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)

Despite detailed evaluation of disease-associated prognostic factors, little is known about the impact of overweight in autograft programs for non-Hodgkin's lymphoma (NHL) patients. In order to address this issue, 121 NHL patients were retrospectively evaluated. They had been upfront (92 patients) or in relapse (29 patients) and received high-dose sequential (HDS) chemotherapy including peripheral blood progenitor cell (PBPC) autograft. Body mass index (BMI) was calculated as weight in kilograms divided by the square of the height in meters; overweight was defined as BMI > or = 28. Univariate and multivariate analyses were used to determine the prognostic implication of overweight and other known prognostic indicators on overall (OS) and event-free (EFS) survival for the entire group and overweight and non-overweight (reference) subgroups. With a median follow-up of 3 years, the estimated 5-year OS and EFS for the entire group were 58% and 49%, respectively. Twenty-eight patients (23%) had BMI > or = 28. Their median OS and EFS were 2.2 and 1.4 years, respectively, whereas median OS and EFS for the reference group have not been reached, with a 5-year projection of 65 and 55%, respectively (P < 0.002). On multivariate analysis, the risk of death among overweight patients was 2.9 (CI, 1.3-6.2) times that of the reference group; using EFS as the end point, a similar association between overweight and survival was observed. In conclusion, in high-risk NHL patients undergoing intensive chemotherapy and PBPC autografting overweight is associated with a poorer outcome.
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PMID:Overweight as an adverse prognostic factor for non-Hodgkin's lymphoma patients receiving high-dose chemotherapy and autograft. 1114 29

In an era of rapidly increasing prevalence of human obesity and associated health problems, leptin gene polymorphisms have drawn much attention in biomedical research. Leptin gene polymorphisms have furthermore drawn much attention from animal scientists for their possible roles in economically important production and reproduction traits. Of the polymorphisms reported for exonic, intronic, and promoter regions of the leptin gene, 16 have been included in association studies in humans, 19 in cattle, and 6 (all exonic or intronic) in pigs. In humans, associations have been found with overweight or (early-onset) obesity, non-insulin-dependent diabetes mellitus, prostate cancer, and non-Hodgkin's lymphoma. In cattle, associations have been found with feed intake, milk yield traits, carcass traits, and reproduction-related traits, and in pigs with feed intake, average daily gain, carcass traits (backfat/leanness), and reproduction performance traits. Many of the polymorphisms were only included in a limited number of association studies, or the phenotypes studied varied largely for a given polymorphism between studies. Therefore, many of the associations found for these polymorphisms need to be confirmed in future studies before firm conclusions can be drawn.
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PMID:Leptin gene polymorphisms and their phenotypic associations. 1611 75

Obesity is associated with altered immune and inflammatory responses and it may therefore influence the risk of non-Hodgkin's lymphoma. However, epidemiologic findings on obesity in relation to non-Hodgkin's lymphoma have been inconsistent. We conducted a meta-analysis to summarize the epidemiologic evidence on the association between excess body weight and risk of non-Hodgkin's lymphoma. Relevant studies were identified by searching MEDLINE (1966 to February 2007) and the reference lists of retrieved publications. We included cohort and case-control studies that reported relative risk (RR) estimates with 95% confidence intervals (CIs) for the association of body mass index (BMI) with non-Hodgkin's lymphoma incidence or mortality. A random-effects model was used to combine results from individual studies. Sixteen studies (10 cohorts and 6 case-control studies), with 21,720 cases, met the inclusion criteria. Compared to individuals of normal weight (BMI < 25.0 kg/m(2)), the summary RRs of non-Hodgkin's lymphoma were 1.07 (95% CI, 1.01-1.14) for overweight individuals (BMI between 25 and 30 kg/m(2)) and 1.20 (95% CI, 1.07-1.34) for those who were obese (BMI >/=>/=>/=>/= 30.0 kg/m(2)). Meta-analysis stratified by histologic subtypes showed that obesity was associated with a statistically significant increased risk of diffuse large B-cell lymphoma (RR, 1.40; 95% CI, 1.18-1.66; n = 6 studies) but not of follicular lymphoma (RR, 1.10; 95% CI, 0.82-1.47; n = 6 studies) or small lymphocytic lymphoma/chronic lymphocytic leukemia (RR, 0.95; 95% CI, 0.76-1.20; n = 3 studies). These findings indicate that excess body weight is associated with an increased risk of non-Hodgkin's lymphoma, especially of diffuse large B-cell lymphoma.
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PMID:Obesity and risk of non-Hodgkin's lymphoma: a meta-analysis. 1744 95

