Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was performed in 62 patients with non-Hodgkin's lymphoma (ATL included) who were hospitalized between 1985 and 1991 and who underwent bone marrow aspiration and biopsy before or after treatment or at the time of recurrence. The relationships between the extent of bone marrow fibrosis and other prognostic factors as well as the effects of chemotherapy and bone marrow fibrositic prognosis were examined. The results were as follows: 1) The periods of survival in patients with high degree of fibrosis in bone marrow were significantly shortened. 2) The extent of bone marrow fibrosis significantly correlated with the presence or general symptoms, bone marrow invasion, and blood levels of LDH and Ca on blood biochemical examinations. 3) Effective therapy reduced collagen fibers as well as reticulin fibers in bone marrow. 4) Sixty-four percent of relapsing cases showed increase of bone marrow fibrosis. These results suggest that understanding the state of bone marrow fibrosis over the clinical course may give a good guide of indication the prognosis of malignant lymphoma.
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PMID:[Clinical evaluation of bone marrow fibrosis in non-Hodgkin's lymphomas]. 157 32

Fibrin deposits were observed in the involved lymph nodes and/or spleens of 15 patients with Hodgkin's disease by specific immunofluorescence and by electron microscopy. Two basic patterns of fibrin deposition were observed: 1) intercellular deposits, chiefly associated with nonneoplastic-appearing lymphoid cells and 2) deposits associated with the collagen fibers of young connective tissue. In addition, coarse fibrin deposits were observed in areas of necrosis, presumably a non-specific finding. Fibronectin was also observed in intercellular areas, but staining was less intense than for fibrin. Fibrin deposits were also observed in 3 of 6 cases of non-Hodgkin's lymphoma, indicating that the finding is not an exclusive feature of Hodgkin's disease. The pathogenesis and possible significance of fibrin deposition in Hodgkin's disease are related to earlier observations of activation of the coagulation system on neoplasia and cell-mediated immunity and to the possible role of fibrin, fibronectin, and their breakdown products in angiogenesis and fibroplasia.
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PMID:Fibrin deposits in Hodgkin's disease. 704 53

Combination chemotherapy regimens using multiple agents have been reported to produce long term survival in patients with non-Hodgkin's lymphoma (NHL). However, the adverse effects of those regimens, particularly pulmonary complications, have resulted in fatalities. We measured P-III-P and type IV collagen-7S level in the serum and BALF of 23 previously untreated NHL patients who underwent COP-BLAM III chemotherapy in which a high dose of bleomycin (BLM) was used, and studied the relationship between those parameters and the pulmonary functions in those patients. The parameters and pulmonary function were measured before the first course and after the completion of the fourth course of chemotherapy. As for pulmonary function, chemotherapy produced an increment of %DLCO value but no change in PaO2, %VC, and %FEV1.0. While serum P-III-P levels remained unchanged, P-III-P levels in BALF slightly decreased after the chemotherapy. Type IV collagen-7S levels both in serum and BALF showed no change after the chemotherapy. Serum P-III-P levels after the chemotherapy were significantly correlated with both total cell counts and lymphocyte counts in the BALF. But there was no correlation between serum P-III-P levels and %DLCO. Mild and early-Stage fibrosis was observed in the lungs of the patients who were treated with COP-BLAM III. Pulmonary adverse effects are not likely to be associated with the total administered dose of BLM, but are associated with individual susceptibility to BLM toxicity. Our results suggest that the chemotherapy should be discontinued or the dose of BLM should be reduced if the P-III-P level in BALF increases.
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PMID:[Type III procollagen N-terminal peptide and type IV collagen-7S level in the serum and BALF of patients with non-Hodgkin's lymphoma before and after chemotherapy]. 752 40

