[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 38 of about 38
1. Rao VK, Carrasquillo JA, Dale JK, Bacharach SL, Whatley M, Dugan F, Tretler J, Fleisher T, Puck JM, Wilson W, Jaffe ES, Avila N, Chen CC, Straus SE: Fluorodeoxyglucose positron emission tomography (FDG-PET) for monitoring lymphadenopathy in the autoimmune lymphoproliferative syndrome (ALPS). Am J Hematol; 2006 Feb;81(2):81-5
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fluorodeoxyglucose positron emission tomography (FDG-PET) for monitoring lymphadenopathy in the autoimmune lymphoproliferative syndrome (ALPS).
  • Autoimmune lymphoproliferative syndrome (ALPS) is associated with mutations that impair the activity of lymphocyte apoptosis proteins, leading to chronic lymphadenopathy, hepatosplenomegaly, autoimmunity, and an increased risk of lymphoma.
  • We investigated the utility of fluorodeoxyglucose positron emission tomography (FDG-PET) in discriminating benign from malignant lymphadenopathy in ALPS.
  • We report that FDG avidity of benign lymph nodes in ALPS can be high and, hence, by itself does not imply presence of lymphoma; but FDG-PET can help guide the decision for selecting which of many enlarged nodes in ALPS patients to biopsy when lymphoma is suspected.
  • [MeSH-major] Fluorodeoxyglucose F18. Lymphatic Diseases / diagnosis. Lymphoma / diagnosis. Lymphoproliferative Disorders / diagnosis. Positron-Emission Tomography / methods
  • [MeSH-minor] Autoimmune Diseases / diagnosis. Autoimmune Diseases / pathology. Biopsy. Diagnosis, Differential. Female. Humans. Lymph Nodes / pathology. Male. Mutation. Prospective Studies

  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • MedlinePlus Health Information. consumer health - Lymphatic Diseases.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2006 Wiley-Liss, Inc.
  • [ErratumIn] Am J Hematol. 2006 May;81(5):389
  • (PMID = 16432855.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Case Reports; Clinical Trial; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
  •  go-up   go-down


2. Dowdell KC, Niemela JE, Price S, Davis J, Hornung RL, Oliveira JB, Puck JM, Jaffe ES, Pittaluga S, Cohen JI, Fleisher TA, Rao VK: Somatic FAS mutations are common in patients with genetically undefined autoimmune lymphoproliferative syndrome. Blood; 2010 Jun 24;115(25):5164-9
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatic FAS mutations are common in patients with genetically undefined autoimmune lymphoproliferative syndrome.
  • Autoimmune lymphoproliferative syndrome (ALPS) is characterized by childhood onset of lymphadenopathy, hepatosplenomegaly, autoimmune cytopenias, elevated numbers of double-negative T (DNT) cells, and increased risk of lymphoma.
  • Most cases of ALPS are associated with germline mutations of the FAS gene (type Ia), whereas some cases have been noted to have a somatic mutation of FAS primarily in their DNT cells.
  • We sought to determine the proportion of patients with somatic FAS mutations among a group of our ALPS patients with no detectable germline mutation and to further characterize them.
  • Similar to ALPS type Ia patients, the somatic ALPS patients had increased DNT cell numbers and elevated levels of serum vitamin B(12), interleukin-10, and sFAS-L.
  • These data support testing for somatic FAS mutations in DNT cells from ALPS patients with no detectable germline mutation and a similar clinical and laboratory phenotype to that of ALPS type Ia.
  • These findings also highlight the potential role for somatic mutations in the pathogenesis of nonmalignant and/or autoimmune hematologic conditions in adults and children.

  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • Genetics Home Reference. consumer health - autoimmune lymphoproliferative syndrome.
  • Genetics Home Reference. consumer health - FAS gene.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYANOCOBALAMIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 1999 Oct 15;94(8):2575-82 [10515860.001]
  • [Cites] Hum Mol Genet. 1999;8(10):1893-900 [10469842.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1652-9 [15870181.001]
  • [Cites] Clin Immunol. 2006 Jan;118(1):59-65 [16257267.001]
  • [Cites] Mol Cell Probes. 2006 Feb;20(1):21-6 [16271851.001]
  • [Cites] BMC Bioinformatics. 2006;7:166 [16551372.001]
  • [Cites] J Mol Diagn. 2007 Feb;9(1):1-6 [17251329.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 22;104(21):8953-8 [17517660.001]
  • [Cites] Cell. 2007 Jul 13;130(1):25-35 [17632054.001]
  • [Cites] Br J Haematol. 2009 Apr;145(1):101-6 [19208097.001]
  • [Cites] Blood. 2009 Mar 26;113(13):3027-30 [19176318.001]
  • [Cites] Pediatr Blood Cancer. 2009 Jul;52(7):847-52 [19214977.001]
  • [Cites] Nat Protoc. 2009;4(7):1073-81 [19561590.001]
  • [Cites] Nature. 2009 Oct 1;461(7264):659-63 [19794494.001]
  • [Cites] J Allergy Clin Immunol. 2010 Apr;125(4):946-949.e6 [20227752.001]
  • [Cites] Am J Surg Pathol. 2005 Jul;29(7):903-11 [15958855.001]
  • [Cites] Radiology. 1999 Jul;212(1):257-63 [10405750.001]
  • [Cites] Science. 2000 Jun 30;288(5475):2354-7 [10875918.001]
  • [Cites] Blood. 2001 May 15;97(10):3161-70 [11342444.001]
  • [Cites] Leuk Lymphoma. 2001 May;41(5-6):501-11 [11378568.001]
  • [Cites] Blood. 2001 Jul 1;98(1):194-200 [11418480.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2466-73 [11588044.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1811-6 [11861299.001]
  • [Cites] Nucleic Acids Res. 2002 Sep 1;30(17):3894-900 [12202775.001]
  • [Cites] Nucleic Acids Res. 2003 Jul 1;31(13):3812-4 [12824425.001]
  • [Cites] Bioinformatics. 2004 May 22;20(8):1322-4 [14871869.001]
  • [Cites] N Engl J Med. 2004 Sep 30;351(14):1388-90 [15459299.001]
  • [Cites] N Engl J Med. 2004 Sep 30;351(14):1409-18 [15459302.001]
  • [Cites] J Clin Invest. 1992 Aug;90(2):334-41 [1386609.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1341-8 [9028957.001]
  • [Cites] J Pediatr. 1997 Mar;130(3):388-93 [9063413.001]
  • [Cites] Bone Marrow Transplant. 1998 Aug;22(4):375-80 [9722073.001]
  • [Cites] Am J Pathol. 1998 Nov;153(5):1541-50 [9811346.001]
  • [Cites] J Clin Invest. 1999 Feb;103(3):355-63 [9927496.001]
  • [Cites] Ann Intern Med. 1999 Apr 6;130(7):591-601 [10189330.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1002-14 [10090885.001]
  • [CommentIn] Blood. 2010 Dec 2;116(23):5072-3 [21127186.001]
  • [CommentIn] Blood. 2010 Jun 24;115(25):5125-6 [20576815.001]
  • (PMID = 20360470.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / PHS HHS / / HHSN261200800001E; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / FAS protein, human; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / IL10 protein, human; 130068-27-8 / Interleukin-10; P6YC3EG204 / Vitamin B 12
  • [Other-IDs] NLM/ PMC2892951
  •  go-up   go-down


3. Rao VK, Dowdell KC, Dale JK, Dugan F, Pesnicak L, Bi LL, Hoffmann V, Penzak S, Avila NA, Fleisher TA, Puck JM, Straus SE: Pyrimethamine treatment does not ameliorate lymphoproliferation or autoimmune disease in MRL/lpr-/- mice or in patients with autoimmune lymphoproliferative syndrome. Am J Hematol; 2007 Dec;82(12):1049-55
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pyrimethamine treatment does not ameliorate lymphoproliferation or autoimmune disease in MRL/lpr-/- mice or in patients with autoimmune lymphoproliferative syndrome.
  • Autoimmune lymphoproliferative syndrome (ALPS) is an inherited disorder of lymphocyte apoptosis leading to childhood onset of marked lymphadenopathy, hepatosplenomegaly, autoimmune cytopenias, and increased risk of lymphoma.
  • Most cases are associated with heterozygous mutations in the gene encoding Fas protein.
  • Prolonged use of immunosuppressive drugs that do ameliorate its autoimmune complications fail to consistently lessen lymphoproliferation in ALPS.
  • A case series had described children with ALPS, whose spleens (SPL) and lymph nodes decreased in size when treated weekly with pyrimethamine and sulfadoxine; parallel in vitro studies showed only pyrimethamine to promote apoptosis.
  • Moreover, seven children with ALPS enrolled in a study of escalating dose of pyrimethamine alone given twice weekly for 12 weeks to determine if their lymphadenopathy and/or splenomegaly would diminish, as assessed by standardized computerized tomography.
  • Neither pyrimethamine alone or with sulfadoxine in the MRL/lpr-/- mice, nor pyrimethamine alone in ALPS patients proved efficacious.
  • We conclude that these drugs do not warrant further use empirically or as part of clinical trials in ALPS Type Ia as a lympholytic agent.
  • [MeSH-major] Autoimmune Diseases / drug therapy. Lymphoproliferative Disorders / drug therapy. Lymphoproliferative Disorders / immunology. Pyrimethamine / therapeutic use

  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Pyrimethamine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17674358.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] Z3614QOX8W / Pyrimethamine
  •  go-up   go-down


Advertisement
4. Venkataraman G, McClain KL, Pittaluga S, Rao VK, Jaffe ES: Development of disseminated histiocytic sarcoma in a patient with autoimmune lymphoproliferative syndrome and associated Rosai-Dorfman disease. Am J Surg Pathol; 2010 Apr;34(4):589-94
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of disseminated histiocytic sarcoma in a patient with autoimmune lymphoproliferative syndrome and associated Rosai-Dorfman disease.
  • Patients with autoimmune lymphoproliferative syndrome (ALPS) have defective lymphocyte apoptosis with increased risk for lymphoid malignancies.
  • Herein, we report a patient with ALPS who developed histiocytic sarcoma in a background of sinus histiocytosis and massive lymphadenopathy or Rosai- Dorfman disease.
  • This patient had documented ALPS type Ia with a germline missense mutation in exon 9 of the TNFRSF6 gene (973 A>T, D244V) encoding Fas (CD95/Apo-1).
  • He presented at 10 months with hepatosplenomegaly and autoimmune hemolytic anemia and was diagnosed with ALPS.
  • At the age of 6 (1/2) years, he developed classic Hodgkin lymphoma which was treated using standard chemotherapy.
  • Two years later, a biopsy of a positron emission tomography-positive axillary node showed features of ALPS and focal involvement by sinus histiocytosis and massive lymphadenopathy.
  • Thereafter, the patient continued to have continued lymphadenopathy and progressive splenomegaly, leading to exploratory surgery at the age of 13 years for suspicion of lymphoma.
  • The occurrence of malignancies involving 2 separate hematopoietic lineages in ALPS has not been reported earlier.
  • Given the central role of defective Fas signaling in ALPS, histiocytes may be yet another lineage at risk for neoplastic transformation secondary to a block in apoptosis.
  • [MeSH-major] Autoimmune Lymphoproliferative Syndrome / pathology. Histiocytic Sarcoma / pathology. Histiocytosis, Sinus / pathology

