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)

Growth impairment is one of the most important late sequelae in childhood malignancies. In the last few years, the contribution of cytotoxic agents to growth retardation has been a subject of investigation. The aim of this study was to evaluate the growth impairment in children treated for non-Hodgkin's lymphoma (NHL). The study group comprised 41 children (eight girls, 33 boys) treated for NHL with three different chemotherapy protocols. All patients were in remission at the last visit. The control group consisted of 41 healthy age- and sex-matched children. All patients' standing heights and body weights were measured regularly from the time of diagnosis. Growth parameters were measured both at the time of diagnosis and at the end of treatment (median treatment time: 6 months). Height and weight velocities were calculated at 6 month intervals after the diagnosis until the last visit. The mean height SDS of the patients was -0.66 +/- 1.42 at the diagnosis and 0.29 +/- 1.21 at the last visit. Height SDS of the patients showed a significant improvement at the end of the 2nd year after the diagnosis (p = 0.005) and at the last visit (p = 0.022) (median follow-up time: 48 months after diagnosis). The height velocity SDS increase at the end of the 2nd year was particularly remarkable in short-term protocols such as BFM-90 B-NHL. The sitting height, the sitting height/height ratio and serum insulin-like growth factor-I (IGF-I) levels were found to be lower in the patients than those of control group at the last visit. One can conclude that chemotherapy might cause a reduction in growth velocity during treatment. The cumulative dosages of anti-neoplastic agents and serum IGF-I levels could have been implied in the pathogenesis of growth retardation.
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PMID:Late effects of treatment on growth in childhood non-Hodgkin's lymphoma. 1692 58

The number of cancer cases caused by being obese is estimated to be 20% with the increased risk of malignancies being influenced by diet, weight change, and body fat distribution together with physical activity. Reports from the International Agency for Research into Cancer and the World Cancer Research Fund (WCRF) have shown that the strongest evidence exists for an association of obesity with the following cancer types: endometrial, esophageal adenocarcinoma, colorectal, postmenopausal breast, prostate, and renal, whereas the less common malignancies are leukemia, non-Hodgkin's lymphoma, multiple myeloma, malignant melanoma, and thyroid tumours. To be able to develop novel methods in prevention and treatment, we first must understand the underlying processes which link cancer to obesity. Four main systems have been identified as potential producers of cancer in obesity: insulin, insulin-like growth factor-I, sex steroids, and adipokines. Various novel candidate mechanisms have been proposed: chronic inflammation, oxidative stress, crosstalk between tumour cells and surrounding adipocytes, migrating adipose stromal cells, obesity-induced hypoxia, shared genetic susceptibility, and the functional defeat of immune function. Herein, we review the major pathogenic links between obesity and susceptibility to cancer.
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PMID:Obesity as a major risk factor for cancer. 2407 32