Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One to three-month-old A-strain mice, inoculated subcutaneously with 2 x 10(6) viable syngeneic C1300 neuroblastoma cells (clone NB9R) developed a palpable tumor within 9-12 days and died within 28-30 days. A transient glomerulopathy developed after 16-24 days. Despite a normal histologic appearance, the nephropathy was clearly demonstrated by electron microscopy and was classified as a focal mesangiopathic glomerulonephritis. Deposits of host 7S-G immunoglobulins and C3 complement fragments were detected in these same kidneys by immunofluorescence. Radioimmunoprecipitin determinations on sera obtained from mice at different intervals from tumor cell inoculation, revealed that untreated mice contained circulating antibodies capable of reacting with 125I-labeled gp69-71 glycoprotein from Gross murine leukemia virus (MuLV). Antibodies to p30 MuLV antigen and to crude membrane antigen (s) (CMA) solubilized from NB9R cells were found in sera only after tumor cell inoculation. Circulating immune complexes formed by host 7S-G immunoglobulins were clearly detected from day 16 to 22. Antibodies eluted from kidneys with nephropathy were shown to react with NB9R cells in vitro and to react specifically with CMA and the p30 MuLV antigen.
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PMID:Antibody formation and transient immune complex glomerulopathy in A-strain mice with C1300 neuroblastoma tumors. 14 55

The histopathologic study of 103 patients with Hodgkin's disease including 5 cases who had staging laparotomy during the last 10 years were reviewed. The following conclusions were drawn: 1. No significant sex difference among subtypes were noted. 2. Associated glomerulopathy, nephrotic syndromes, and amyloidosis were occasionally found. 3. In childhood lymphomas excluding leukemia are the most frequent malignacies. Among the lymphomas, Hodgkin's disease predominates. 4. The most frequent subtype both in the original biopsy and after staging laparotomy was mixed cellularity. The nodular sclerosis type was the rarest. The subtypes generally did not change in the subsequent biopsies and in laparatomy done up to 6 months later. 5. It is most frequently noted in cervical area. Males are affected more than females. The peak incidence was in the first decade of age group. A brief review of the literature and discussion on the comparison of data from other countries is given.
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PMID:Hodgkin's disease in childhood. 38 4

The histopathologic studies of 103 patients under 16-years old with Hodgkin's disease including 5 cases who had staging laparotomy during the last 10 years were reviewed. The following conclusions were drawn: 1. No significant sex differences among subtypes were noted. 2. Associated glomerulopathy, nephrotic syndromes, and amyloidosis were occasionally found. 3. In childhood, lymphomas excluding leukemia are the most frequent malignancies. Among the lymphomas, Hodgkin's disease predominates. 4. The most frequent subtype both in the original biopsy and after staging laparatomy was mixed cellularity. The nodular sclerosis type was the rarest. The subtypes generally did not change during the subsequent biopsies and in laparotomy done up to 6 months later. 5. Lymphomas were most frequently noted in cervical area. Males are affected more severely than females. The peak incidence was around 8 years. A brief review and discussion on the comparison of data from other countries are also given.
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PMID:Histopathological subtypes of Hodgkin's disease in childhood in Iraq. 52 87

A review is presented of the association between a glomerular disease and a malignancy. The incidence of Hodgkin's disease in patients with glomerulopathy is very low, but the incidence of a solid tumour in a patient with glomerulopathy varies between 3 and 13%, mean 7%, and may be as high as 22% in patients over 60 years of age with a membranous nephropathy. A solid tumour was found most frequently in patients with membranous nephropathy. On the other hand, minimal change nephropathy is often associated with Hodgkin's disease and membrano-proliferative glomerulopathy with chronic lymphatic leukaemia. In Hodgkin's disease-associated glomerulopathy, a defect in the function of T lymphocytes is probably important, but the precise pathogenesis has not yet been elucidated. The other glomerulopathies may be mediated by immune complexes, containing tumour-derived antigens and their antibodies, either formed in situ or deposited as complexes from the circulation.
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PMID:Glomerulopathy as a paraneoplastic phenomenon. 267 59

A 51-year-old man presented with a T-cell leukemia of large granular lymphocytes and rapidly developed a nephrotic syndrome due to presumptive minimal-change glomerulopathy. The E-rosette+, Ia+ cells demonstrated cytotoxic activity similar to that of natural killer lymphocytes but lacked other T-subset markers, except that one third of them bore Fc(IgG) receptors. Cytogenetic analysis revealed loss of chromosome 10 and the translocation (1;10)(p11;q11) in all metaphases. Regression of the leukemia after chemotherapy was accompanied by a dramatic resolution of the nephrotic syndrome, suggesting that the activated granular lymphocytes induced the renal lesion. The close association of a clonal T-lymphoproliferative disorder with minimal-change nephrotic syndrome lends further support to current views implicating activated T cells or their products in the pathogenesis of this glomerulopathy.
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PMID:Nephrotic syndrome associated with a clonal T-cell leukemia of large granular lymphocytes with cytotoxic function. 348 48