  • Genetic Alliance. consumer health - Rosai-Dorfman disease.
  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Histopathology. 1999 Dec;35(6):525-33 [10583576.001]
  • [Cites] Nature. 2009 Oct 1;461(7264):659-63 [19794494.001]
  • [Cites] Blood. 2001 Jul 1;98(1):194-200 [11418480.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3452-7 [15150097.001]
  • [Cites] Science. 1985 Jun 21;228(4706):1440-3 [3874430.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):6961-5 [1871110.001]
  • [Cites] J Clin Invest. 1992 Aug;90(2):334-41 [1386609.001]
  • [Cites] Science. 1995 Jun 2;268(5215):1347-9 [7539157.001]
  • [Cites] Cell. 1995 Jun 16;81(6):935-46 [7540117.001]
  • [Cites] Br J Haematol. 1995 Oct;91(2):415-8 [8547085.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1341-8 [9028957.001]
  • [Cites] J Immunol. 1997 Feb 15;158(4):1912-8 [9029133.001]
  • [Cites] Cytokine. 1998 Jan;10(1):32-7 [9505143.001]
  • [Cites] J Pediatr. 1998 Nov;133(5):629-33 [9821419.001]
  • [Cites] Ann Intern Med. 1999 Apr 6;130(7):591-601 [10189330.001]
  • [Cites] Hepatogastroenterology. 1999 Mar-Apr;46(26):1202-5 [10370692.001]
  • [Cites] Inflammation. 2004 Jun;28(3):139-45 [15527169.001]
  • [Cites] Cancer Cell. 2005 May;7(5):425-31 [15894263.001]
  • [Cites] Am J Surg Pathol. 2005 Jul;29(7):903-11 [15958855.001]
  • [Cites] Indian J Pathol Microbiol. 2006 Oct;49(4):509-15 [17183839.001]
  • [Cites] Pathol Int. 2007 Aug;57(8):474-84 [17610471.001]
  • [Cites] Am J Surg Pathol. 2008 Feb;32(2):329-34 [18223337.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5433-9 [18272816.001]
  • [Cites] Blood. 2001 May 15;97(10):3161-70 [11342444.001]
  • (PMID = 20216376.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 SC000550-27; United States / Intramural NIH HHS / / ZIA SC000550-29
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Biomarkers, Tumor; 0 / FAS protein, human
  • [Other-IDs] NLM/ NIHMS190086; NLM/ PMC2861546
  •  go-up   go-down


5. Vacek MM, Schäffer AA, Davis J, Fischer RE, Dale JK, Adams S, Straus SE, Puck JM: HLA B44 is associated with decreased severity of autoimmune lymphoproliferative syndrome in patients with CD95 defects (ALPS type Ia). Clin Immunol; 2006 Jan;118(1):59-65
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HLA B44 is associated with decreased severity of autoimmune lymphoproliferative syndrome in patients with CD95 defects (ALPS type Ia).
  • Autoimmune lymphoproliferative syndrome (ALPS) is a disorder of lymphocyte apoptosis characterized by non-malignant lymphadenopathy and splenomegaly, expansion of T cells without either CD4 or CD8 surface markers, and increased incidence of autoimmune diseases and lymphoma.
  • Most patients with ALPS have dominant, heterozygous mutations in tumor necrosis factor receptor superfamily member 6 (TNFRSF6), which encodes CD95, also known as Fas, a mediator of apoptosis.
  • Penetrance and range of disease manifestations in ALPS are highly variable, even among family members who share the same dominant TNFRSF6 mutation.
  • To evaluate HLA as a candidate modifier locus, we typed HLA A, B (including subtypes), and DQB alleles in 356 individuals from 63 unrelated families with defined TNFRSF6 mutations associated with ALPS.
  • Among the healthier, mutation-bearing individuals, transmission of HLA B44 was significantly overrepresented (nominal P<0.0074) as compared to transmission in patients with severe clinical features of ALPS.
  • The B44 allele may exert a protective role in ALPS.
  • [MeSH-major] Antigens, CD95 / genetics. Autoimmune Diseases / genetics. HLA-B Antigens / genetics. HLA-B Antigens / physiology. Lymphoproliferative Disorders / genetics. Lymphoproliferative Disorders / immunology. Severity of Illness Index
  • [MeSH-minor] Alleles. Data Interpretation, Statistical. Gene Frequency. HLA-B44 Antigen. HLA-DQ Antigens / genetics. HLA-DQ beta-Chains. Histocompatibility Testing. Humans. Mutation. Receptors, Tumor Necrosis Factor / genetics. Syndrome

  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16257267.001).
  • [ISSN] 1521-6616
  • [Journal-full-title] Clinical immunology (Orlando, Fla.)
  • [ISO-abbreviation] Clin. Immunol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / FAS protein, human; 0 / HLA-B Antigens; 0 / HLA-B44 Antigen; 0 / HLA-DQ Antigens; 0 / HLA-DQ beta-Chains; 0 / HLA-DQB1 antigen; 0 / HLA-Dx antigen; 0 / Receptors, Tumor Necrosis Factor
  •  go-up   go-down


6. Hong YH, Lee CK: Autoimmune lymphoproliferative syndrome-like syndrome presented as lupus-like syndrome with mycobacterial joint infection evolved into the lymphoma. Rheumatol Int; 2009 Mar;29(5):569-73
MedlinePlus Health Information. consumer health - Mycobacterial Infections.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autoimmune lymphoproliferative syndrome-like syndrome presented as lupus-like syndrome with mycobacterial joint infection evolved into the lymphoma.
  • The autoimmune lymphoproliferative syndrome (ALPS) and ALPS-like syndrome are variable clinical conditions characterized by lymphoproliferative disease, autoimmune cytopenias and susceptibility to malignancy.
  • A low-grade fever, intermittent hypotension and confusion were associated with the pain.
  • But with the symptoms worsening, the patient developed cervical lymph node enlargements and was diagnosed as a diffuse large B cell lymphoma with hemophagocytosis on biopsy.
  • [MeSH-major] Autoimmune Diseases / pathology. Joints / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoproliferative Disorders / pathology. Mycobacterium Infections / pathology
  • [MeSH-minor] Anti-Bacterial Agents / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Female. Glucocorticoids / therapeutic use. Humans. Lupus Erythematosus, Systemic / pathology. Middle Aged. Syndrome

  • Genetic Alliance. consumer health - Lupus.
  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18820932.001).
  • [ISSN] 1437-160X
  • [Journal-full-title] Rheumatology international
  • [ISO-abbreviation] Rheumatol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Glucocorticoids
  •  go-up   go-down


7. Prochorec-Sobieszek M, Wagner T: [Lymphoproliferative disorders in Sjögren's syndrome]. Otolaryngol Pol; 2005;59(4):559-64
MedlinePlus Health Information. consumer health - Sjogren's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Lymphoproliferative disorders in Sjögren's syndrome].
  • INTRODUCTION: Sjögren's syndrome [SS] is an autoimmune disease that mainly affects the exocrine glands.
  • B-cell lymphoproliferation is a characteristic feature of this syndrome and the lesion may range from benign to malignant.
  • RESULTS: Patients with Sjögren's syndrome [SS] have over 40-fold increased risk of the development B-cell non-Hodgkin's lymphoma.
  • Most cases of lymphomas complicating the course of SS arise in mucosal extranodal sites, especially in the salivary gland, and are classified as low grade marginal zone B-cell lymphoma with long-term survival.
  • The main problem in salivary lymphoproliferation in Sjögren's syndrome consists in the difficulties in the differential diagnosis of lymphoma.
  • Genotypic studies have documented the rearrangement of immunoglobulin genes across the full spectrum of lymphoid infiltrates in the salivary gland including cases regarded as reactive lymphoepithelial sialadenitis [LESA], borderline cases with halos of monocytoid cells surrounding epimyoepithelial islets, and cases with fully developed marginal zone lymphoma [MZL].
  • The pathophysiology of lymphoma in SS remains still unknown.
  • Viral infection, hyperstimulation of B cells, disregulation in the process of apoptosis, and unknown oncogenes are suspected to initiate the start of lymphoma.
  • The main clinical features associated with the development of lymphoma in SS include persistent major salivary gland enlargement (> 2 months), persistent lymphadenopathy or splenomegaly, monoclonal gammapathy and type II mixed cryoglobulinemia.
  • The treatment and prognosis of lymphoma associated with SS depend on the type and stage of lymphoma.
  • CONCLUSION: Patients with SS develop a variety B lymphoproliferative disorders.
  • [MeSH-major] Lymphoma, B-Cell / diagnosis. Lymphoma, B-Cell / etiology. Salivary Gland Neoplasms / etiology. Sjogren's Syndrome / complications

  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16273862.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD20
  • [Number-of-references] 25
  •  go-up   go-down


8. Rao VK, Price S, Perkins K, Aldridge P, Tretler J, Davis J, Dale JK, Gill F, Hartman KR, Stork LC, Gnarra DJ, Krishnamurti L, Newburger PE, Puck J, Fleisher T: Use of rituximab for refractory cytopenias associated with autoimmune lymphoproliferative syndrome (ALPS). Pediatr Blood Cancer; 2009 Jul;52(7):847-52
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of rituximab for refractory cytopenias associated with autoimmune lymphoproliferative syndrome (ALPS).
  • BACKGROUND: ALPS is a disorder of apoptosis resulting in accumulation of autoreactive lymphocytes, leading to marked lymphadenopathy, hepatosplenomegaly, and multilineage cytopenias due to splenic sequestration and/or autoimmune destruction often presenting in childhood.
  • We summarize our experience of rituximab use during the last 8 years in 12 patients, 9 children, and 3 adults, out of 259 individuals with ALPS, belonging to 166 families currently enrolled in studies at the National Institutes of Health.
  • METHODS: Refractory immune thrombocytopenia (platelet count <20,000) in nine patients and autoimmune hemolytic anemia (AIHA) in three patients led to treatment with rituximab.
  • RESULTS: In seven out of nine patients with ALPS and thrombocytopenia, rituximab therapy led to median response duration of 21 months (range 14-36 months).
  • Long-term follow-up of ALPS patients with cytopenias after any treatment is necessary to determine relative risks and benefits.

