Therapeutic radiation for lymphoma: risk of malignant mesothelioma

BACKGROUND: Ionizing radiation has been used since the 1950s to treat a variety of cancers. Cancer patients who are treated with radiotherapy have shown increased risks for a variety of second malignancies, including mesothelioma, in several recent reports. The only existing study of Hodgkin lymphoma (HL) and subsequent mesothelioma had a short observation period. METHODS: The authors used Surveillance, Epidemiology, and End Results data over a 30-year period to identify patients with HL and non-Hodgkin lymphoma (NHL) who also were diagnosed with mesothelioma. Standardized incidence ratios (SIR) and absolute excess risks were calculated by sex and treatment modality for both types of lymphoma. RESULTS: Twenty-six patients were identified who had mesothelioma as second primaries based on 21,881 diagnoses of HL and 101,001 diagnoses of NHL. There was a statistically significant increase in mesothelioma (4 diagnoses; SIR, 6.59; 95% confidence interval [95% CI], 1.79-16.87) among men with HL who received radiation, but no women survivors were identified who had a diagnosis of mesothelioma. For NHL survivors, there was a nonsignificant excess of mesothelioma among men (SIR, 1.91; 95% CI, 0.77-3.93) and women (SIR, 3.75; 95% CI, 0.77-10.95) who had received radiation treatment. There were no increases among patients who were unirradiated. CONCLUSIONS: Mesothelioma rates for patients who had received radiotherapy were increased for survivors of HL and NHL. No increases were observed among the unirradiated. These findings and the existing body of supporting studies confirmed that radiotherapy is a cause of mesothelioma.     

Maternal smoking during pregnancy and childhood lymphoma: a meta-analysis

Results from epidemiological studies exploring the association between childhood lymphoma and maternal smoking during pregnancy have been contradictory. This meta-analysis included all published cohort (n = 2) and case-control (n = 10) articles; among the latter, the data of the Greek Nationwide Registry for Childhood Hematological Malignancies study were updated to include all recently available cases (-2008). Odds ratios (ORs), relative risks and hazard ratios were appropriately pooled in three separate analyses concerning non-Hodgkin lymphoma (NHL, n = 1,072 cases), Hodgkin lymphoma (HL, n = 538 cases) and any lymphoma (n = 1,591 cases), according to data availability in the included studies. An additional metaregression analysis was conducted to explore dose-response relationships. A statistically significant association between maternal smoking (any vs. no) during pregnancy and risk for childhood NHL was observed (OR = 1.22, 95% confidence interval, CI: 1.03-1.45, fixed effects model), whereas the risk for childhood HL was not statistically significant (OR = 0.90, 95% CI: 0.66-1.21, fixed effects model). The analysis on any lymphoma did not reach statistical significance (OR = 1.10, 95% CI = 0.96-1.27, fixed effects model), possibly because of the case-mix of NHL to HL. No dose-response association was revealed in the metaregression analysis. In conclusion, this meta-analysis points to a modest increase in the risk for childhood NHL, but not HL, among children born by mothers smoking during pregnancy. Further investigation of dose-response phenomena in the NHL association, however, warrants accumulation of additional data.     

Risk of second malignant neoplasms among lymphoma patients with a family history of cancer

Radiotherapy and chemotherapy are known risk factors for second cancers after lymphoma. The role of genetic influences, however, remains largely unknown. We assessed risk of second cancers associated with family history of any cancer in 41,181 patients with Hodgkin lymphoma (HL) (n = 7,476), non-Hodgkin lymphoma (NHL) (n = 25,941), or chronic lymphocytic leukemia (CLL) (n = 7,764), using a large population-based database. Family history of cancer was based on a diagnosis of any cancer in 110,862 first-degree relatives. We found increased relative risk (RR) (1.81, 95% confidence interval (CI): 1.04-3.16) of breast cancer among HL patient with positive (vs. negative) family history of cancer. Among CLL patients with positive (vs. negative) family history of cancer, we observed elevated risks of bladder (RR = 3.53, 95% CI: 1.31-9.55) and prostate cancer (RR = 2.15, 95% CI: 1.17-3.94). For NHL patients with positive (vs. negative) family history of cancer, we observed non-significantly increased risk of non-melanoma skin cancer (RR = 1.94, 95% CI: 0.86-4.38) and lung cancer (RR = 1.99, 95% CI: 0.73-5.39). Our observations suggest that genetic factors, as measured by positive family history of cancer, may be influential risk-factors for selected second tumors following lymphoproliferative disorders.     