In selected patients with early-stage breast cancer, conservative surgery and radiation represent an alternative equal to mastectomy in terms of local recurrence, distant metastasis, survival, and long-term complications. Patients with early-stage breast cancer who are candidates for conservative surgery and radiation include those whose primary tumor is less than 4 to 5 cm in size without evidence of gross multicentricity or diffuse microcalcifications. Patients with an extensive intraductal component may be appropriate candidates provided that margins of resection are negative. Young age is not a contraindication to the conservative treatment. A preexisting history of collagen vascular disease or prior mantle irradiation for Hodgkin's or non-Hodgkin's lymphoma represents a contraindication to conservative surgery and radiation because of the potential for severe complications. An additional contraindication is the pregnant woman in whom delivery cannot be accomplished before the initiation of radiation. Mammography is essential in the pretreatment evaluation and posttreatment follow-up of the conservatively treated patient. The goal of the pretreatment mammogram is to assess the extent of disease in the ipsilateral breast as well as to evaluate the contralateral breast. In patients who present with microcalcifications, a postbiopsy mammogram before radiation is essential to document complete removal of all malignant-appearing microcalcifications. Mammography is an essential part of the follow-up program in order to detect a recurrence in the treated breast as well as a cancer in the contralateral breast cancer. The optimal interval for follow-up mammography has not been determined, although programs employing mammography on a yearly basis after treatment have been associated with the detection of early recurrences and excellent survival after salvage mastectomy for these recurrences.
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PMID:Conservative surgery and radiation for early-stage breast cancer. 821 Dec 36

An extremely rare case of a meningioma in the posterior fossa without dural attachment has been reported. The patient was a 56-year-old male whose chief manifestation was the abnormality of his CT scan. His past history included gastric and colonic polyp when he was 54, 55 years old, and non-Hodgkin's lymphoma before hospitalization in our department. CT scan showed a small round non-enhancing lesion located at the lateral site of the right cerebellar cortex. T1 weighted image of MRI showed a homogeneous low intensity lesion with partial enhancing with Gd-DTPA. Proton image showed a remarkable low intensity lesion which showed an extramedullary mass. Right retromastoid craniectomy was performed. The mass was an extramedullary tumor which had no relation with the cerebellar cortex and dura matter. The arachnoid membrane around the tumor was intact. The tumor was totally resected and the patient had no neurological deficits. Histopathologically, the tumor was delineated into laminar structures by collagen fiber. Tumor cells were spindle in shape and made a whorling formation. There was no psammoma body and it had a hyperchromatic nuclei without mitotic features. Electron microscopic studies revealed no typical interdigitation but irregularity of the cell membrane. Abundant collagen fibers were in contact with basement membrane of the tumor. According to these findings, we diagnosed fibroblastic meningioma with atypical forms. Meningiomas without dural attachment are rare in adults, especially extremely rare of the posterior fossa. There are only 23 previous reports of "meningioma of the posterior fossa without dural attachment". Cantore divided these meningiomas into three groups (IV ventricle, inferior tela choroidea and cisterna magna).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A meningioma in the posterior fossa without dural attachment: case report]. 837 6

Samples of lymph nodes from 88 patients with B-cell non-Hodgkin's lymphoma (B-NHL) grouped by the Working Formulation (WF) and from 15 patients with benign lymphadenopathies were investigated immunohistochemically and ultrastructurally for changes in angiogenesis and stromal distribution of two subendothelial basement membrane (BM) components, namely laminin and type IV collagen. The microvessel number was usually low in lymphadenopathies, and increased significantly in low-grade B-NHL. Intermediate-grade tumors displayed a further significant increase that was mainly due to their diffuse subtypes rather than to the follicular subtype. High-grade B-NHL showed the highest counts. By contrast with the lymphadenopathies studied, the stroma of B-NHL reacted intensely with both BM components, whose linear co-expression was significantly associated with low-grade and follicular intermediate-grade B-NHL, while expression of laminin alone in a granular pattern was detected in diffuse intermediate-grade and high-grade tumors. Ultrastructural analysis revealed immature vessels more frequently in diffuse intermediate-grade, and in high-grade B-NHL. These in situ data suggest that angiogenesis occurring in B-NHL increases along their progression path, and emphasize the importance of angiogenesis as an epigenetic phenomenon of B-NHL progression.
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PMID:Angiogenesis spectrum in the stroma of B-cell non-Hodgkin's lymphomas. An immunohistochemical and ultrastructural study. 859 93