  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • [Cites] Leuk Lymphoma. 2001 May;41(5-6):501-11 [11378568.001]
  • [Cites] Blood. 2001 Jul 1;98(1):194-200 [11418480.001]
  • [Cites] Blood. 2001 Aug 15;98(4):952-7 [11493438.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2466-73 [11588044.001]
  • [Cites] Br J Haematol. 2002 Apr;117(1):176-88 [11918552.001]
  • [Cites] Br J Haematol. 2002 Sep;118(4):1078-81 [12199788.001]
  • [Cites] Nature. 2002 Sep 26;419(6905):395-9 [12353035.001]
  • [Cites] Blood. 2003 May 15;101(10):3857-61 [12531800.001]
  • [Cites] Curr Opin Rheumatol. 2003 Jul;15(4):417-21 [12819469.001]
  • [Cites] N Engl J Med. 2004 Sep 30;351(14):1409-18 [15459302.001]
  • [Cites] J Pediatr. 1967 Jun;70(6):891-9 [4165068.001]
  • [Cites] J Clin Invest. 1992 Aug;90(2):334-41 [1386609.001]
  • [Cites] Science. 1995 Jun 2;268(5215):1347-9 [7539157.001]
  • [Cites] Cell. 1995 Jun 16;81(6):935-46 [7540117.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1341-8 [9028957.001]
  • [Cites] Am J Pathol. 1998 Nov;153(5):1541-50 [9811346.001]
  • [Cites] Ann Intern Med. 1999 Apr 6;130(7):591-601 [10189330.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1002-14 [10090885.001]
  • [Cites] Br J Haematol. 2005 May;129(4):534-8 [15877736.001]
  • [Cites] Hum Genet. 2006 Apr;119(3):284-94 [16446975.001]
  • [Cites] Blood. 2006 Apr 1;107(7):2639-42 [16352811.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1965-71 [16757690.001]
  • [Cites] J Pediatr Hematol Oncol. 2006 Dec;28(12):824-6 [17164652.001]
  • [Cites] J Pediatr. 2007 Apr;150(4):338-44, 344.e1 [17382107.001]
  • [Cites] Br J Haematol. 2007 May;137(4):349-54 [17456057.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 22;104(21):8953-8 [17517660.001]
  • [Cites] BMC Med Genet. 2007;8:41 [17605793.001]
  • [Cites] Eur J Haematol. 2007 Oct;79(4):363-6 [17725802.001]
  • [Cites] Arthritis Rheum. 2007 Sep;56(9):3044-56 [17763423.001]
  • [Cites] Am J Hematol. 2007 Dec;82(12):1049-55 [17674358.001]
  • [Cites] Blood. 2008 Jan 15;111(2):705-14 [17925488.001]
  • [Cites] Br J Haematol. 2008 Apr;141(2):149-69 [18318765.001]
  • [Cites] Pathology. 2008 Apr;40(3):288-94 [18428049.001]
  • [Cites] Blood. 2008 Jul 15;112(2):277-86 [18319398.001]
  • [Cites] Pediatr Blood Cancer. 2009 Feb;52(2):259-62 [18937333.001]
  • [Cites] Exp Hematol. 2009 Apr;37(4):487-94 [19217201.001]
  • (PMID = 19214977.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / Intramural NIH HHS / / Z99 AI999999; United States / PHS HHS / / HHSN261200800001E
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Immunosuppressive Agents; 4F4X42SYQ6 / Rituximab
  • [Other-IDs] NLM/ NIHMS123735; NLM/ PMC2774763
  •  go-up   go-down


9. Gualco G, van den Berg A, Koopmans S, Bacchi LM, Carneiro SS, Ruiz E Jr, Vecchi AP, Chan JK: Autoimmune lymphoproliferative syndrome in a patient with a new minimal deletion in the death domain of the FAS gene. Hum Pathol; 2008 Jan;39(1):137-41
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autoimmune lymphoproliferative syndrome in a patient with a new minimal deletion in the death domain of the FAS gene.
  • We present a case of autoimmune lymphoproliferative syndrome (ALPS) caused by a previously undescribed minimal deletion in the death domain of the FAS gene.
  • ALPS is an uncommon disease associated with an impaired Fas-mediated apoptosis.
  • The patient presented with a history of splenomegaly since 4 months of age, associated with cervical lymphadenopathy, which improved with oral corticosteroid treatment.
  • Some clear cells were also present, raising the suspicion of malignant lymphoma.
  • [MeSH-major] Autoimmune Diseases / genetics. Fas-Associated Death Domain Protein / genetics. Lymphoproliferative Disorders / genetics. Sequence Deletion

  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18070632.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 070058; United States / NCI NIH HHS / CA / CA 082274
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Fas-Associated Death Domain Protein
  •  go-up   go-down


10. Libra M, Indelicato M, De Re V, Zignego AL, Chiocchetti A, Malaponte G, Dianzani U, Nicoletti F, Stivala F, McCubrey JA, Mazzarino MC: Elevated Serum Levels of Osteopontin in HCV-Associated Lymphoproliferative Disorders. Cancer Biol Ther; 2005 Nov;4(11):1192-4
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated Serum Levels of Osteopontin in HCV-Associated Lymphoproliferative Disorders.
  • Hepatitis C virus (HCV) infection is associated with chronic hepatitis, cirrhosis, and hepatocellular carcinoma.
  • Recent evidences have also suggested that HCV infection contributes to development of autoimmune disorders and B-cell nonHodgkin's lymphoma (NHL).
  • Increased serum osteopontin (OPN) levels have been associated with several autoimmune diseases as well as a variety of cancers.
  • However, the association between OPN and B-cell NHL or HCV-associated B-cell proliferation has not previously been reported.
  • In the present study, we determined whether serum OPN differences were associated with HCV infection, type II mixed cryglobulinemia (MC) syndrome and B-cell NHL.
  • Our results show that high serum OPN levels are associated with B-cell NHL and HCV infection.
  • Interestingly, highest serum OPN concentrations were found among HCV-infected patients with concomitant type II MC syndrome with and without B-cell NHL.
  • These data indicate that OPN is involved in the lymphomagenesis, especially, in the context of HCV infection and autoimmune diseases.
  • [MeSH-major] Cryoglobulinemia / virology. Hepatitis C / complications. Lymphoma, B-Cell / virology. Sialoglycoproteins / blood

  • MedlinePlus Health Information. consumer health - Hepatitis C.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16177564.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA098195
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral; 0 / SPP1 protein, human; 0 / Sialoglycoproteins; 106441-73-0 / Osteopontin
  •  go-up   go-down


11. Dowdell KC, Pesnicak L, Hoffmann V, Steadman K, Remaley AT, Cohen JI, Straus SE, Rao VK: Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, diminishes lymphoproliferation in the Fas -deficient MRL/lpr(-/-) murine model of autoimmune lymphoproliferative syndrome (ALPS). Exp Hematol; 2009 Apr;37(4):487-94
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, diminishes lymphoproliferation in the Fas -deficient MRL/lpr(-/-) murine model of autoimmune lymphoproliferative syndrome (ALPS).
  • OBJECTIVE: Autoimmune lymphoproliferative syndrome (ALPS) is a disorder of apoptosis, often presenting in childhood.
  • Similarly, MRL/lpr(-/-) mice homozygous for Fas mutations develop an ALPS-like disease with autoimmunity, lymphadenopathy, splenomegaly, and expansion of double-negative T cells.
  • Currently, there are no proven therapies with adequate safety margins for sustained abolition of the lymphoproliferation associated with ALPS.
  • MATERIALS AND METHODS: Human peripheral blood mononuclear cells from patients with ALPS and normal controls were tested in vitro to determine the efficacy of VPA at inducing cell death.
  • VPA was used in vivo to control lymphoproliferation in MRL/lpr(-/-) mice, a model for ALPS.
  • CONCLUSION: Based on our data, VPA is effective at reducing lymphoproliferation in mice, and is currently being studied in a clinical trial as a lympholytic agent in patients with ALPS.
  • [MeSH-major] Apoptosis / drug effects. Autoimmune Diseases / drug therapy. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Lymphoproliferative Disorders / drug therapy. T-Lymphocytes / drug effects. Valproic Acid / pharmacology
  • [MeSH-minor] Animals. Antigens, CD95 / genetics. Cell Proliferation / drug effects. Cells, Cultured. Disease Models, Animal. Female. Humans. Leukocytes, Mononuclear / cytology. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. Mice. Mice, Knockout. Reference Standards. Syndrome

  • Genetic Alliance. consumer health - Autoimmune Lymphoproliferative Syndrome.
  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. VALPROIC ACID .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 May 15;97(10):3161-70 [11342444.001]
  • [Cites] Mol Cancer Ther. 2005 Dec;4(12):1912-22 [16373706.001]
  • [Cites] Leuk Res. 2002 May;26(5):495-502 [11916526.001]
  • [Cites] J Clin Invest. 2003 Feb;111(4):539-52 [12588892.001]
  • [Cites] FEBS Lett. 2003 May 8;542(1-3):74-8 [12729901.001]
  • [Cites] Int J Oncol. 2004 Mar;24(3):679-85 [14767553.001]
  • [Cites] Clin Cancer Res. 2004 Feb 1;10(3):1141-9 [14871994.001]
  • [Cites] J Immunol. 2004 Sep 15;173(6):4171-8 [15356168.001]
  • [Cites] N Engl J Med. 2004 Sep 30;351(14):1409-18 [15459302.001]
  • [Cites] J Natl Cancer Inst. 2004 Oct 6;96(19):1447-57 [15467034.001]
  • [Cites] Nature. 1992 Mar 26;356(6367):314-7 [1372394.001]
  • [Cites] J Clin Invest. 1992 Aug;90(2):334-41 [1386609.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1341-8 [9028957.001]
  • [Cites] Am J Pathol. 1998 Nov;153(5):1541-50 [9811346.001]
  • [Cites] Oncogene. 2006 Jan 26;25(4):512-24 [16186804.001]
  • [Cites] Neuroscience. 2006 Jul 21;140(4):1149-56 [16600518.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1965-71 [16757690.001]
  • [Cites] Anticancer Drugs. 2006 Nov;17(10):1141-50 [17075313.001]
  • [Cites] Blood. 2006 Dec 15;108(13):3967-75 [16926289.001]
  • [Cites] Int J Oncol. 2007 Mar;30(3):573-82 [17273758.001]
  • [Cites] Neurobiol Dis. 2007 May;26(2):464-72 [17398106.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 22;104(21):8953-8 [17517660.001]
  • [Cites] Br J Cancer. 2007 Jul 16;97(2):177-82 [17579623.001]
  • [Cites] J Reprod Dev. 2007 Aug;53(4):903-13 [17558190.001]
  • [Cites] Exp Hematol. 2007 Oct;35(10):1527-37 [17697742.001]
  • [Cites] Endocr Relat Cancer. 2007 Sep;14(3):839-45 [17914112.001]
  • [Cites] Am J Hematol. 2007 Dec;82(12):1049-55 [17674358.001]
  • [Cites] Gynecol Oncol. 2008 Jan;108(1):27-33 [17920664.001]
  • [Cites] Mol Med. 2008 Jan-Feb;14(1-2):20-7 [17973028.001]
  • [Cites] Blood. 2008 Jan 15;111(2):705-14 [17925488.001]
  • [Cites] Biomed Pharmacother. 2008 Feb;62(2):85-93 [17644301.001]
  • [Cites] Int J Mol Med. 2008 Mar;21(3):325-33 [18288380.001]
  • [Cites] Immunol Lett. 2008 Apr 15;117(1):45-9 [18222547.001]
  • [Cites] Chem Biol Interact. 2008 Apr 15;172(3):235-44 [18313654.001]
  • [Cites] Radiology. 1999 Jul;212(1):257-63 [10405750.001]
  • [Cites] Clin Immunol. 1999 Oct;93(1):34-45 [10497009.001]
  • [Cites] Mol Cancer Ther. 2004 Nov;3(11):1397-402 [15542778.001]
  • [Cites] J Cereb Blood Flow Metab. 2004 Nov;24(11):1226-34 [15545916.001]
  • [Cites] Br J Cancer. 2005 Feb 28;92(4):751-9 [15685243.001]
  • [Cites] Clin Cancer Res. 2005 Nov 1;11(21):7945-52 [16278420.001]
  • [Cites] FEBS Lett. 2005 Dec 19;579(30):6716-20 [16313906.001]
  • [Cites] J Proteome Res. 2005 Nov-Dec;4(6):2032-42 [16335948.001]
  • [Cites] Surgery. 2005 Dec;138(6):979-84; discussion 984-5 [16360381.001]
  • [Cites] Leuk Lymphoma. 2001 May;41(5-6):501-11 [11378568.001]
  • (PMID = 19217201.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 AI999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Enzyme Inhibitors; 0 / Fas protein, mouse; 0 / Histone Deacetylase Inhibitors; 614OI1Z5WI / Valproic Acid
  • [Other-IDs] NLM/ NIHMS106599; NLM/ PMC2693256
  •  go-up   go-down


