Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

p53 is a tumor suppressor gene that commonly undergoes mutations in human tumors, including lymphomas. Because p53 mutations are not restricted to a single locus, immunohistochemistry is useful to detect p53 expression and correlate this finding with lymphoma phenotype. Cryostat sections from 125 cases of lymphoma were analyzed for p53 expression using three different monoclonal antibodies (pAb 421, 1801, 240) which react with human cellular p53 and a common conformational epitope on mutant p53. A control antibody (pAb 246) reacts only with wild type p53 of murine origin and was negative in all cases. Tissue from 29 cases of lymphoid hyperplasia, including six from human immunodeficiency virus-positive (HIV+) patients, were negative for p53. p53 was predominantly localized in nuclei of high-grade lymphomas, including 14 of 46 cases of B cell immunoblastic lymphomas and two of five T cell immunoblastic lymphomas. p53 expression was relatively common in lymphomas from HIV+ patients, and unusual in intermediate and low-grade lymphomas of follicular center cell type. Low-grade lymphoma of small lymphocytic type disclosed p53+ large cells (paraimmunoblasts) that may play a role in tumor progression in this lymphoma subtype. p53 was also strongly expressed in the nuclei of Reed Sternberg cells from 19 of 37 cases of Hodgkin's disease, including six cases of mixed cellularity, and 13 cases of nodular sclerosing type. Immunohistochemical staining is a rapid method to identify p53 expression in lymphomas.
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PMID:Immunohistochemical analysis of p53 expression in malignant lymphomas. 146 98

Many of the advances in the management of non-Hodgkin's lymphomas have been based on more precise understanding of the various cell types that constitute these disorders. During the past year, we have seen some dramatic changes in the therapeutic approach to low-grade lymphomas. Until recently, the usual approach to these disorders was a purely palliative one, but a number of publications from the past year describe a more intensive approach with the goal of developing a curative modality. The use of combination chemotherapy in addition to radiation therapy for the early Ann Arbor stages as well as the use of high-dose chemotherapy with bone marrow transplantation in patients with high-risk factors has been reported recently. In the area of intermediate-grade lymphomas, most of the recent publications have described prognostic factors associated with various chemotherapy protocols. One of the most interesting recent developments is related to the dose-intensity issue. A consensus appears to be developing in regard to the correlation of dose intensity with clinical outcome. Despite the fact that new third-generation regimens have been associated with cures in 50% to 66% of the patients, a significant fraction of patients require salvage chemotherapy. Some of the new salvage regimens are discussed, as is the use of calcium channel blockers to reverse multiple-drug resistance. Finally, management of the high-grade lymphomas, specifically the small noncleaved cell type, has been associated with a cure rate in the range of 50% in two recently published studies. Patients who are human immunodeficiency virus-positive with small noncleaved cell lymphoma can be cured of their underlying malignancy, but many of them later develop complications of acquired immunodeficiency syndrome, to which they usually succumb.
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PMID:Treatment of non-Hodgkin's lymphoma. 175 77

Although dramatic progress has been made in the treatment of advanced non-Hodgkin's lymphoma, a majority of patients eventually die from this disease. Improvements in histopathology, staging techniques, immunophenotyping, and knowledge of prognostic factors have improved our ability to choose appropriate treatment. Most low-grade lymphomas can be effectively palliated for many years, but eventually convert to large-cell lymphomas or become resistant to chemotherapy. Intermediate-grade lymphomas, especially diffuse large-cell lymphomas, may be cured in 30% to 60% of the cases with aggressive combination chemotherapy. The high-grade lymphomas require treatment similar to regimens designed to treat acute lymphocytic leukemia, including central nervous system (CNS) prophylaxis. Non-Hodgkin's lymphomas are becoming more common in patients with acquired immunodeficiency syndrome (AIDS), and may be effectively controlled before the immunodeficiency becomes too severe. All patients with high-grade lymphoma and others at high risk should be tested for human immunodeficiency virus (HIV). Patients who relapse may be salvaged with chemotherapy, and their diseases are potentially curable with autologous or allogeneic bone marrow transplantation. New treatments using monoclonal antibodies, biological response modifiers, and growth factors, should improve palliation and survival.
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PMID:Treatment of advanced non-Hodgkin's lymphoma in adults. 184 59