Understanding the validity of self-reported positive family history of lymphoma in extended families to facilitate genetic epidemiology and clinical practice

The validity of self-reported information about familial Hodgkin lymphoma (HL), important for epidemiologic research and clinical practice, is undetermined. We attempted to validate 55 familial lymphomas previously reported by 48 subjects in a population-based case - control study of HL in women. Of 44 diagnoses (80%) reported by 40 (83%) recontacted subjects, we obtained medical documentation for 36 (82%). Twenty-nine (81%) were validated as lymphoma, with accuracy better for first-degree relatives and subjects with larger nuclear families and other family illness. Fourteen reports of familial HL were validated as lymphoma for 13 (93%) and as HL for nine (64%). Fifteen reports of familial NHL were validated as lymphoma for 10 (67%) and as NHL for 10 (67%). Thus, familial HL reported by HL patients and controls is highly likely to be lymphoma even in extended family members but less likely to be HL per se. Validity may vary with the subject's family size and medical history.     

Healthy lifestyle and the risk of lymphoma in the European Prospective Investigation into Cancer and Nutrition study

Limited evidence exists on the role of modifiable lifestyle factors on the risk of lymphoma. In this work, the associations between adherence to healthy lifestyles and risks of Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL) were evaluated in a large-scale European prospective cohort. Within the European Prospective Investigation into Cancer and Nutrition (EPIC), 2,999 incident lymphoma cases (132 HL and 2,746 NHL) were diagnosed among 453,808 participants after 15 years (median) of follow-up. The healthy lifestyle index (HLI) score combined information on smoking, alcohol intake, diet, physical activity and BMI, with large values of HLI expressing adherence to healthy behavior. Cox proportional hazards models were used to estimate lymphoma hazard ratios (HR) and 95% confidence interval (CI). Sensitivity analyses were conducted by excluding, in turn, each lifestyle factor from the HLI score. The HLI was inversely associated with HL, with HR for a 1-standard deviation (SD) increment in the score equal to 0.78 (95% CI: 0.66, 0.94). Sensitivity analyses showed that the association was mainly driven by smoking and marginally by diet. NHL risk was not associated with the HLI, with HRs for a 1-SD increment equal to 0.99 (0.95, 1.03), with no evidence for heterogeneity in the association across NHL subtypes. In the EPIC study, adherence to healthy lifestyles was not associated with overall lymphoma or NHL risk, while an inverse association was observed for HL, although this was largely attributable to smoking. These findings suggest a limited role of lifestyle factors in the etiology of lymphoma subtypes.     

Food groups and risk of non-Hodgkin lymphoma: a multicenter, case-control study in Italy

Incidence of non-Hodgkin lymphoma (NHL) has been rising worldwide, but the reasons are undefined. Dietary habits may play a role in the etiology of NHL by influencing the metabolic pathways of several cells of the immune system. This case-control study investigated the relation between food consumption and NHL risk. Between 1999 and 2002, we conducted a hospital-based case-control study on NHL in 2 areas of Italy. Cases were 190 patients (median age 58 years) with incident NHL admitted to specialized and general hospitals. Controls were 484 patients (median age 63 years) with acute non-neoplastic conditions admitted to the same hospitals network of cases. A validated food-frequency questionnaire was used to assess habitual diet 2 years before interview. Unconditional multiple logistic regression was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals (CI), with allowance for energy intake, according to the residual model. Consumption of highest versus lowest quartile of pasta/rice (OR = 1.87, 95% CI: 1.04-3.36) and cheese (OR = 1.66, 95% CI: 0.98-2.83) were associated with a significantly increased NHL risk. Inverse association was found for vegetables (OR = 0.49, 95% CI: 0.28-0.87), fruits (OR = 0.51, 95% CI: 0.30-0.85), and egg consumption (OR = 0.59, 95% CI: 0.36-0.97). The association of pasta/rice was also supported by an increased risk of high glycemic load levels (OR = 1.86, 95% CI: 1.04-3.32). In conclusion, our results suggested that diet could affect NHL risk.     