12. Papiris SA, Tsonis IA, Moutsopoulos HM: Sjögren's Syndrome. Semin Respir Crit Care Med; 2007 Aug;28(4):459-71
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sjögren's Syndrome.
  • Sjögren's syndrome (SS) is a chronic, slowly progressive, inflammatory, autoimmune disease characterized by (1) lymphocytic infiltration of the exocrine glands leading to diminished or absent glandular secretion, and (2) marked B-lymphocytic cell hyperreactivity manifested initially by a variety of serum autoantibodies, including those against the Ro(SSA) and La(SSB) ribonucleoproteins, ending in the development of B cell non-Hodgkin's lymphoma in a substantial number of patients.
  • (2) a wide spectrum of lymphoproliferative diseases, ranging from bronchus-associated lymphoid tissue (BALT) hyperplasia, lymphoid interstitial pneumonia, and B cell non-Hodgkin's lymphoma mainly of the extranodal marginal zone B-cell lymphoma of BALT-type or rarely of higher-grade malignancy; and (3) other interstitial pneumonias.
  • Pleuritis can be seen in SS patients with associated systemic lupus erythematosus or rheumatoid arthritis.
  • [MeSH-major] Lung Diseases, Interstitial / etiology. Respiratory Tract Diseases / etiology. Sjogren's Syndrome / complications
  • [MeSH-minor] Humans. Lymphoproliferative Disorders / etiology. Prognosis. Respiratory Function Tests

  • MedlinePlus Health Information. consumer health - Interstitial Lung Diseases.
  • MedlinePlus Health Information. consumer health - Sjogren's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17764063.001).
  • [ISSN] 1069-3424
  • [Journal-full-title] Seminars in respiratory and critical care medicine
  • [ISO-abbreviation] Semin Respir Crit Care Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 128
  •  go-up   go-down


13. Ramos-Casals M, De Vita S, Tzioufas AG: Hepatitis C virus, Sjögren's syndrome and B-cell lymphoma: linking infection, autoimmunity and cancer. Autoimmun Rev; 2005 Jan;4(1):8-15
MedlinePlus Health Information. consumer health - Sjogren's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatitis C virus, Sjögren's syndrome and B-cell lymphoma: linking infection, autoimmunity and cancer.
  • An increased prevalence of hematologic malignancies is often described in patients with Sjögren's syndrome (SS).
  • Viruses have been proposed as possible etiologic or triggering agents of systemic autoimmune diseases (SADs), with hepatitis C virus (HCV) being one of the viruses most frequently associated with autoimmune features and with systemic autoimmune diseases such as mixed cryoglobulinemia or SS.
  • Moreover, the association between HCV infection and hematologic malignancies, mainly non-Hodgkin's lymphoma (NHL), is supported by several studies.
  • For these reasons, the recognized association of specific systemic autoimmune diseases (mainly SS and mixed cryoglobulinemia) with HCV infection, added to the possible evolution of any one of these entities into a B-cell NHL, suggests the possibility of a close relationship among SS, HCV and B-cell lymphoproliferative disorders, especially in patients with type II mixed cryoglobulinemia.
  • [MeSH-major] Autoimmunity / immunology. Hepacivirus / immunology. Hepatitis C / immunology. Lymphoma, B-Cell / immunology. Sjogren's Syndrome / immunology

  • Genetic Alliance. consumer health - C Syndrome.
  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Hepatitis C.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15652773.001).
  • [ISSN] 1568-9972
  • [Journal-full-title] Autoimmunity reviews
  • [ISO-abbreviation] Autoimmun Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Ribonucleoproteins; 0 / SS-A antigen; 0 / SS-B antigen
  • [Number-of-references] 32
  •  go-up   go-down


14. Grulich AE, Vajdic CM: The epidemiology of non-Hodgkin lymphoma. Pathology; 2005 Dec;37(6):409-19
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The epidemiology of non-Hodgkin lymphoma.
  • Non-Hodgkin lymphoma (NHL) includes a group of more than 20 different malignant lymphoproliferative diseases that originate from lymphocytes.
  • The best described risk factor for NHL is immune deficiency; rates of NHL are greatly increased, with relative risks of 10-100 or more, in people with immune deficiency associated with immune suppressive therapy after transplantation, HIV/AIDS, and congenital conditions.
  • In addition, some NHL subtypes are associated with specific infections.
  • These include immune-deficiency-associated central nervous system NHL (Epstein-Barr virus); gastric mucosa-associated lymphoid tissue NHL (Helicobacter pylori); adult T-cell leukemia/lymphoma (human T-lymphotrophic virus type 1) and body cavity-based lymphoma (human herpesvirus 8).
  • Specific autoimmune conditions, including rheumatoid arthritis, systemic lupus erythema, Sjogren's syndrome, psoriasis and coeliac disease are associated with moderately increased risk of NHL.
  • On the other hand, allergic and atopic conditions and their correlates such as early birth order, appear to be associated with a decreased risk of NHL.A variety of other exposures are less strongly related to NHL risk.
  • Recently, two studies have reported that sun exposure is associated with a decreased risk of NHL.
  • Smoking appears to be weakly positively associated with risk of follicular NHL, and alcohol intake is associated with a decreased risk of NHL.
  • [MeSH-major] Lymphoma, Non-Hodgkin / epidemiology

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16373224.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 147
  •  go-up   go-down


15. Quartuccio L, Fabris M, Salvin S, Maset M, De Marchi G, De Vita S: Controversies on rituximab therapy in sjögren syndrome-associated lymphoproliferation. Int J Rheumatol; 2009;2009:424935

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Controversies on rituximab therapy in sjögren syndrome-associated lymphoproliferation.
  • Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by chronic inflammation of salivary and lachrymal glands, and frequently accompanied by systemic symptoms.
  • A subgroup of SS patients develops malignant B cell non-Hodgkin's lymphoma (NHL), usually of the mucosa-associated lymphoid tissue (MALT) type and very often located in the major salivary glands.
  • Rituximab (RTX), a chimeric monoclonal antibody targeting the CD20 antigen on the B cell surface, has been successfully investigated in other autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, ANCA-associated vasculitis, and mixed cryoglobulinemic syndrome.
  • Preliminary experiences of RTX therapy in SS patients with or without a lymphoproliferative disorder suggest that SS patients with more residual exocrine gland function might better benefit from RTX.
  • Efficacy of RTX in SS-associated B-cell lymphoma, mainly in low-grade salivary gland lymphomas, remains an open issue.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Open Rheumatol J. 2008;2:38-43 [19088870.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4029-38 [18263783.001]
  • [Cites] Clin Rev Allergy Immunol. 2008 Feb;34(1):80-4 [18270861.001]
  • [Cites] Clin Rev Allergy Immunol. 2007 Jun;32(3):265-74 [17992593.001]
  • [Cites] Arthritis Rheum. 2007 May;56(5):1464-77 [17469105.001]
  • [Cites] Ann Rheum Dis. 2007 Mar;66(3):351-7 [16950808.001]
  • [Cites] Ann Rheum Dis. 2006 Aug;65(8):1033-7 [16322082.001]
  • [Cites] Arthritis Rheum. 2005 Sep;52(9):2740-50 [16142737.001]
  • [Cites] Ann Rheum Dis. 2005 Jun;64(6):958-60 [15576414.001]
  • [Cites] Ann Rheum Dis. 2005 Jun;64(6):913-20 [15550531.001]
  • [Cites] Lupus. 2004;13(12):969-71 [15645755.001]
  • [Cites] Curr Dir Autoimmun. 2005;8:243-65 [15564724.001]
  • [Cites] Am J Med. 1964 Apr;36:529-40 [14142406.001]
  • [Cites] Arthritis Rheum. 1999 Aug;42(8):1765-72 [10446879.001]
  • [Cites] J Clin Invest. 1998 Sep 1;102(5):938-46 [9727062.001]
  • [Cites] Arthritis Rheum. 1997 Feb;40(2):318-31 [9041944.001]
  • [Cites] Curr Opin Oncol. 1996 May;8(3):232-7 [8804813.001]
  • [Cites] Br J Rheumatol. 1995 Apr;34(4):326-33 [7788146.001]
  • [Cites] Ann Intern Med. 1978 Dec;89(6):888-92 [102228.001]
  • [Cites] Rheumatology (Oxford). 2004 Oct;43(10):1309-10 [15448217.001]
  • [Cites] Rheumatology (Oxford). 2004 Aug;43(8):1050-3 [15187246.001]
  • [Cites] J Pathol. 2004 Apr;202(4):496-502 [15095277.001]
  • [Cites] Arthritis Rheum. 2003 Nov;48(11):3181-6 [14613281.001]
  • [Cites] Arthritis Rheum. 2003 Jun 15;49(3):394-8 [12794796.001]
  • [Cites] Lab Invest. 2003 Mar;83(3):357-65 [12649336.001]
  • [Cites] Ann Rheum Dis. 2003 Feb;62(2):168-71 [12525388.001]
  • [Cites] Arthritis Rheum. 2002 Aug;46(8):2029-33 [12209504.001]
  • [Cites] Clin Nucl Med. 2002 Feb;27(2):142-3 [11786752.001]
  • [Cites] Semin Arthritis Rheum. 2000 Apr;29(5):296-304 [10805354.001]
  • [Cites] Arthritis Rheum. 2000 Jan;43(1):94-102 [10643704.001]
  • [Cites] J Exp Med. 1999 Dec 6;190(11):1697-710 [10587360.001]
  • (PMID = 20148068.001).
  • [ISSN] 1687-9279
  • [Journal-full-title] International journal of rheumatology
  • [ISO-abbreviation] Int J Rheumatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2817502
  •  go-up   go-down


16. Quartuccio L, De Re V, Fabris M, Marzotto A, Franzolini N, Gasparotto D, Caggiari L, Ferraccioli G, Scott CA, De Vita S: Atypical lymphoproliferation progressing into B-cell lymphoma in rheumatoid arthritis treated with different biological agents: clinical course and molecular characterization. Haematologica; 2006 May;91(5):691-4
Hazardous Substances Data Bank. CYCLOSPORIN A .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical lymphoproliferation progressing into B-cell lymphoma in rheumatoid arthritis treated with different biological agents: clinical course and molecular characterization.
  • A patient with rheumatoid arthritis (RA) developed an atypical lymphoproliferative disorder (LPD) after methotrexate and cyclosporine A, which regressed after suspension of both drugs.
  • Anti-tumor necrosis factor a therapy was used when the arthritis relapsed, but an aggressive B-cell non Hodgkin's lymphoma developed.
  • A minor clone with significant sequence homology to B-cell lymphomas arising in Sjogren's syndrome and mixed cryoglobulinemia syndrome, given rise to the non-Hodgkin's lymphoma.
  • Treatment of rheumatoid arthritis associated with lymphoproliferation represents a clinical challenge, and common pathogenetic pathways to lymphoma may occur in different autoimmune diseases.
  • [MeSH-major] Antirheumatic Agents / therapeutic use. Arthritis, Rheumatoid / complications. Immunosuppressive Agents / therapeutic use. Lymphoma, Large B-Cell, Diffuse / etiology. Lymphoproliferative Disorders / complications
  • [MeSH-minor] Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Autoimmune Diseases / complications. Cyclosporine / adverse effects. Cyclosporine / therapeutic use. DNA, Neoplasm / genetics. Disease Progression. Disease Susceptibility. Etanercept. Female. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Gene Rearrangement, B-Lymphocyte, Light Chain. Genes, Immunoglobulin. Humans. Immunocompromised Host. Immunoglobulin G / adverse effects. Immunoglobulin G / contraindications. Immunoglobulin G / therapeutic use. Methotrexate / adverse effects. Methotrexate / therapeutic use. Neoplasm Proteins / analysis. Neoplasm Proteins / genetics. Receptors, Tumor Necrosis Factor / therapeutic use. Rituximab. Tumor Necrosis Factor-alpha / antagonists & inhibitors