The present study was undertaken to establish the incidence of t(14;18) (q32:q21) chromosomal translocations detectable by a polymerase chain reaction (PCR) assay on fixed lymphoma biopsies. DNA samples from 113 formalin-fixed, paraffin-embedded tissue biopsies (non-Hodgkin's lymphomas, 96 cases; Hodgkin's disease, six cases; reactive, 11 cases) were amplified by the PCR. Of the 96 non-Hodgkin's lymphoma cases, 56 had a follicular pattern and 40 had a diffuse pattern. Polymerase chain reaction-amplifiable t(14;18) chromosomal translocations were detected in 23 of 43 follicular low-grade lymphomas, one of eight follicular intermediate grade lymphomas, one of five follicular high-grade lymphomas, and one of 10 diffuse large-cell lymphomas. The remaining 30 diffuse lymphomas represented the spectrum of the Working Formulation classification. There were six biopsy specimens of Hodgkin's disease and 11 biopsy specimens of follicular hyperplasia; all were negative. The translocation was not detected in 16 biopsies (non-Hodgkin's lymphomas, seven cases; follicular hyperplasia, nine cases) from patients infected with the human immunodeficiency virus. Since this procedure uses the widely available fixed paraffin-embedded material, correlative studies between histology and genetic aberrations can be readily undertaken.
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PMID:Detection of specific t(14;18) chromosomal translocations in fixed tissues. 230 46

Organized lymphoid aggregates are normally found within the walls of bronchi in many species and may occur, under conditions of disease, in humans. This bronchus-associated lymphoid tissue (BALT) can be viewed as an organizing principle to explain the behavior and distribution of many pulmonary lymphoid proliferations, both hyperplastic and neoplastic. The extent of lymphoid hyperplasia can vary, from multifocal proliferations that arise in and remain in the airway walls (follicular hyperplasia of BALT) to those that form a solitary mass or nodule (nodular lymphoid hyperplasia of BALT or "pseudolymphoma") to multifocal or diffuse lymphoid hyperplasia of BALT ("lymphoid interstitial pneumonitis"). It seems likely that more than one cause accounts for these proliferations. Of interest is the hypothesis that many examples of diffuse lymphoid hyperplasia associated with the acquired immune deficiency syndrome may have a viral cause, possibly human immunodeficiency virus or, in some cases, Epstein-Barr virus (EBV). Most pulmonary lymphomas are low-grade B cell lymphomas. They exhibit histological diversity in any given case, characterized by small lymphocytes with irregular nuclei and pale cytoplasm (so-called "centrocytelike" cells), scattered immunoblasts, and lymphoplasmacytic or plasma cells. Reactive germinal centers are frequently present, and this, along with the benign clinical behavior of these tumors, may cause diagnostic confusion with reactive lesions. Both the histological appearance and the clinical behavior (in particular, the tendency to recur in extranodal sites) of these low-grade lymphomas can be explained on the basis of origin in BALT. T cell lymphoproliferative processes can occur in the lung but are rare. Lymphomatoid granulomatosis (angioimmunoproliferative lesion) is an angiocentric and necrotizing, polymorphous lymphoid lesion that presents as multiple masses in the lung, involves skin and central nervous system (among other organs), may progress to histologically overt lymphoma, and is immunophenotypically predominantly a T cell process. Microscopically, a lymphohistiocytic infiltrate, including variable numbers of atypical cells, is present. Recent in situ hybridization and immunohistochemical studies have served to show EBV localized to the large cells. In addition, these atypical cells often show B cell immunophenotypic features and are present in a background of small, reactive T cells. It is therefore possible that lymphomatoid granulomatosis is a family of T cell rich lymphoproliferations driven by EBV infection of B cells and/or T cells, analagous to the EBV-associated, posttransplantation B cell lymphoproliferative disorders.
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PMID:Pulmonary lymphoid disorders. 763 48