Second cancers in patients with brain tumours--impact of treatment

The records of the Finnish Cancer Registry from 1953 to 1994 were used to assess the risk of subsequent primary cancer among 14,493 brain tumour patients. They had been treated with surgery only (n = 9804), radiotherapy (n = 4099), chemotherapy and radiotherapy (n = 493) or chemotherapy alone (n = 97). By the end of 1994, 403 subsequent primary cancers were registered in these patients, whilst the expected number based on national incidence was 332. The standardised incidence ratio (SIR) was 1.2 (95% confidence interval (CI) 1.1-1.3). A significant excess risk of tumours in the central nervous system (CNS) including meningeomas (SIR 2.6, 95% CI 1.7-3.8), non-Hodgkin's lymphoma (SIR 2.6, 95% CI 1.6-4.1) and skin melanoma (SIR 1.9, 95% CI 1.0-3.1) was observed. CNS tumours were observed in excess among patients treated with surgery alone (SIR 2.0, 95% CI 1.2-3.2) and with radiotherapy (SIR 5.1, 95% CI 2.5-9.4). In conclusion, brain tumours are associated with an increased risk of both CNS second tumours and non-CNS second cancers, especially non-Hodgkin's lymphoma and melanoma. A moderately increased risk of second tumours in the CNS was observed among brain tumour patients treated with surgery only and a larger excess among those treated with radiotherapy.     

Is birth weight associated with childhood lymphoma? A meta‐analysis

Several risk factors have been identified for childhood lymphomas. The purpose of this meta-analysis was to synthesize current evidence regarding the association between birth weight with primarily the risk for non-Hodgkin lymphoma (NHL), given its similarity to acute lymphoblastic leukemia, Hodgkin lymphoma (HL) and any category of lymphoma. Two cohort (278,751 children) and seven case-control studies (2,660 cases and 69,274 controls) were included. Effects estimates regarding NHL, HL and any lymphoma were appropriately pooled using fixed or random effects model in two separate analyses: specifically, high was compared to normal or any birth weight. Similarly, low was compared to normal or any birth weight. No statistically significant association was found between high birth weight, as compared to normal birth weight, and risk for NHL plus Burkitt lymphoma (OR = 1.17, 95% CI = 0.76-1.80, random effects), HL (OR = 0.94, 95% CI = 0.64-1.38, fixed effects) or any plus Burkitt lymphoma (OR = 1.09, 95% CI = 0.76-1.56, fixed effects). A null association emerged when low was compared with normal birth weight for NHL plus Burkitt lymphoma (OR = 1.07, 95% CI = 0.71-1.62, random effects), HL (OR = 0.94, 95% CI = 0.54-1.65, fixed effects) or any plus Burkitt lymphoma (OR = 1.02, 95% CI = 0.79-1.33, fixed effects). Accordingly, no association was found when high or low birth weight was compared to any birth weight. Although current evidence suggests no association, birth weight might be a too crude indicator to reveal a genuine association of fetal growth with specific lymphoma categories; hence, there is an emerging need for use of more elaborate proxies, at least those accounting for gestational week.     

The incidence of lymphoma in first-degree relatives of patients with Hodgkin disease and non-Hodgkin lymphoma: results and limitations of a registry-linked study

BACKGROUND: The precise incidence of familial Hodgkin disease (HD) and non-Hodgkin lymphoma (NHL) in first-degree relatives is unknown. Through record linkage using two population-based sources, the authors estimated the risk of HD and NHL in family members of lymphoma probands. METHODS: The authors identified 8,037 first-degree relatives of 2,606 lymphoma cases (28.5% HD, 71.5% NHL) treated between 1970 and 1993 in 3 hospitals in Israel via the family file of the Population Registry. The authors linked this file with the Israel Cancer Registry, then calculated the standardized incidence ratio (SIR) by dividing the observed number of cases with the expected, adjusting for age, gender, calendar year, and continent of origin. RESULTS: The family file yielded incomplete ascertainment of relatives (for 771 probands, no relatives were identified). Twenty cases of lymphoma--6 HD and 14 NHL--were identified among relatives of lymphoma patients. The SIR for HD was 1.15 (95% confidence interval [CI]: 0.42-2.51) and for NHL 1.71 (95% CI: 0.93-2.87), considering the entire population of first-degree relatives. SIRs among siblings of lymphoma probands were 3.12 (95% CI: 1.01-7.29) for HD, 2.16 (95% CI: 0.45-6.31) for NHL, and 2.68 (95% CI: 1.15-5.27) for all lymphomas. There were 4 HD/HD, 1 NHL/NHL, and 3 NHL/HD sibling pairs. For HD/HD and NHL/NHL sibling pairs, the interval between lymphoma occurrence in proband and sibling was 1-4 years, whereas for HD/NHL pairs this ranged from 16 to 21 years. CONCLUSIONS: The risk of lymphoma among siblings of lymphoma probands was over 2.5-fold that of the general population and lower among other family members. The temporal proximity of HD/HD and NHL/NHL sibling pairs argues for environmental as well as genetic etiology. This method was hampered by incomplete data.     

