during the L-asparaginase therapy is not commonly used.
  • We measured L-asparaginase activity in the serum of ten children (aged 3-13 y) with ALL (ALL NOPHO-92 standard or intermediate risk groups) during their L-asparaginase therapy.
  • L-asparaginase was given 30,000 IU/m2 IM during days 37-46 of the induction therapy and no other chemotherapeutic drug except for prednisone was given at the same time.
  • There was also a relationship between the area under the L-asparaginase activity-time curve (AUC) and even peak L-asparaginase activity in serum during the enzyme therapy and neutropenia after the therapy in the patients: the higher the AUC or peak value was, the more severe was the neutropenia in the patients after treatment.
  • Monitoring L-asparaginase in serum could be useful in optimization of the therapy with this toxic drug.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Asparaginase / adverse effects. Neutropenia / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Area Under Curve. Child. Child, Preschool. Drug Monitoring. Humans

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  • (PMID = 12142634.001).
  • [ISSN] 0163-4356
  • [Journal-full-title] Therapeutic drug monitoring
  • [ISO-abbreviation] Ther Drug Monit
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.5.1.1 / Asparaginase
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