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

A 64-year-old male developed pain and marked swelling of his left calf muscle in September, 1989. Deep-vein thrombophlebitis was suspected, and therapy with warfarin sodium followed by urokinase was instituted. Because of unsatisfactory effect of the therapy, the patient was referred to another hospital on January 3rd 1990. A CT scan of the left leg showed a soft-tissue mass adjacent to the fibula. A biopsy of the mass revealed non-Hodgkin's lymphoma of diffuse medium-sized cell type. Immunohistologic examination confirmed B cell type. He was admitted to our hospital on January 31st 1990. A chest roentgenogram showed right pleural effusion. A CT scan of the abdomen revealed a space-occupying lesion in the liver. A Gallium scintigraphy showed markedly increased isotope uptake in the left calf and liver. He was classed as a Stage IV B. He responded well to combination chemotherapy with cyclophosphamide, THP-adriamycin, VP-16, and prednisolone and achieved a complete remission. Although prominent infiltration of lymphoma cells in skeletal muscles is rarely reported, it is important to perform the biopsy promptly when the mass is found in a muscle. In this case report, we describe a rare case of non-Hodgkin's lymphoma with muscle invasion presented as marked calf muscle swelling.
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PMID:[Non-Hodgkin's lymphoma with marked infiltration in calf muscle]. 202 Jan 18

An evaluation of totally implanted venous access systems inserted in 163 consecutive children with cancer is reported. From 1988 to 1994, 180 subcutaneous ports were inserted in children more than 1 year old. Initial diagnosis was acute leukaemia (n = 79), non-Hodgkin's lymphoma (n = 33), and solid tumour (n = 51). Median age was 85 months. All venous procedures were performed through the device. Chemotherapy was either moderate (n = 13) or intensive (n = 119) or very intensive (n = 48), including 16 patients undergoing marrow transplantation. Cumulative venous access totalled 55,770 patient days with a mean of 305 days/subcutaneous port. The cause of device removal was, end of treatment (n = 111), death due to malignancy (n = 20), catheter related infection (n = 7), and occlusion of the system (n = 4). Mechanical complications occurred in 19 ports; 16 were due to clots, of which 14 were cleared with instillation of urokinase. Documented infectious episodes occurred in 47 ports, recurred once in 14, and twice in five cases. Among these infections, 47 were septicaemic; 31 due to Staphylococcus epidermidis. Twenty seven of initial septic episodes were considered to be catheter related; the rate was 15%/subcutaneous port or 0.05/100 catheter days. Risk factors for the development of a first infection were age below 4 years and the time of use. Since February 1993, vancomycin (50 micrograms/ml) has been given and this has reduced the rate of S epidermidis infection from 26/83 subcutaneous port to 4/97. Life table analysis showed that the infection free interval for staphylococcus was significantly better after this technique ws initiated (log rank rest=0.02). Time saved was approximately 30minutes/patient/week compared with external catheters, or 45 hours/month for the cohort of children treated. Subcutaneous ports in paediatric cancer patients are reliable, safe, and durable and may offer an attractive alternative to external catheters for prolonged venous access and intensive treatment.
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PMID:Morbidity using subcutaneous ports and efficacy of vancomycin flushing in cancer. 776 65

A 38-year-old man with a non-Hodgkin's lymphoma of intermediate grade malignancy attained partial remission after three courses of CHOP (cyclophosphamide+hydroxydaunorubicin+vincristine+prednisolone). He was assigned to undergo autologous bone marrow transplantation (ABMT). The conditioning regimen consisted of cyclophosphamide and whole body irradiation. Two weeks later he developed veno-occlusive disease (VOD) of the liver. Doppler sonography confirmed the diagnosis showing a reversal of the blood flow in the portal vein. In addition a large thrombus was present in the inferior caval vein. Protein C level was strongly reduced (28%). Because of clinical deterioration intravenous urokinase was started. The transaminases normalised rapidly and the patient showed a dramatic clinical improvement. There were no major bleeding complications. Repeat Doppler sonography showed a normal antegrade flow in the portal vein. This case suggests that a coagulopathy in the hepatic vascular bed might contribute to the development of VOD and that patients with VOD are at risk for other thrombotic complications. Furthermore it shows that urokinase with platelet support can be given safely and effectively to a patient with VOD and severe thrombocytopenia.
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PMID:Successful treatment of veno-occlusive disease of the liver with urokinase in a patient with non-Hodgkin's lymphoma. 848 32

Oncogene c-Myc is frequently amplified and activated in human cancers. Deregulation of c-Myc protein has been shown to occur in 30% of all human cancers, especially in hematopoietic malignancies. As a transcription factor, c-Myc has been shown to regulate up to 15% of all human genome genes, controlling diverse cellular activities including cell cycle, ribosome biogenesis, protein synthesis, metabolism, apoptosis and angiogenesis. In this report, we provide evidence that the RNA helicase DHX33 is a critical downstream target of c-Myc. Myc binds to DHX33 upstream promoter region and stimulates its transcription. Elevated DHX33 protein is pivotal for c-Myc to drive tumor formation. Knockdown of DHX33 to basal levels in c-Myc overexpressing cells significantly reduced cell proliferation, cell migration and anchorage-independent cell growth in vitro and in vivo. Additionally, we found that DHX33 promotes MMP9, MMP14 and urokinase-type plasminogen activator (PLAU) transcription by directly binding to their promoters, thus promoting cancer cell migration. DHX33 protein was overexpressed in a certain subset of human non-Hodgkin's lymphoma tissues. Finally, knockdown of DHX33 significantly inhibits the development of Myc-induced acute myeloid leukemia. Overall, our results implicate the important role for DHX33 in Myc-induced cancer and point toward its potential therapeutic value in Myc driven cancers.
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PMID:Role of DHX33 in c-Myc-induced cancers. 2849 93