Family history of hemolymphopoietic and other cancers and risk of non-Hodgkin's lymphoma.

We investigated the risk of lymphomas, hemolymphopoietic (HLP) cancers (including lymphomas), and non-HLP cancers in first-degree relatives of non-Hodgkin's lymphoma (NHL) cases in an Italian case-control study on 225 patients (median age, 59 years) with a new diagnosis of NHL and 504 hospital controls (median age, 63 years), admitted for a wide spectrum of acute, nonneoplastic, nonimmune conditions. We estimated odds ratios (OR) adjusted for sex, age, family size, and other potential confounders. We also built the cohort of all first-degree relatives and computed age and sex adjusted hazard ratios (HR) using proportional hazard models. A history of lymphoma in first-degree relatives was reported by 5 NHL cases and 3 controls [OR, 3.2; 95% confidence interval (95% CI), 0.7-14.4] whereas 14 cases and 11 controls reported a family history of HLP cancers (OR, 3.0; 95% CI, 1.2-7.0). The HR of relatives of NHL cases, compared with relatives of controls, was 4.5 (95% CI, 1.1-18.8) for lymphomas, 3.5 (95% CI, 1.5-7.4) for HLP cancers, 1.6 (95% CI, 1.3-2.0) for all cancers, and 1.0 (95% CI, 0.9-1.1) for all causes of deaths. The HRs were higher for relatives of NHL cases diagnosed before the age of 50 years: 7.1 for HLP cancers, 2.0 for all cancers, and 1.6 for all deaths. A family history of cancer of the liver (OR, 2.1; 95% CI, 1.0-4.2), breast (OR, 2.0; 95% CI, 1.0-3.6), and kidney (OR, 4.6; 95% CI, 1.0-20.9) increased NHL risk. The OR was also elevated for all cancer sites (OR, 1.7 95% CI, 1.2-2.4) and the risk increased with the number of affected relatives also when HLP cancers were excluded.     

Sex- and kindred-specific familial risk of non-Hodgkin's lymphoma.

A family history of non-Hodgkin's lymphoma (NHL) confers increased risk of NHL, but it is unknown whether the excess risk in males and females varies by the sex or kinship of the affected relative. We linked nationwide Swedish registries to identify parents and siblings of NHL patients who developed NHL between January 1, 1961 and December 31, 2002. In males, parental risks were approximately the same from fathers and mothers, whereas sibling risks were higher from brothers [standardized incidence ratio (SIR), 1.8; 95% confidence interval (95% CI), 1.0-2.9] than sisters (SIR, 0.9; 95% CI, 0.2-1.9). In females, parental and sibling risks were higher from same-sex relatives (SIR from mothers, 1.9; 95% CI, 1.2-2.7; SIR from sisters, 6.3; 95% CI, 4.0-9.3) than from opposite-sex relatives (SIR from fathers, 1.2; 95% CI, 0.7-1.9; SIR from brothers, 0.7; 95% CI, 0.2-1.6). These findings did not vary substantially by the age of diagnosis of the offspring. Risk of NHL in offspring was also increased among those with a parent diagnosed with multiple myeloma or leukemia. The relative risk of NHL among those with a parent diagnosed with any hematopoietic cancer was 1.5 (95% CI, 1.4-1.7) and that for having a sibling with any hematopoietic cancer was also 1.5 (95% CI, 1.2-1.9). Our results suggest that part of the familial risk of NHL may be attributable to shared environmental exposures, particularly between same-sex siblings.     