Excess body weight (overweight and obesity) is characterized by chronic hyperinsulinaemia and insulin resistance, and is implicated both in cancer risk and cancer mortality. The list of cancers at increased risk of development in an "obesogenic" environment include common adult cancers such as endometrium, post-menopausal breast, colon and kidney, but also less common malignancies such as leukaemia, multiple myeloma, and non-Hodgkin's lymphoma. The pathophysiological and biological mechanisms underpinning these associations are only starting to be understood. Insulin resistance is at the heart of many, but there are several other candidate systems including insulin-like growth factors, sex steroids, adipokines, obesity-related inflammatory markers, the nuclear factor kappa beta (NF-kappa B) system and oxidative stresses. With such as diversity of obesity-related cancers, it is unlikely that there is a "one system fits all" mechanism. While public health strategies to curb the spread of the obesity epidemic appear ineffective, there is a need to better understand the processes linking obesity and cancer as a pre-requisite to the development of new approaches to the prevention and treatment of obesity-related cancers.
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PMID:Obesity and cancer: pathophysiological and biological mechanisms. 1846 61

The aggregate of epidemiological studies indicates a significantly elevated risk for cancer in people with a high body mass index (BMI); a "dose-response" effect exists with increasing risk as BMI increases from the normal to overweight to obese categories. Successful sustained weight loss decreases future risk. The relationship of being overweight to the risk for leukemia in the aggregate has been supported in several large cohort studies and two meta-analyses of cohort and case-control studies. One meta-analysis found an elevated risk for each of the four major subtypes of leukemia. A significant association between the risk for non-Hodgkin's lymphoma and elevated BMI was supported by a meta-analysis of 13 cohort and nine case-control studies. The risk for diffuse large B-cell lymphoma may be especially significant. A high BMI increases the risk for myeloma, as judged by a meta-analysis of 11 cohort and four case-control studies. The biological relationship of obesity to the risk for cancer (biological plausibility) is unresolved. The two major causal final pathways could be "inductive" or "selective." The metabolic, endocrinologic, immunologic, and inflammatory-like changes resulting from obesity may increase the cell mutation rate, dysregulate gene function, disturb DNA repair, or induce epigenetic changes, favoring the induction of neoplastic transformation (inductive). Alternatively, obesity may create an environment in which pre-existing clones that are dormant are permitted (selected) to emerge.
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PMID:Obesity and the risk for a hematological malignancy: leukemia, lymphoma, or myeloma. 2093 95