  • Genetic Alliance. consumer health - Arthritis.
  • Genetic Alliance. consumer health - Rheumatoid arthritis.
  • MedlinePlus Health Information. consumer health - Rheumatoid Arthritis.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. Etanercept .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16670074.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antirheumatic Agents; 0 / DNA, Neoplasm; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Neoplasm Proteins; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; 4F4X42SYQ6 / Rituximab; 83HN0GTJ6D / Cyclosporine; OP401G7OJC / Etanercept; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


17. Papiris SA, Kalomenidis I, Malagari K, Kapotsis GE, Harhalakis N, Manali ED, Rontogianni D, Roussos C, Moutsopoulos HM: Extranodal marginal zone B-cell lymphoma of the lung in Sjögren's syndrome patients: reappraisal of clinical, radiological, and pathology findings. Respir Med; 2007 Jan;101(1):84-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extranodal marginal zone B-cell lymphoma of the lung in Sjögren's syndrome patients: reappraisal of clinical, radiological, and pathology findings.
  • BACKGROUND: Primary Sjögren's syndrome (pSs) is an autoimmune rheumatic disease that may express in a small number of patients a spectrum of lymphoproliferative diseases.
  • The aim of this study was to describe clinical, imaging and pathology features of the extranodal marginal zone B-cell lymphoma (MZCL) of the lung of mucosa-associated lymphoid tissue (MALT) type in patients with pSs.
  • CONCLUSIONS: Lung MZCL associated with pSs are characterized by an important dissociation between clinical expression and radiological pattern.
  • [MeSH-major] Lymphoma, B-Cell / complications. Lymphoma, B-Cell, Marginal Zone / complications
  • [MeSH-minor] B-Lymphocytes / pathology. Biomarkers / analysis. CD4-Positive T-Lymphocytes / pathology. Female. Humans. Immunohistochemistry / methods. Keratins / analysis. Lung / pathology. Lung / radiography. Male. Sjogren's Syndrome / complications. Sjogren's Syndrome / pathology. Sjogren's Syndrome / radiography. Tomography, X-Ray Computed

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16735112.001).
  • [ISSN] 0954-6111
  • [Journal-full-title] Respiratory medicine
  • [ISO-abbreviation] Respir Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 68238-35-7 / Keratins
  •  go-up   go-down


18. Yeh S, Li Z, Sen HN, Lim WK, Gill F, Perkins K, Rao VK, Nussenblatt RB: Scleritis and multiple systemic autoimmune manifestations in chronic natural killer cell lymphocytosis associated with elevated TCRalpha/beta+CD3+CD4-CD8- double-negative T cells. Br J Ophthalmol; 2010 Jun;94(6):748-52
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scleritis and multiple systemic autoimmune manifestations in chronic natural killer cell lymphocytosis associated with elevated TCRalpha/beta+CD3+CD4-CD8- double-negative T cells.
  • BACKGROUND/AIMS: Chronic natural killer lymphocytosis (CNKL) has been associated with systemic autoimmunity; however, its association with scleritis or ocular autoimmunity has not been characterised.
  • The natural killer (NK) cell function and immunophenotype of a patient with CNKL who developed bilateral scleritis and multiple systemic autoimmune findings were evaluated.
  • RESULTS: A 56-year-old woman with vitiligo, psoriatic arthritis, thyroiditis, erythema nodosum, bilateral anterior scleritis and Sjogren syndrome was managed with multiple immunosuppressive medications, including prednisone, mycophenolate mofetil and methotrexate.
  • An abnormal elevation of TCRalpha/beta(+) CD3(+)CD4(-)CD8(-) T cells suggestive of autoimmune lymphoproliferative syndrome was observed; however, apoptosis dysfunction was not found.
  • [MeSH-major] Autoimmune Diseases / immunology. Killer Cells, Natural / immunology. Lymphocytosis / immunology. Scleritis / immunology. T-Lymphocyte Subsets / immunology

  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Immunol. 2002 Jul;104(1):21-30 [12139944.001]
  • [Cites] Autoimmun Rev. 2008 May;7(5):384-90 [18486926.001]
  • [Cites] Br J Dermatol. 2003 Jul;149(1):160-4 [12890211.001]
  • [Cites] J Autoimmun. 2003 Aug;21(1):83-92 [12892739.001]
  • [Cites] Ophthalmology. 2004 Mar;111(3):501-6 [15019326.001]
  • [Cites] Brain. 2004 Sep;127(Pt 9):1917-27 [15229129.001]
  • [Cites] Arthritis Rheum. 1983 Aug;26(8):954-60 [6882489.001]
  • [Cites] Ophthalmology. 1985 Nov;92(11):1542-9 [3878485.001]
  • [Cites] Arch Dermatol Res. 1986;278(4):264-9 [3740937.001]
  • [Cites] Clin Exp Immunol. 1988 May;72(2):299-302 [3409548.001]
  • [Cites] Cancer. 1989 Jan 1;63(1):90-5 [2783378.001]
  • [Cites] J Neurol Sci. 1989 Dec;94(1-3):115-23 [2614463.001]
  • [Cites] Ophthalmology. 1991 Apr;98(4):472-9 [1828871.001]
  • [Cites] Blood. 1994 Oct 15;84(8):2721-5 [7919384.001]
  • [Cites] Leuk Lymphoma. 1996 Jan;20(3-4):245-8 [8624463.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1341-8 [9028957.001]
  • [Cites] Am J Pathol. 1997 Feb;150(2):653-66 [9033278.001]
  • [Cites] J Neuroimmunol. 1998 Jun 15;86(2):123-33 [9663557.001]
  • [Cites] J Biol Chem. 2005 Feb 11;280(6):4772-8 [15563472.001]
  • [Cites] J Immunol. 2005 May 1;174(9):5187-91 [15843513.001]
  • [Cites] Intern Med. 2007;46(5):251-4 [17329922.001]
  • [Cites] Immunol Res. 2008;40(1):87-92 [18193364.001]
  • [Cites] Br J Ophthalmol. 2008 Mar;92(3):417-9 [18303163.001]
  • [Cites] Nat Immunol. 2002 Sep;3(9):807-13 [12205470.001]
  • (PMID = 20508050.001).
  • [ISSN] 1468-2079
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 EY000393-06; United States / Intramural NIH HHS / / ZIA EY000376-09
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-2; 0 / Receptors, Antigen, T-Cell, alpha-beta
  • [Other-IDs] NLM/ NIHMS320628; NLM/ PMC3172679
  •  go-up   go-down


19. Berger F, Traverse-Glehen A, Felman P, Callet-Bauchu E, Baseggio L, Gazzo S, Thieblemont C, Ffrench M, Magaud JP, Salles G, Coiffer B: Clinicopathologic features of Waldenstrom's macroglobulinemia and marginal zone lymphoma: are they distinct or the same entity? Clin Lymphoma; 2005 Mar;5(4):220-4
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathologic features of Waldenstrom's macroglobulinemia and marginal zone lymphoma: are they distinct or the same entity?
  • Waldenstrom's macroglobulinemia (WM) is considered in the World Health Organization classification as a clinical syndrome associated with monoclonal immunoglobulin (Ig) M secretion, mainly observed in patients with lymphoplasmacytic lymphoma (LPL) and occasionally with other small B-cell lymphomas.
  • Some authors consider it a rare distinct lymphoproliferative disorder with primary bone marrow infiltration and IgM monoclonal gammopathy.
  • Extranodal mucosa-associated lymphoid tissue (MALT) lymphoma, nodal MZL (NMZL), and splenic MZL (SMZL) are distinct entities displaying common morphologic, immunophenotypic, and genetic characteristics.
  • MALT lymphoma is clearly distinct from LPL, although bone marrow infiltration and IgM paraprotein are not rare.
  • Splenic MZL and NMZL are incompletely characterized, but a plasmacytoid/plasmacytic differentiation, autoimmune manifestations, and monoclonal component are frequent in both diseases.
  • [MeSH-major] Antigens, CD. Leukemia, Lymphocytic, Chronic, B-Cell / classification. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / pathology. Waldenstrom Macroglobulinemia / classification. Waldenstrom Macroglobulinemia / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15794852.001).
  • [ISSN] 1526-9655
  • [Journal-full-title] Clinical lymphoma
  • [ISO-abbreviation] Clin Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Immunoglobulin M
  • [Number-of-references] 38
  •  go-up   go-down


20. Liu X, Karnell JL, Yin B, Zhang R, Zhang J, Li P, Choi Y, Maltzman JS, Pear WS, Bassing CH, Turka LA: Distinct roles for PTEN in prevention of T cell lymphoma and autoimmunity in mice. J Clin Invest; 2010 Jul;120(7):2497-507
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct roles for PTEN in prevention of T cell lymphoma and autoimmunity in mice.
  • Mutations in the tumor-suppressor gene phosphatase and tensin homolog deleted on chromosome 10 (Pten) are associated with multiple cancers in humans, including T cell malignancies.
  • Targeted deletion of Pten in T cells induces both a disseminated "mature phenotype" lymphoma and a lymphoproliferative autoimmune syndrome in mice.
  • These data suggest multiple and distinct regulatory roles for PTEN in the molecular pathogenesis of lymphoma and autoimmunity.

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Annu Rev Biochem. 2002;71:101-32 [12045092.001]
  • [Cites] J Exp Med. 2009 Oct 26;206(11):2441-54 [19808258.001]
  • [Cites] J Exp Med. 2004 Oct 4;200(7):883-94 [15452180.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Ann N Y Acad Sci. 1975 Jun 30;254:505-15 [52321.001]
  • [Cites] Science. 1986 May 16;232(4752):884-6 [3486470.001]
  • [Cites] Immunity. 2001 May;14(5):523-34 [11371355.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3788-93 [11891328.001]
  • [Cites] Science. 1986 Nov 21;234(4779):982-5 [3490692.001]
  • [Cites] Oncogene. 1988 Feb;2(2):195-200 [2966921.001]
  • [Cites] Cancer Genet Cytogenet. 1990 Oct 1;49(1):69-74 [2397475.001]
  • [Cites] Leukemia. 1991 Jan;5(1):60-5 [1705637.001]
  • [Cites] Nature. 1992 Nov 19;360(6401):225-31 [1359428.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):355-8 [7566092.001]
  • [Cites] Clin Diagn Lab Immunol. 1996 Jul;3(4):374-7 [8807199.001]
  • [Cites] Science. 1997 Mar 28;275(5308):1943-7 [9072974.001]
  • [Cites] Nat Genet. 1997 May;16(1):64-7 [9140396.001]
  • [Cites] Cancer Res. 1997 Dec 1;57(23):5221-5 [9393738.001]
  • [Cites] Hum Mol Genet. 1998 Mar;7(3):507-15 [9467011.001]
  • [Cites] J Biol Chem. 1998 May 29;273(22):13375-8 [9593664.001]
  • [Cites] Science. 1998 Jul 17;281(5375):416-9 [9665885.001]
  • [Cites] Science. 1999 Sep 24;285(5436):2122-5 [10497129.001]
  • [Cites] Eur J Immunol. 2005 Mar;35(3):964-70 [15719363.001]
  • [Cites] J Exp Med. 2005 Oct 3;202(7):893-900 [16186188.001]
  • [Cites] Eur J Cancer. 2005 Nov;41(17):2620-9 [16239105.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • [Cites] Nat Rev Genet. 2006 Aug;7(8):606-19 [16847462.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] J Immunol. 2006 Oct 1;177(7):4262-6 [16982858.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Cell. 2007 Jan 12;128(1):25-8 [17218252.001]
  • [Cites] Cell. 2007 Jan 12;128(1):157-70 [17218262.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Cell. 2007 Jul 13;130(1):25-35 [17632054.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2022-7 [18250301.001]
  • [Cites] Leukemia. 2008 Mar;22(3):608-19 [18046443.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] Nature. 2008 May 22;453(7194):529-33 [18463637.001]
  • [Cites] Nature. 2008 Dec 11;456(7223):819-23 [18849970.001]
  • [Cites] Blood. 2009 Jul 16;114(3):647-50 [19458356.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1417-25 [19340001.001]
  • [Cites] Cell. 2002 Jun 28;109(7):811-21 [12110179.001]
  • (PMID = 20516645.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI047833; United States / NIAID NIH HHS / AI / AI047833; United States / NCI NIH HHS / CA / R01 CA125195; United States / NIAID NIH HHS / AI / AI 43620; United States / NCI NIH HHS / CA / CA119070; United States / NIAID NIH HHS / AI / P01 AI043620; United States / NCI NIH HHS / CA / CA125195; United States / NCI NIH HHS / CA / P01 CA119070
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2898609
  •  go-up   go-down