Smoking and non-Hodgkin lymphoma: case-control study in Italy

Tobacco smoking is a well-documented risk factor for several cancers, but the role of cigarette smoking in the etiology of non-Hodgkin lymphoma (NHL) is inadequately understood. Hepatitis C virus (HCV) has been associated with NHL, but the interaction between HCV and smoking habits has not yet been studied. Between 1999 and 2002, we conducted a case-control study on the association of HCV, smoking habits and NHL in 2 areas of northern and southern Italy. Cases were 225 consecutive patients (median age, 59 years) with a new diagnosis of NHL that were admitted to reference and general hospitals. Controls were 504 patients (median age, 63 years) admitted to the same hospitals as cases, for a wide spectrum of acute, nonneoplastic, nonimmune-, nor tobacco-related conditions. Current, heavy smokers (> or = 20 cigarettes/day) had an odds ratio (OR) of NHL of 2.10 (95% confidence interval, CI: 1.07-4.12) compared to never smokers. The association between smoking and NHL was consistent across strata of sex and age. Compared to never smokers, current smokers of > or = 20 cigarettes/day had ORs of 1.14 (95% CI: 0.37-3.56) for B-cell-low-grade, 2.10 (95% CI: 0.94-4.67) for B-cell-intermediate and high-grade, and 25.84 (95% CI: 1.95-342.17) for T-cell NHL. The effect of tobacco smoking and HCV were independent on the relative risk, leading a 4-fold elevated risk in current smokers HCV positive subjects. Tobacco smoking and hepatitis C virus (HCV) have been associated to non-Hodgkin lymphoma (NHL), but the interaction between HCV and smoking habits has not yet been studied. Our study confirms that tobacco is related to NHL, and reports on the combined effect of tobacco smoking and HCV. Infection acted together according to a multiplicative model, leading to a 4-fold elevated risk in current smokers HCV positive subjects.     

Alcohol consumption and risk of hematological malignancies: A meta‐analysis of prospective studies

Current convincing evidence suggests that alcohol intake increases the risk of several carcinomas, which might subsequently lead to a recommendation toward limiting alcohol consumption. However, there are accumulating data worth meta‐analyzing that show a different effect on the risk of hematological malignancies. Eligible cohort studies were sought in PubMed database up to August 31, 2016. Separate analyses were performed by subtype of hematological malignancy (non‐Hodgkin lymphoma [NHL] and subtypes, Hodgkin lymphoma [HL], leukemia and subtypes), time status (ever, current, former), level of consumption (light, moderate, heavy), alcoholic beverage (total alcohol, beer, liquor, wine) and gender. Moderate and heavy alcohol consumption were significantly associated with reduced risk of NHL (relative risk [RR] = 0.85, 95% confidence interval [CI]: 0.80–0.90 and RR = 0.73, 95%CI: 0.60–0.89, respectively); a protective trend was also shown for light alcohol intake (RR = 0.93, 95%CI: 0.87–1.00). Specifically, beer consumption was associated with reduced NHL risk (RR = 0.88, 95%CI: 0.81–0.95). However, the association regarding other alcoholic beverages seemed null. The beneficial effects of alcohol mainly pertained to Diffuse Large B‐Cell Lymphoma (DLBCL) (RR = 0.83, 95%CI: 0.77–0.89) and Follicular Lymphoma (FL) (RR = 0.85, 95%CI: 0.78–0.93). There was also no association between alcohol consumption and risk of HL or leukemias. In contrast to most solid malignancies, alcohol seems to confer a protective effect on NHL risk, especially on DLBCL and FL subtypes, with beer being notably beneficial.     

Hepatitis C virus and risk of non-Hodgkin lymphoma in British Columbia, Canada

We investigated Hepatitis C virus (HCV) seropositivity and the risk of non-Hodgkin lymphoma (NHL) in a population-based case-control study in British Columbia, Canada. Cases were aged 20-79, diagnosed between March 2000 and February 2004, and resident in greater Vancouver or Victoria. Cases with HIV or a prior transplant were excluded. Controls were chosen from the Client Registry of the British Columbia (BC) Ministry of Health, and were age/sex/region frequency matched to cases. Antibodies for HCV were measured in 795 cases and 697 control subjects. HCV seropositivity was 2.4% in cases and 0.7% in controls [odds ratio (OR) = 2.6, 95% confidence interval (CI) = 0.9-7.4]. A significantly elevated risk was observed for B-cell lymphoma (OR = 2.9, 95%CI = 1.0-8.6). The highest risks were associated with diffuse large B-cell lymphoma (OR = 7.3, 95%CI = 2.1-25.0) and marginal zone lymphoma (OR = 6.1, 95%CI = 1.1-33.9). Our results provide further evidence that HCV infection contributes to NHL risk.     