We describe a 44-year-old man with non-Hodgkin's lymphoma receiving granulocyte colony-stimulating factor (G-CSF) who developed an acute arterial thrombosis. The removed thrombus contained large amounts of platelet aggregation. A rapid increase of platelets and increased adenosine diphosphate (ADP)- and collagen-induced platelet aggregation were observed at the time of the thrombotic event. A challenge test of G-CSF showed an increase in the platelet count and an augmentation of ADP- and collagen-induced platelet aggregation. In the use of GCSF. patients who produce a rapid increase in platelet levels could be at greater risk for thrombotic events and need to be followed-up carefully.
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PMID:Acute arterial thrombosis due to platelet aggregation in a patient receiving granulocyte colony-stimulating factor. 875 7

Hepatocyte growth factor (HGF)/scatter factor (SF) is the ligand for a tyrosine kinase cell surface receptor encoded by the MET protooncogene (c-MET). HGF/SF can induce proliferation and motility in epithelial cells and promotes invasion of carcinoma cells and NIH3T3 fibroblasts transfected with both HGF/SF and c-MET genes. Our results show that HGF/ SF and c-MET also play a role in adhesion and invasion of human lymphoma cells. c-MET mRNA is expressed in hemopoietic cells, such as hemopoietic progenitor cells (CD34+ cells) in bone marrow (BM) and mobilized peripheral blood, immature B cells in cord blood and BM, and germinal center B-centroblasts. In normal peripheral blood B cells, which are c-MET-, c-MET expression was induced by PMA, ConA, HGF/ SF, and Epstein-Barr virus (EBV) infection. Using immunohistochemistry, we detected c-MET on the cell surface of large activated centroblasts in lymph nodes from patients with B-non-Hodgkin's lymphoma and Hodgkin's disease. In the latter group, c-MET expression correlated well with the presence of EBV. Because HGF/SF and c-MET promote metastasis of carcinoma cells, we studied the effects of c-MET stimulation by HGF/SF of B-lymphoma cells on properties relevant for metastasis, ie, adhesion, migration, and invasion. HGF/SF stimulated adhesion of the c-MET+ B-cell lines to the extracellular matrix molecules fibronectin (FN) and collagen (CN) in a dose dependent manner. However, adhesion to laminin was not affected by HGF/SF. Adhesion to FN was mediated by beta 1-integrins alpha 4 beta 1 (VLA4) and alpha 5 beta 1 (VLA5) since blocking antibodies against beta 1- (CD29), alpha 4-(CD49d), or alpha 5- (CD49e) integrin subunits, completely reversed the effect of HGF/SF. Furthermore, HGF/SF induced adhesion was abrogated by addition of genistein, which blocks protein tyrosine kinases, including c-MET. Addition of HGF/SF resulted in a sixfold increase in migration of c-MET B-lymphoma cells through Matrigel, compared to medium alone. In rat fibroblast cultures, HGF/SF doubled the number of c-MET+ B-lymphoma cells that invaded the fibroblast monolayer. In these adhesion, migration and invasion assays HGF/SF had no effect on c-MET- cell lines. In conclusion, c-MET is expressed or can be induced on immature, activated, and certain malignant B cells. HGF/SF increased adhesion of c-MET+ B-lymphoma cells to FN and CN, mediated via beta 1-integrins alpha 4 beta 1 and alpha 5 beta 1, and furthermore promoted migration and invasion.
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PMID:Hepatocyte growth factor/scatter factor promotes adhesion of lymphoma cells to extracellular matrix molecules via alpha 4 beta 1 and alpha 5 beta 1 integrins. 902 31