21. Manganelli P, Fietta P, Quaini F: Hematologic manifestations of primary Sjögren's syndrome. Clin Exp Rheumatol; 2006 Jul-Aug;24(4):438-48
MedlinePlus Health Information. consumer health - Sjogren's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematologic manifestations of primary Sjögren's syndrome.
  • Sjögren's syndrome (SS) is a chronic autoimmune disorder, primarily characterized by the mononuclear cell infiltration of exocrine glands exiting in parenchymal damage and secretory impairment.
  • The spectrum of the disease extends from an autoimmune exocrinopathy to a systemic process with extraglandular manifestations.
  • SS is defined as primary (pSS) when isolated, or secondary when associated with another autoimmune disease.
  • Patients with pSS may present hematologic abnormalities, such as anemia, hemocytopenias, monoclonal gammopathies and lymphoprolipherative disorders, predominantly non-Hodgkin's lymphoma of B-cell origin.
  • [MeSH-major] Hematologic Diseases / etiology. Sjogren's Syndrome / complications
  • [MeSH-minor] Autoimmunity. Humans. Lymphoproliferative Disorders

  • MedlinePlus Health Information. consumer health - Blood Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16956437.001).
  • [ISSN] 0392-856X
  • [Journal-full-title] Clinical and experimental rheumatology
  • [ISO-abbreviation] Clin. Exp. Rheumatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 147
  •  go-up   go-down


22. Tran H, Nourse J, Hall S, Green M, Griffiths L, Gandhi MK: Immunodeficiency-associated lymphomas. Blood Rev; 2008 Sep;22(5):261-81
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunodeficiency-associated lymphomas.
  • This article covers lymphoproliferative disorders in patients with primary or acquired immunodeficiencies.
  • Primary immunodeficiences include Ataxia Telangiectasia and X-linked disorders such as Wiskott-Aldrich syndrome.
  • Evidence for lymphoma developing as a result of treatment with methotrexate or Tumour Necrosis Factor Antagonists for autoimmune entities will also be reviewed.
  • Lastly, discussion will centre on mechanisms utilized by lymphomas in the immunodeficient as these may have applications to lymphomas in the "immunocompetent", by serving as a paradigm for the altered immunoregulatory environment present in many lymphoma sub-types.
  • [MeSH-major] Immunocompromised Host / immunology. Immunologic Deficiency Syndromes / immunology. Lymphoma / immunology

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18456377.001).
  • [ISSN] 0268-960X
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 175
  •  go-up   go-down


23. Alcântara C, Gomes MJ, Ferreira C: Rituximab therapy in primary Sjögren's syndrome. Ann N Y Acad Sci; 2009 Sep;1173:701-5
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rituximab therapy in primary Sjögren's syndrome.
  • Primary Sjögren's syndrome is an autoimmune disease characterized by lymphocytic infiltration of glandular tissues leading to sicca symptoms, namely, dry eyes and dry mouth.
  • A small but not insignificant percentage of those patients evolve to B cell lymphoma.
  • The increased expression of B cell survival factors, such as B cell activating factor, may promote the perpetuation of a B cell clone and precede the lymphoproliferative disease.
  • Rituximab, a chimeric monoclonal antibody to CD20, leads to B cell depletion and may have a role in Sjögren systemic manifestations as well as in preventing and treating Sjögren-associated lymphoma.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD20 / immunology. Sjogren's Syndrome / drug therapy

  • MedlinePlus Health Information. consumer health - Sjogren's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19758218.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antirheumatic Agents; 0 / B-Cell Activating Factor; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


24. Ramos-Casals M, Brito-Zerón P, Yagüe J, Akasbi M, Bautista R, Ruano M, Claver G, Gil V, Font J: Hypocomplementaemia as an immunological marker of morbidity and mortality in patients with primary Sjogren's syndrome. Rheumatology (Oxford); 2005 Jan;44(1):89-94
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypocomplementaemia as an immunological marker of morbidity and mortality in patients with primary Sjogren's syndrome.
  • OBJECTIVE: To analyse the prevalence and clinical significance of hypocomplementaemia in a large series of patients with primary Sjogren's syndrome (SS), focusing on the association of low complement levels with clinical manifestations, immunological features, lymphoproliferative disorders and mortality.
  • We also analysed complement levels in 46 patients with SS associated with hepatitis C virus (HCV) infection and 184 with HCV-related cryoglobulinaemia as control groups.
  • In the multivariate analysis, patients with low C4 levels showed a higher prevalence of peripheral neuropathy, cutaneous vasculitis, RF, cryoglobulins and lymphoma compared with those with normal C4 levels.
  • CONCLUSION: Hypocomplementaemia is closely associated with systemic expression and adverse outcomes (lymphoma development and death) in patients with primary SS.
  • [MeSH-major] Complement System Proteins / deficiency. Sjogren's Syndrome / immunology
  • [MeSH-minor] Aged. Biomarkers / blood. Complement C3 / analysis. Complement C3 / deficiency. Complement C4 / analysis. Complement C4 / deficiency. Complement Hemolytic Activity Assay. Female. Hepatitis C, Chronic / complications. Hepatitis C, Chronic / immunology. Humans. Lymphoma / etiology. Lymphoma / immunology. Male. Middle Aged. Prospective Studies. Survival Analysis

  • MedlinePlus Health Information. consumer health - Sjogren's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15381790.001).
  • [ISSN] 1462-0324
  • [Journal-full-title] Rheumatology (Oxford, England)
  • [ISO-abbreviation] Rheumatology (Oxford)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Complement C3; 0 / Complement C4; 9007-36-7 / Complement System Proteins
  •  go-up   go-down


25. Fabris M, Quartuccio L, Sacco S, De Marchi G, Pozzato G, Mazzaro C, Ferraccioli G, Migone TS, De Vita S: B-Lymphocyte stimulator (BLyS) up-regulation in mixed cryoglobulinaemia syndrome and hepatitis-C virus infection. Rheumatology (Oxford); 2007 Jan;46(1):37-43
MedlinePlus Health Information. consumer health - Hepatitis C.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B-Lymphocyte stimulator (BLyS) up-regulation in mixed cryoglobulinaemia syndrome and hepatitis-C virus infection.
  • OBJECTIVES: To investigate the role of B-Lymphocyte stimulator (BLyS) in mixed cryoglobulinaemia syndrome (MCsn), a systemic vasculitis associated with a high risk to develop lymphoma, since BLyS up-regulation may favour both autoimmunity and lymphoproliferation.
  • High BLyS levels were significantly associated only with MCsn-related overt lymphoproliferative disorder.
  • CONCLUSIONS: BLyS is up-regulated and may play a pathogenetic role in a fraction of patients with MCsn, similarly to other autoimmune diseases.
  • [MeSH-major] Autoimmune Diseases / immunology. B-Cell Activating Factor / blood. Cryoglobulinemia / immunology. Hepatitis C / immunology. Up-Regulation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antiviral Agents / therapeutic use. Enzyme-Linked Immunosorbent Assay / methods. Female. Humans. Male. Middle Aged. Syndrome

  • Genetic Alliance. consumer health - C Syndrome.
  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16735452.001).
  • [ISSN] 1462-0324
  • [Journal-full-title] Rheumatology (Oxford, England)
  • [ISO-abbreviation] Rheumatology (Oxford)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / B-Cell Activating Factor
  •  go-up   go-down


26. Ramos-Casals M, Font J: Extrahepatic manifestations in patients with chronic hepatitis C virus infection. Curr Opin Rheumatol; 2005 Jul;17(4):447-55
MedlinePlus Health Information. consumer health - Autoimmune Diseases.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE OF REVIEW: Chronic hepatitis C virus infection often has autoimmune clinical and analytic features.
  • This review analyzes recent data on the close association of chronic hepatitis C virus infection with autoimmune and lymphoproliferative processes.
  • RECENT FINDINGS: Hepatitis C virus infection has been associated with both organ-specific (thyroiditis, diabetes) and systemic autoimmune diseases.
  • Experimental, virologic, and clinical evidence has demonstrated a close association between hepatitis C virus infection and Sjögren syndrome, with hepatitis C virus-associated Sjögren syndrome being indistinguishable in most cases from the primary form.
  • Hepatitis C virus has also been associated with an atypical presentation of antiphospholipid syndrome, as well as with the development of sarcoidosis.
  • A higher prevalence of hematologic processes in patients with hepatitis C virus infection has recently been reported, including cytopenias and lymphoproliferative disorders.
  • Recent data are available on the use of new immunosuppressive and biologic agents (mainly mycophenolate mofetil, anti-tumor necrosis factor agents, and rituximab) in patients with hepatitis C virus infection and autoimmune or lymphoproliferative manifestations.
  • SUMMARY: There is increasing evidence of a close association of hepatitis C virus infection with autoimmune and hematologic processes.
  • The sialotropism of hepatitis C virus may explain the close association with Sjögren syndrome, and its lymphotropism links the virus to cryoglobulinemia, autoimmune cytopenias, and lymphoma.
  • The substantial overlap between cryoglobulinemic features and the classification criteria for some systemic autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, and polyarteritis nodosa) make the differentiation between mimicking and coexistence difficult.
  • [MeSH-major] Autoimmune Diseases / complications. Hepatitis C, Chronic / complications. Lymphoproliferative Disorders / complications

  • Genetic Alliance. consumer health - Hepatitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15956842.001).
  • [ISSN] 1040-8711
  • [Journal-full-title] Current opinion in rheumatology
  • [ISO-abbreviation] Curr Opin Rheumatol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 111
  •  go-up   go-down