Rare cases of low-grade lymphomas have been described in patients with human immunodeficiency virus (HIV) infection. However, this is the first reported case of mantle-cell lymphoma, a type of low-grade lymphoma, in a patient who also had HIV infection. Salient clinical features included lymphocytosis, lymphadenopathy, splenomegaly, and involvement of the bone marrow and meninges. The disease proved to be unusually aggressive and response to chemotherapy was insignificant. The patient survived only 4 months.
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PMID:Mantle-cell lymphoma in a patient with human immunodeficiency viral infection. 763 49

We report two cases of marginal zone B-cell lymphoma in two patients 6 and 18 years of age, respectively (cases 1 and 2) who had no clinical evidence of immunodeficiency or risk factors for human immunodeficiency virus (HIV) infection. Histologic analysis in both cases revealed diffuse nodal effacement by a monotonous population of atypical lymphoid cells with abundant pale cytoplasm and round to oval nuclei, with very infrequent mitotic activity. The neoplastic cells in both cases were of B-cell lineage (CD20 and CD79a positive), with CD43 coexpression. One case showed monoclonal light chain expression, and polymerase chain reaction analysis demonstrated clonal rearrangements of the immunoglobulin heavy chain gene in both cases. Abnormal cytogenetic findings were detected in case 2, in which metaphase spreads revealed trisomy 13 (karyotype 47, XY, +13). Although trisomy 13 has been described in association with acute nonlymphocytic leukemias and myelodysplastic syndromes, this case represents the first documented association of trisomy 13 with marginal zone B-cell lymphoma. Interphase cytogenetics analysis for trisomy 3, reported to be associated with mucosa-associated lymphoid tissue (MALT) lymphomas, was negative in both cases. Although low-grade lymphomas of the MALT type have been reported in HIV-positive patients, the two cases reported here are unique in that they occurred in young patients without HIV infection or any other evidence of immunodeficiency.
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PMID:Marginal zone B-cell lymphoma with monocytoid B-cell lymphocytes in pediatric patients without immunodeficiency. A report of two cases. 898 Mar 74

The uptake of fluorine-18 fluorodeoxyglucose (FDG) is increased in processes with enhanced glycolysis, including malignancy. It is this property of FDG which is exploited in positron emission tomography (PET) imaging for lymphoma. FDG, whilst a good oncology tracer, is not perfect and there are limitations to its use. FDG may have low uptake in some types of lymphoma, predominantly low-grade lymphomas. High physiological uptake may occur within the bowel, urinary tract, muscle, salivary glands and lymphoid tissue. FDG is not specific for malignancy and increased uptake occurs in benign conditions with increased glycolysis such as infection, inflammation and granulomatous disease. Benign conditions usually have lower uptake than malignancy but there is overlap. These limitations of FDG mean that tumour may be 'missed', 'masked' or 'mimicked' by other pathology. These limitations are described in this article and methods to circumvent them where possible are discussed. These include performing baseline scans at presentation with lymphoma for comparison with post-treatment scans, simple manoeuvres to reduce physiological uptake such as administration of frusemide and diazepam and remaining alert to the possibility of alternative pathology in immunosuppressed patients. Patients with disease secondary to human immunodeficiency virus are a particular challenge in this regard as they often have dual or multiple pathology. One of the most important skills in PET reporting may be to recognise its limitations and be clear when a definitive answer cannot be given to the referring clinician's question. This may require using PET to direct the clinician to biopsy the site most likely to yield the correct diagnosis.
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PMID:Limitations of PET for imaging lymphoma. 1274 31