Proposed mechanisms of action for ascorbic acid (ascorbate, vitamin C) in the prevention and treatment of cancer include enhancement of the immune system, stimulation of collagen formation necessary for "walling off" tumors, inhibition of hyaluronidase which keeps the ground substance around the tumor intact and prevents metastasis, prevention of oncogenic viruses, correction of an ascorbate deficiency often seen in cancer patients, expedition of wound healing after cancer surgery, enhancement of the effect of certain chemotherapy drugs, reduction of the toxicity of other chemotherapeutic agents such as Adriamycin, prevention of free radical damage, and neutralization of carcinogenic substances. Scottish as well as Japanese studies have pointed to the potential benefit of high dose vitamin C for the treatment of "terminal" cancer. Mayo Clinic studies, however, have contradicted the Scottish and Japanese findings, resulting in accusations of methodological flaws from both sides. Numerous epidemiological studies have pointed to the importance of dietary and supplemental ascorbate in the prevention of various types of cancer including bladder, breast, cervical, colorectal, esophageal, lung, pancreatic, prostate, salivary gland, stomach, leukemia, and non-Hodgkin's lymphoma.
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PMID:Ascorbic acid in the prevention and treatment of cancer. 963 Jul 35

Acquired von Willebrand syndrome (AVWS) associated with hypothyroidism is of type I, results from a decreased synthesis of factor VIII and von Willebrand factor (VWF), responds to desmopressin with normal half-life times for factor VIII and VWF parameters, and disappears after treatment with I-thyroxine. AVWS type I or III, which occurs in a minority of patients with Wilms' tumour in the complete absence of an inhibitor against VWF and no absorption of factor VIII or VWF onto nephroblastoma cells, responds to chemotherapy and/or tumour resection. Hyaluronic acid produced by nephroblastoma cells may be the causative factor in atypical AVWS in Wilms' tumour. AVWS associated with thrombocythaemia of various myeloproliferative disorders is characterized by normal factor VIII and von Willebrand factor antigen (VWF: Ag) levels and a selective deficiency of functional ristocetin co-factor activity (VWF: RCo) and collagen-binding activity (VWF: CBA). AVWS type II in thrombocythaemia is caused by a platelet-dependent proteolysis of large VWF multimers, given the inverse relationship between platelet count and large VWF multimers in plasma and specific increases in the number of proteolytic VWF fragments in plasma. The laboratory findings of AVWS associated with systemic lupus erythematosus or IgG benign monoclonal gammopathy are characterized by a prolonged bleeding time and activated partial thromboplastin time, decreased or absent ristocetin-induced platelet activity, low to very low levels of factor VIII coagulant activity (mean 15%), VWF: Ag (mean 10.7%) and VWF: RCo (mean 6.2%), and a type II multimeric pattern of VWF. Neutralizing and non-neutralizing anti-VWF autoantibodies, usually IgG, have been detected in patient plasma either free or tightly bound to the intermediate and high molecular weight VWF factor VIII particles. The bound auto antibody-antigen complex is rapidly cleared from the circulation, resulting in low levels of factor VIII, VWF parameters as documented by a poor response to desmopressin and VWF factor VIII concentrate. High-dose intravenous immunoglobulin transiently corrects the factor VIII coagulant and VWF levels, lasting for a few weeks in AVWS type II associated with systemic lupus erythematosus or IgG benign monoclonal gammopathy. Prednisolone is effective in AVWS associated with autoimmune disorder. Prednisolone and chemotherapy will not affect AVWS associated with IgG benign monoclonal gammopathy because the monoclonal IgG protein remains to act as an anti-VWF autoantibody. An absorption of VWF to malignant cells has been documented in a few patients with various lymphoproliferative disorders or adrenal carcinoma and suggested to result in a depletion of VWF. The clinical picture of AVWS associated with early-stage IgG multiple myeloma, chronic lymphocytic leukaemia or non-Hodgkin's lymphoma without a paraprotein or no detectable underlying disorder is similar to that of AVWS type II in IgG benign monoclonal gammopathy but poorly documented with regard to the underlying immune mechanism of AVWS. The mechanical destruction of large VWF multimers may be of relevance in conditions in which the shear rate of flowing blood is increased, as may occur in cases of aortic stenosis, other heart valve defects or stenosed vessels. Drug-induced AVWS has been described in association with the use of pesticides valproic acid, ciprofloxacin, griseofulvin, tetracycline, thrombolytic agents and hydroxyethyl starch.
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PMID:Acquired von Willebrand syndromes: clinical features, aetiology, pathophysiology, classification and management. 1168 7


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