27. Silvana B, Antonella LM, Basilia P, Trombetta D, Saija A, Salpietro C: Rituximab for the treatment of post-bone marrow transplantation refractory hemolytic anemia in a child with Omenn's syndrome. Pediatr Transplant; 2007 Aug;11(5):552-6
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rituximab for the treatment of post-bone marrow transplantation refractory hemolytic anemia in a child with Omenn's syndrome.
  • Omenn's syndrome is a rare severe combined immunodeficiency that kills affected subjects before the end of the first year of life unless patients are treated with bone marrow transplantation (BMT).
  • Unfortunately, post-BMT patients may develop autoimmune diseases, such as autoimmune hemolytic anemia (AIHA), which sometimes fails to respond to standard therapies.
  • Rituximab is currently only labeled for treatment of B-cell lymphoproliferative disorders, such as B-cell non-Hodgkin's lymphoma and follicular lymphoma; however, it is also employed in the treatment of a variety of disorders mediated by auto-antibodies, such as AIHA and transplant-related autoimmune disorders.
  • Herein, we describe the case of a 23-month-old male child with Omenn's syndrome, who had undergone BMT and was successfully treated with rituximab (375 mg/m(2) intravenously, weekly for three times) for refractory post-BMT hemolytic anemia.
  • Our findings evidence that rituximab should be considered for treatment of post-BMT AIHA refractory to traditional therapy also in children with primary immunodeficiencies; furthermore, rituximab might represent a means to obtain remissions without the toxic effects associated with corticosteroid and immunosuppressive agents.
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antigens, CD20. Follow-Up Studies. Humans. Infant. Injections, Intravenous. Male. Postoperative Complications. Rituximab. Syndrome

  • Genetic Alliance. consumer health - CHILD Syndrome.
  • Genetic Alliance. consumer health - Anemia.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17631027.001).
  • [ISSN] 1397-3142
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Immunologic Factors; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


28. Zignego AL, Ferri C, Pileri SA, Caini P, Bianchi FB, Italian Association of the Study of Liver Commission on Extrahepatic Manifestations of HCV infection: Extrahepatic manifestations of Hepatitis C Virus infection: a general overview and guidelines for a clinical approach. Dig Liver Dis; 2007 Jan;39(1):2-17
MedlinePlus Health Information. consumer health - Hepatitis C.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hepatitis C Virus is associated with a wide series of extrahepatic manifestations.
  • Hepatitis C Virus-related lymphoproliferative disorders, whose prototype is mixed cryoglobulinaemia, represent the most closely related extrahepatic manifestations of Hepatitis C Virus.
  • Other Hepatitis C Virus-associated disorders include nephropathies, thyreopathies, sicca syndrome, idiopathic pulmonary fibrosis, porphyria cutanea tarda, lichen planus, diabetes, chronic polyarthritis, cardiopathy and atherosclerosis.
  • The aim of the present paper is to outline the most recent evidence concerning extrahepatic disorders that are possibly associated with Hepatitis C Virus infection.
  • [MeSH-minor] Autoimmune Diseases / etiology. Autoimmune Diseases / immunology. Cryoglobulinemia / etiology. Cryoglobulinemia / immunology. Humans. Lichen Planus / etiology. Lichen Planus / immunology. Lymphoma, B-Cell / etiology. Lymphoma, B-Cell / immunology. Lymphoproliferative Disorders / epidemiology. Lymphoproliferative Disorders / etiology. Paraproteinemias / etiology. Paraproteinemias / immunology. Porphyria Cutanea Tarda / etiology. Porphyria Cutanea Tarda / immunology

  • Genetic Alliance. consumer health - Hepatitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Dig Liver Dis. 2008 Aug;40(8):707-8; author reply 708 [18450527.001]
  • (PMID = 16884964.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Practice Guideline; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 236
  •  go-up   go-down


29. Cugno M, Castelli R, Cicardi M: Angioedema due to acquired C1-inhibitor deficiency: a bridging condition between autoimmunity and lymphoproliferation. Autoimmun Rev; 2008 Dec;8(2):156-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Angioedema due to an acquired deficiency in the inhibitor of the first component of human complement (CI-INH) is a rare syndrome that is usually identified as acquired angioedema (AAE).
  • AAE is frequently associated with lymphoproliferative diseases ranging from monoclonal gammopathies of uncertain significance (MGUS) to non-Hodgkin's lymphoma (NHL) and/or anti-C1-INH inactivating autoantibodies.
  • The coexistence of true B cell malignancy, non-malignant B cell proliferation and pathogenic autoimmune responses suggests that AAE patients are all affected by altered B cell proliferation control although their clinical evolution may vary.
  • [MeSH-major] Angioedema / etiology. Autoimmunity. Complement C1 Inhibitor Protein / metabolism. Lymphoproliferative Disorders / immunology

  • Genetic Alliance. consumer health - Acquired Angioedema.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19014872.001).
  • [ISSN] 1873-0183
  • [Journal-full-title] Autoimmunity reviews
  • [ISO-abbreviation] Autoimmun Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Complement C1 Inhibitor Protein
  • [Number-of-references] 30
  •  go-up   go-down


30. De Re V, Caggiari L, Simula MP, De Vita S, Mazzaro C, Lenzi M, Massimo GM, Monti G, Ferri C, Zignego AL, Gabrielli A, Sansonno D, Dammacco F, Libra M, Sacchi N, Talamini R, Spina M, Tirelli U, Cannizzaro R, Dolcetti R: Role of the HLA class II: HCV-related disorders. Ann N Y Acad Sci; 2007 Jun;1107:308-18
MedlinePlus Health Information. consumer health - Hepatitis C.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The paper highlights the role of different HLA class II molecules in hepatic and lymphoproliferative HCV-related disorders.
  • Thus, by reducing the complexity of HLA II polymorphism, characteristics that unite different HLA molecules with specific HCV-associated pathologies may be recognized with greater case.
  • Results show that HLA clusters associated with better dlimination of the virus are protective against HCC development, while the same clusters are associated with a higher risk of developing cryoglobulinemic syndrome and the concomitant NHL.
  • These data added further acknowledgements on pathogenetic mechanisms associated with HCV infection.
  • Results also highlight differences of NHL occurring in HCV-positive subjects, with or without a concomitant type II autoimmune cryoglobulinemic syndrome, suggesting that cryoglobulinemic background associated with NHL should be considered in the evaluation of the effectiveness of new therapies in the course of HCV-associated NHLs.
  • [MeSH-minor] Autoimmune Diseases / immunology. Autoimmune Diseases / pathology. Cryoglobulinemia / immunology. Cryoglobulinemia / pathology. Fibrosis / immunology. Fibrosis / pathology. Fibrosis / virology. Hepacivirus / immunology. Hepacivirus / pathogenicity. Humans. Liver Neoplasms / immunology. Liver Neoplasms / pathology. Liver Neoplasms / virology. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / pathology. T-Lymphocytes, Helper-Inducer / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17804559.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class II
  •  go-up   go-down


31. Tilakaratne W, Dissanayake M: Paraneoplastic pemphigus: a case report and review of literature. Oral Dis; 2005 Sep;11(5):326-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Paraneoplastic pemphigus (PNP) is an autoimmune mucocutaneous disease frequently associated with lymphoproliferative disorders.
  • Most patients develop very severe oral ulceration and conjunctival ulceration with or without genital ulceration resembling the features of Steven's Johnson's syndrome or most severe forms of drug eruptions.
  • We document a case of PNP in a 29-year-old female who suffers from non-Hodgkin's lymphoma.
  • [MeSH-major] Lymphoma, Non-Hodgkin / complications. Oral Ulcer / etiology. Paraneoplastic Syndromes / pathology. Pemphigus / pathology

  • Genetic Alliance. consumer health - Pemphigus.
  • MedlinePlus Health Information. consumer health - Pemphigus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16120122.001).
  • [ISSN] 1354-523X
  • [Journal-full-title] Oral diseases
  • [ISO-abbreviation] Oral Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents
  •  go-up   go-down


32. Bryce AH, Dispenzieri A, Kyle RA, Lacy MQ, Rajkumar SV, Inwards DJ, Yasenchak CA, Kumar SK, Gertz MA: Response to rituximab in patients with type II cryoglobulinemia. Clin Lymphoma Myeloma; 2006 Sep;7(2):140-4
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Type II cryoglobulinemia (CG) is a heterogeneous, generally indolent disorder caused by a monoclonal antibody with activity against polyclonal antibodies and is commonly associated with hepatitis C, lymphoproliferative disorders (LPDs), or autoimmune diseases.
  • Six patients had an LPD, and 4 of them had concomitant disorders (2 with hepatitis C and 2 with Sjogren syndrome).
  • Cutaneous manifestations were the most responsive; renal disease and lymphoma were more refractory.

  • Genetic Alliance. consumer health - Cryoglobulinemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17026826.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-62242
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Blood Proteins; 0 / Immunologic Factors; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


33. Liebman H: Other immune thrombocytopenias. Semin Hematol; 2007 Oct;44(4 Suppl 5):S24-34
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Commonly occurring conditions associated with secondary ITP include lymphoproliferative disorders (chronic lymphocytic leukemia [CLL], Hodgkin's disease and non-Hodgkin's lymphomas), autoimmune collagen vascular diseases (systemic lupus erythematosus [SLE], thyroid disease, antiphospholipid syndrome [APS]), and chronic infections (human immunodeficiency virus [HIV], Helicobacter pylori, hepatitis C virus [HCV]).
  • The mechanism of platelet destruction in thrombocytopenias associated with lymphoproliferative disorders and collagen vascular diseases is identical to the autoimmune mechanism seen in primary ITP.
  • Platelet destruction in infection-associated ITP occurs via various mechanisms including accelerated platelet clearance due to immune complex disease as seen in HIV infection or cross-reactivity of anti-platelet glycoprotein antibodies and viral antigens in HIV, HCV, and H pylori infections (antigenic mimicry).
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / complications. Acquired Immunodeficiency Syndrome / drug therapy. Acquired Immunodeficiency Syndrome / immunology. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / drug therapy. Antiphospholipid Syndrome / immunology. Diagnosis, Differential. Female. Helicobacter Infections / complications. Helicobacter Infections / drug therapy. Helicobacter Infections / immunology. Hepatitis C / complications. Hepatitis C / drug therapy. Hepatitis C / immunology. Humans. Leukemia / complications. Leukemia / drug therapy. Leukemia / immunology. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / drug therapy. Lupus Erythematosus, Systemic / immunology. Lymphoma / complications. Lymphoma / immunology. Lymphoma / therapy. Male. Platelet Count. Thyroid Diseases / complications. Thyroid Diseases / immunology. Thyroid Diseases / therapy

  • HIV InSite. treatment guidelines - Pneumocystosis and HIV .
  • HIV InSite. treatment guidelines - Human Herpesvirus-8 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18096469.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 152
  •  go-up   go-down


34. Vezzoli P, Berti E, Marzano AV: Rationale and efficacy for the use of rituximab in paraneoplastic pemphigus. Expert Rev Clin Immunol; 2008 May;4(3):351-63
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Paraneoplastic pemphigus (PNP) is a life-threatening, autoimmune, blistering-skin disease, associated with various neoplasms, particularly lymphoproliferative disorders.
  • To define this condition, the encompassing term 'paraneoplastic autoimmune multiorgan syndrome' has also been suggested.
  • The anti-CD20 monoclonal antibody, rituximab, was successfully administered to two patients with PNP and CD20(+) follicular lymphoma in 2001.
  • Since then, good responses to rituximab by different refractory autoimmune disorders have been reported, but further controlled trials are warranted to evaluate the effectiveness and safety of this agent as a second-line treatment for PNP.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20476925.001).
  • [ISSN] 1744-8409
  • [Journal-full-title] Expert review of clinical immunology
  • [ISO-abbreviation] Expert Rev Clin Immunol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


35. Mascia MT, Ferrari D, Campioli D, Sandri G, Mussini C, Ferri C: Non HCV-related mixed cryoglobulinemia. Dig Liver Dis; 2007 Sep;39 Suppl 1:S61-4
Genetic Alliance. consumer health - Cryoglobulinemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Interestingly, patients with Sjögren's syndrome or lymphoma had higher levels of cryocrit with cryoglobulinemic syndrome comparable to that found in HCV-positive MC patients.
  • MC is a multifactorial disorder; considering possible etiological factors and clinical associations the disease may present different subsets: the prevalent group of HCV-positive MC; HCV-positive MC associated with different autoimmune lymphoproliferative disorders; two MC subsets without any apparent causative agent: those with well-known autoimmune lymphoproliferative disorders and the rare cases of "essential" MC; and finally MC associated with other infectious agents.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17936226.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