Chronic lymphocytic leukemia (CLL), the most common form of leukemia in Western countries, rarely induces glomerular disease, but membranoproliferative glomerulonephritis or immunotactoid glomerulopathy has been reported. The proliferating cells in CLL are of mature B-cell origin and produce monoclonal immunoglobulin (Ig), thus leading to various kinds of autoimmune disorders or immunotactoid glomerulopathy. Although there have been a few reported cases of amyloidosis accompanying CLL, the type of amyloid fibrils has not been demonstrated nor described in detail, particularly regarding monoclonal Ig productivity. We report a rare case of amyloidosis associated with CLL, in which we detected ?-light chain type monoclonal Ig in the sera, urine, and on the surface membrane of lymphocytes, and discuss an association between monoclonal Ig-related disease and non-Hodgkin's lymphoma.
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PMID:Amyloidosis associated with chronic lymphocytic leukemia. 1601 91

Kidney disease frequently complicates malignancy and its treatment. Although many solid and hematologic cancers may involve the renal parenchyma, clinical sequelae are usually not prominent. Published reports cite membranous nephropathy as the most common malignancy-associated glomerulopathy, occurring with many carcinomas and occasionally with leukemia and lymphoma followed by minimal change disease. Rarely membranoproliferative glomerulonephritis (MPGN) has been reported in patients with malignancy. The mechanism by which malignancy induces disease remains unproved, but may involve deposition of tumor antigen in the subepithelial space with in situ immune complex formation and subsequent complement activation. Treatment of the underlying malignancy may lead to resolution of nephrotic syndrome, lending indirect support to this theory. We report a rare autopsy case of a patient with metastatic carcinoma (with unknown primary) associated with MPGN. The association between MPGN and metastatic carcinoma with unknown primary is uncommon and has not been previously reported in the literature.
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PMID:Membranoproliferative glomerulonephritis in a carcinoma with unknown primary: an autopsy study. 1860 90

We report a case of collapsing glomerulopathy associated with natural killer cell leukemia in a previously healthy 27-year-old African American man. An initial kidney biopsy showed findings concordant with the cellular variant of focal segmental glomerulosclerosis. A repeated biopsy 3 months later showed collapsing glomerulopathy, likely representing a morphologic evolution from a cellular variant into the collapsing glomerulopathy variant of focal segmental glomerulosclerosis. Collapsing glomerulopathy has been described in connection with a number of disparate disorders in which podocyte injury seems to be the common denominator. The close temporal association between clinical presentation and the development of nephropathy provides support for a direct pathogenic link between the underlying lymphoproliferative disorder and the glomerular lesions. We hypothesize that dysregulated cytokine production by the neoplastic cells led to podocyte alterations and eventually to the development of collapsing glomerulopathy.
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PMID:Collapsing glomerulopathy associated with natural killer cell leukemia: a case report and review of the literature. 2190 87

Clofarabine is a purine nucleoside analog indicated for treatment of relapsed or refractory acute lymphoblastic leukaemia in children. The drug is also increasingly used, outside of its FDA approved indication, for treatment of relapsed or refractory acute myeloid leukemia in adults. It acts by inhibiting DNA synthesis, the enzyme ribonucleotide reductase and repair and activation of mitochondrial repair processes. We describe a case of a 48-year-old male with refractory acute myeloid leukemia with acute kidney injury associated with clofarabine treatment. We conducted a review of the literature and utilized the Food and Drug Administration Adverse Event Reporting System to identify spontaneous reporting of renal adverse events with this drug in 29 other cases. Since clofarabine inhibits ribonucleotide reductase, we postulate by extrapolation from the animal studies that collapsing glomerulopathy or severe tubular injury or a combination of both may be the mechanism of acute kidney injury observed with this agent. This would be consistent with the observed severe acute kidney injury and proteinuria in humans.
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PMID:Clofarabine-induced kidney toxicity. 2408 Dec 20

Monoclonal gammopathy is characterized by circulating monoclonal immunoglobulin owing to clonal proliferation of immunoglobulin-producing B lymphocytes or plasma cells. Clonal proliferation of B lymphocytes is seen in B-cell lymphoma/leukemia, and clonal plasma cell proliferation is seen in multiple myeloma and monoclonal gammopathy of undetermined significance. The monoclonal immunoglobulin in the setting of a B-cell or plasma cell disorder can cause a proliferative glomerulonephritis via 2 mechanisms: (1) glomerular deposition of the monoclonal immunoglobulin with activation of the classical pathway of complement (direct mechanism), resulting in an immunoglobulin-positive C3-positive glomerulonephritis, and (2) glomerular deposition of complement factors of the alternative and terminal pathway via inhibition of alternative pathway-regulating proteins by the monoclonal immunoglobulin (indirect mechanism), resulting in immunoglobulin-negative C3-positive glomerulonephritis (C3 glomerulopathy). Evaluation should include serum and urine electrophoresis and immunofixation as well as serum-free light-chain assay. If a monoclonal immunoglobulin is detected on these tests, bone marrow biopsy or imaging is needed to exclude more advanced plasma cell dyscrasia. Evaluation of alternative pathway of complement should be done in patients with Ig-negative C3-positive glomerulonephritis. If monoclonal gammopathy is due to an underlying malignant disease such as myeloma, lymphoma, or chronic lymphocytic leukemia, then specific treatment should be aimed at treating the malignant disease, with the goal of eradicating the clonal cells producing the immunoglobulin. In contrast, if monoclonal gammopathy is due to a monoclonal gammopathy of undetermined significance, treatment options include bortezomib, cyclophosphamide, and dexamethasone for a non-IgM monoclonal immunoglobulin and rituximab alone or in combination with cyclophosphamide and dexamethasone for an IgM monoclonal immunoglobulin.
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PMID:Monoclonal gammopathy-associated proliferative glomerulonephritis. 2418 5


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