We conducted a meta-analysis of prospective studies to summarise the epidemiologic evidence regarding the association of body mass index (BMI) with non-Hodgkin's lymphoma (NHL) and Hodgkin's lymphoma (HL) incidence and NHL mortality. Pertinent studies were identified by searching PubMed (1966-May 2011) and the reference lists of retrieved articles. For each study, we estimated a relative risk (RR) for a 5 kg/m(2) increase in BMI. A random-effects model was used to combine the RR estimates from individual studies. The summary RRs for a 5 kg/m(2) increase in BMI were 1.07 (95% confidence intervals (CI), 1.04-1.10) for NHL incidence (16 studies, n=17,291 cases) and 1.14 (95% CI, 1.04-1.26) for NHL mortality (five studies, n=3407 cases). BMI was significantly positively associated with risk of diffuse large B-cell lymphoma (RR, 1.13; 95% CI, 1.02-1.26), but not other NHL subtypes. The difference in risk estimates for subtypes was not statistically significant (P=0.10). There was evidence of a nonlinear association between BMI and HL (P for nonlinearity=0.01) (five studies, n=1557 cases). The summary RRs of HL were 0.97 (95% CI, 0.85-1.12) for overweight and 1.41 (95% CI, 1.14-1.75) for obesity. These results indicate that BMI is positively associated with risk of NHL and HL as well as with NHL mortality.
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PMID:Body mass index and risk of non-Hodgkin's and Hodgkin's lymphoma: a meta-analysis of prospective studies. 2173 76

Overweight and obese individuals frequently restrict caloric intake to lose weight. The resultant weight loss, however, typically is followed by an equal or greater weight gain, a phenomenon called weight cycling. Most attention to weight cycling has focused on identifying its detrimental effects, but preclinical experiments indicating that intermittent caloric restriction or fasting can reduce cancer risk have raised interest in potential benefits of weight cycling. Although hypothesized adverse effects of weight cycling on energy metabolism remain largely unsubstantiated, there is also a lack of epidemiologic evidence that intentional weight loss followed by regain of weight affects chronic-disease risk. In the limited studies of weight cycling and cancer, no independent effect on postmenopausal breast cancer but a modest enhancement of risk for renal cell carcinoma, endometrial cancer, and non-Hodgkin's lymphoma have been reported. An effect of either intermittent caloric restriction or fasting in protecting against cancer is not supported by the majority of rodent carcinogenesis experiments. Collectively, the data argue against weight cycling and indicate that the objective of energy balance-based approaches to reduce cancer risk should be to strive to prevent adult weight gain and maintain body weight within the normal range defined by body mass index.
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PMID:Weight cycling and cancer: weighing the evidence of intermittent caloric restriction and cancer risk. 2198 73

Higher body mass index and adiposopathy have been associated with increased risk of hematologic malignancies such as leukemia, multiple myeloma, myeloproliferative disorders, Hodgkin's and non-Hodgkin's lymphoma, and myelodysplastic syndromes. Adiponectin is a multimeric protein of the white adipose tissue presenting anti-inflammatory, insulin-sensitizing, anti-atherogenic, cardioprotective, and anti-neoplastic properties. Its anti-neoplastic actions are manifested via two mechanisms: (i) direct action on tumor cells by enhancing receptor-mediated signaling pathways and (ii) indirect action by regulating inflammatory responses, influencing cancer angiogenesis, and modulating insulin sensitivity at the target tissue site. In the bone marrow milieu, adiponectin and its main receptors are expressed by the majority of bone marrow stromal cell populations influencing hematopoietic stem cells function. Adiponectin may represent a molecular mediator relating adiposopathy with leukemogenesis and myelomagenesis. Several epidemiological studies conducted to date relate hypoadiponectinemia to the risk of myeloid-derived hematopoietic cancer and multiple myeloma. Adiponectin may be a promising biomarker with potential diagnostic and prognostic utility in determining the likelihood of myeloma and leukemia progression in certain cohorts of monoclonal gammopathy of undetermined significance patients and in myeloid hematologic malignancies, respectively. This review summarizes experimental and epidemiologic data regarding the role of adiponectin in hematologic malignancies in the context of adiposopathy. Enhancement of endogenous adiponectin, adiponectin replacement, or manipulation of adiponectin receptor sensitivity may be an attractive goal for prevention and an effective therapeutic strategy against hematopoietic cancer, specifically in overweight/obese individuals. Further studies are required to elucidate the role of the bone marrow microenvironment adiponectin in complex interactions involved in preleukemic and leukemic states.
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PMID:Adiponectin as a biomarker linking obesity and adiposopathy to hematologic malignancies. 2605 19