36. López-Anglada L, Puig N, Díez-Campelo M, Alonso-Ralero L, Barrena S, Aparicio MA, Gutiérrez NC, García-Sanz R: Monoclonal free light chains can be found in heavy chain diseases. Ann Clin Biochem; 2010 Nov;47(Pt 6):570-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Heavy chain diseases (HCDs) are rare B-cell lymphoproliferative neoplasias characterized by the production of a monoclonal component consisting of a truncated monoclonal Ig heavy chain without the associated light chain.
  • In the work-up of the patient, the underlying anatomopathological lymphoproliferative disease corresponded to a lymphoplasmacytic lymphoma, as it is stated in the current World Health Organization classification (2008), with both lymphadenopathic and bone marrow infiltration.
  • As in other cases, several autoimmune manifestations (antiphospholipidic syndrome and immune thrombocytopenia) were present during the course of the disease in this patient.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20930031.001).
  • [ISSN] 1758-1001
  • [Journal-full-title] Annals of clinical biochemistry
  • [ISO-abbreviation] Ann. Clin. Biochem.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin gamma-Chains
  •  go-up   go-down


37. Martínez-Hernández E, Rosenfeld MR, Pruitt A, Dalmau J: [Neurological complications of transplantation]. Neurologia; 2008 Jul-Aug;23(6):373-86
MedlinePlus Health Information. consumer health - Neurologic Diseases.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Neurological complications associated with these procedures remain frequent.
  • In general, the main neurological problems of HCT and organ transplantation include metabolic and toxic encephalopathies, and central and peripheral neurological disorders caused by coagulopathy, infections, and autoimmune mechanisms.
  • The term post-transplant lymphoproliferative disorder (PTLD) includes a spectrum of disorders ranging from benign polyclonal lymphoid hyperplasia to malignant monoclonal lymphoma, usually related to the Epstein-Barr virus.
  • Some lesser known syndromes such as the immune reconstitution inflammatory syndrome and paraneoplastic neuropathies related with PTLD are increasingly being described and need to be considered in the evaluation of a transplant patient with neurological problems.

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18597192.001).
  • [ISSN] 0213-4853
  • [Journal-full-title] Neurología (Barcelona, Spain)
  • [ISO-abbreviation] Neurologia
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
  • [Number-of-references] 109
  •  go-up   go-down


38. Takacs M, Segesdi J, Banati F, Koroknai A, Wolf H, Niller HH, Minarovits J: The importance of epigenetic alterations in the development of epstein-barr virus-related lymphomas. Mediterr J Hematol Infect Dis; 2009;1(2):e2009012
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Epstein-Barr virus (EBV), a human gammaherpesvirus, is associated with a series of malignant tumors.
  • These include lymphomas (Burkitt's lymphoma, Hodgkin's disease, T/NK-cell lymphoma, post-transplant lymphoproliferative disease, AIDS-associated lymphoma, X-linked lymphoproliferative syndrome), carcinomas (nasopharyngeal carcinoma, gastric carcinoma, carcinomas of major salivary glands, thymic carcinoma, mammary carcinoma) and a sarcoma (leiomyosarcoma).
  • Based on the cell type specific epigenetic marks associated with latent EBV genomes one can distinguish between viral epigenotypes that differ in transcriptional activity in spite of having an identical (or nearly identical) DNA sequence.
  • EBNA3C (EBNA6) seems to be associated both with histone acetylases and deacetylases, although in separate complexes.
  • In epithelial cells LMP1 can up-regulate DNA methyltransferases and, in Hodgkin lymphoma cells, induce the Polycomb group protein Bmi-1.
  • These interactions may result in epigenetic dysregulation and subsequent cellular dysfunctions that may manifest in or contribute to the development of pathological changes (e.g. initiation and progression of malignant neoplasms, autoimmune phenomena, immunodeficiency).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nucleic Acids Res. 1992 May 11;20(9):2287-91 [1594447.001]
  • [Cites] J Gen Virol. 1992 Jul;73 ( Pt 7):1687-92 [1321209.001]
  • [Cites] Virology. 1994 May 1;200(2):661-7 [8178450.001]
  • [Cites] J Virol. 1994 Sep;68(9):5375-83 [8057421.001]
  • [Cites] Science. 1995 Apr 28;268(5210):560-3 [7725102.001]
  • [Cites] Mol Cell Biol. 1995 Nov;15(11):6150-9 [7565767.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3129-36 [8874213.001]
  • [Cites] J Virol. 1997 Mar;71(3):1938-45 [9032325.001]
  • [Cites] Nat Genet. 1998 Jun;19(2):187-91 [9620779.001]
  • [Cites] J Mol Biol. 2005 Jul 22;350(4):631-40 [15967459.001]
  • [Cites] Am J Hematol. 2006 Jan;81(1):5-11 [16369970.001]
  • [Cites] Nature. 2006 Feb 16;439(7078):871-4 [16357870.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2493-500 [16304050.001]
  • [Cites] Cell. 2006 Apr 21;125(2):315-26 [16630819.001]
  • [Cites] RNA. 2006 May;12(5):733-50 [16540699.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7065-70 [16606841.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):2995-3002 [16707594.001]
  • [Cites] PLoS Pathog. 2006 Mar;2(3):e23 [16557291.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):14188-93 [16966603.001]
  • [Cites] J Bacteriol. 2006 Dec;188(23):8160-8 [16997949.001]
  • [Cites] Trends Genet. 2000 Apr;16(4):168-74 [10729832.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(15):5722-35 [10891508.001]
  • [Cites] J Virol. 2001 Mar;75(5):2033-40 [11160707.001]
  • [Cites] J Virol. 2001 Mar;75(6):2584-96 [11222681.001]
  • [Cites] Semin Cancer Biol. 2001 Dec;11(6):469-76 [11669609.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):232-6 [17200670.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):237-42 [17211412.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2597-603 [17148591.001]
  • [Cites] Nat Genet. 2007 Apr;39(4):457-66 [17334365.001]
  • [Cites] Nat Genet. 2007 Apr;39(4):442-3 [17392803.001]
  • [Cites] J Virol. 2007 Jun;81(12):6389-401 [17409162.001]
  • [Cites] EMBO J. 2007 Oct 3;26(19):4252-62 [17853891.001]
  • [Cites] J Virol. 2007 Dec;81(23):13242-7 [17898065.001]
  • [Cites] FEBS Lett. 2008 Mar 5;582(5):705-9 [18258198.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):787-94 [11891177.001]
  • [Cites] J Virol. 2002 May;76(10):4699-708 [11967287.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):10084-9 [12110730.001]
  • [Cites] Blood. 2003 Jan 15;101(2):681-9 [12393683.001]
  • [Cites] J Biol Chem. 2003 Feb 7;278(6):4035-40 [12427740.001]
  • [Cites] J Virol. 2003 Apr;77(7):4261-72 [12634383.001]
  • [Cites] J Gen Virol. 2003 Jun;84(Pt 6):1443-50 [12771413.001]
  • [Cites] J Virol. 2003 Jul;77(14):8166-72 [12829856.001]
  • [Cites] Virus Genes. 2003 Aug;27(1):57-66 [12913358.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11668-76 [17178861.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Dec 19;103(51):19278-83 [17159145.001]
  • [Cites] J Gen Virol. 2008 Jun;89(Pt 6):1364-70 [18474551.001]
  • [Cites] J Cell Physiol. 2008 Aug;216(2):321-6 [18484093.001]
  • [Cites] J Virol. 2008 Nov;82(21):10436-43 [18753206.001]
  • [Cites] J Virol. 2009 Apr;83(7):2930-40 [19129441.001]
  • [Cites] Blood. 2009 Mar 12;113(11):2488-97 [19075189.001]
  • [Cites] Semin Cancer Biol. 2009 Jun;19(3):158-64 [19429479.001]
  • [Cites] J Virol. 2009 Jul;83(14):7109-16 [19403674.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):430-5 [10618435.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(7):2343-9 [10713158.001]
  • [Cites] Genes Dev. 2002 Jan 1;16(1):6-21 [11782440.001]
  • [Cites] Clin Cancer Res. 2002 Jan;8(1):131-7 [11801549.001]
  • [Cites] Adv Cancer Res. 2003;89:133-56 [14587872.001]
  • [Cites] Br J Haematol. 2003 Nov;123(3):475-8 [14617009.001]
  • [Cites] Oncogene. 2004 Feb 12;23(6):1326-31 [14961078.001]
  • [Cites] Science. 2004 Apr 30;304(5671):734-6 [15118162.001]
  • [Cites] Trends Microbiol. 2004 Nov;12(11):495-9 [15488390.001]
  • [Cites] J Virol. 2004 Nov;78(22):12308-19 [15507618.001]
  • [Cites] Science. 1980 Nov 7;210(4470):604-10 [6254144.001]
  • [Cites] J Virol. 1983 May;46(2):446-53 [6302313.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Jun;81(12):3806-10 [6328526.001]
  • [Cites] J Virol. 1998 Sep;72(9):7075-83 [9696800.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):46-56 [9858530.001]
  • [Cites] Science. 1999 May 7;284(5416):967-70 [10320378.001]
  • [Cites] Gene. 1999 Aug 5;236(1):87-95 [10433969.001]
  • [Cites] Lancet. 1964 Mar 28;1(7335):702-3 [14107961.001]
  • [Cites] J Virol. 2004 Dec;78(24):14062-5 [15564516.001]
  • [Cites] Genes Dev. 2005 Mar 1;19(5):542-52 [15706033.001]
  • [Cites] Biochem Cell Biol. 2005 Jun;83(3):286-95 [15959556.001]
  • [Cites] Biochem Cell Biol. 2005 Jun;83(3):344-53 [15959560.001]
  • [Cites] J Gen Virol. 1985 Sep;66 ( Pt 9):1931-40 [2993484.001]
  • [Cites] Nature. 1986 May 15-21;321(6067):209-13 [2423876.001]
  • [Cites] Cell. 1986 Dec 26;47(6):883-9 [3022942.001]
  • [Cites] Adv Cancer Res. 1988;50:95-158 [2837072.001]
  • [Cites] Cell. 1988 Jul 1;54(1):127-35 [2838178.001]
  • [Cites] Cell. 1988 Nov 4;55(3):427-33 [2846181.001]
  • [Cites] J Mol Biol. 1988 Oct 20;203(4):971-83 [3210246.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Sep;86(17):6498-502 [2549539.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 1990 Jan 30;326(1235):179-87 [1968655.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 1990 Jan 30;326(1235):285-97 [1968665.001]
  • [Cites] J Virol. 1990 Nov;64(11):5295-300 [2170673.001]
  • [Cites] EMBO J. 1991 Jan;10(1):143-51 [1846596.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3942-6 [1850841.001]
  • [Cites] J Virol. 1992 Jan;66(1):62-9 [1370095.001]
  • [Cites] J Gen Virol. 1991 Dec;72 ( Pt 12):3025-33 [1662694.001]
  • (PMID = 21416002.001).
  • [ISSN] 2035-3006
  • [Journal-full-title] Mediterranean journal of hematology and infectious diseases
  • [ISO-abbreviation] Mediterr J Hematol Infect Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3033174
  •  go-up   go-down






Advertisement