Family history of cancer and risk of pediatric and adolescent Hodgkin lymphoma: A Children's Oncology Group study

Family history of lymphoid neoplasm (LN) is a strong and consistently observed Hodgkin lymphoma (HL) risk factor, although it has been only marginally examined in pediatric/adolescent patients. Here, healthy control children identified by random digit dialing were matched on sex, race/ethnicity and age to HL cases diagnosed at 0–14 years at Children's Oncology Group institutions in 1989–2003. Detailed histories were captured by structured telephone interviews with parents of 517 cases and 783 controls. Epstein–Barr virus (EBV) RNA detection was performed for 355 available case tumors. Two analytic strategies were applied to estimate associations between family cancer history and pediatric/adolescent HL. In a standard case–control approach, multivariate conditional logistic regression was used to calculate odds ratios and 95% confidence intervals (CIs). In a reconstructed cohort approach, each relative was included as a separate observation, and multivariate proportional hazards regression was used to produce hazard ratios (HRs) and 95% CIs. Using the latter, pediatric/adolescent HL was associated with a positive family history (HR = 1.20, 95% CI: 1.06–1.36), particularly early‐onset cancers (HR = 1.30, 95% CI: 1.06–1.59) and those in the paternal lineage (HR = 1.38, 95% CI: 1.16–1.65), with a suggested association for LN in first‐degree relatives (HR = 3.61, 95% CI: 0.87–15.01). There were no discernable patterns for EBV+ versus EBV– HL. The clustering of LN within pedigrees may signal shared genetic susceptibility or common environmental exposures. Heritable genetic risk variants have only recently begun to be discovered, however. These results are consistent with other studies and provide a compelling rationale for family‐based studies to garner information about genetic susceptibility to HL.     

Associations between statin use and non‐Hodgkin lymphoma (NHL) risk and survival: a meta‐analysis

Evidence on the effect of statin use on non‐Hodgkin lymphoma (NHL) is not clear. We conducted a systematic review and meta‐analysis to examine the associations between statin use and NHL risk and survival. We searched multiple literature sources up to October 2014 and identified 10 studies on the risk of diagnosis with NHL and 9 studies on survival. Random effects model was used to calculate pooled odds ratio (PORs) for risk and pooled hazard ratio (PHR) for survival. Heterogeneity among studies was examined using the Tau‐squared and the I‐squared (I²) tests. Statin use was associated with reduced risk for total NHL (POR = 0.82, 95% CI 0.69–0.99). Among statin users, there was a lower incidence risk for marginal zone lymphoma (POR = 0.54, 95% CI 0.31–0.94), but this was not observed for other types of NHL. However, statin use did not affect overall survival (PHR = 1.02, 95% CI 0.99–1.06) or event‐free survival (PHR = 0.99, 95% CI 0.87–1.12) in diffuse large B‐cell lymphoma. There is suggestive epidemiological evidence that statins decrease the risk of NHL, but they do not influence survival in NHL patients. Copyright © 2015 John Wiley & Sons, Ltd.     

Scholastic achievement of children with lymphoma or Wilms tumor at the end of comprehensive education--a nationwide, register-based study

Cancer treatment may affect school performance. School report grades after childhood lymphomas and Wilms tumor have not been previously reported. All Finnish patients with Wilms tumor (N = 74), Hodgkin lymphoma (HL) (N = 99) and non-Hodgkin lymphoma (NHL) (N = 94) who were born in 1974-1986 and had achieved the age of 16 years were identified from the Finnish cancer registry. Population controls (N = 1329) were matched for age, gender and residence. Their 9th grade school reports were obtained from Statistics Finland. The overall average and grades for mother tongue, first foreign language, mathematics and physical education were compared between the patients and their controls. Almost all the patients (>98%) had finished their comprehensive school. NHL patients had lower overall averages than their controls (difference -0.27 grade units; 95% CI -0.39, -0.15). Irradiation or age at diagnosis did not explain this difference in NHL patients. The grades of NHL patients were significantly lower than those of their controls in each academic school subject, especially in mathematics (-0.45; 95% CI -0.63, -0.27). In mother tongue, girls with irradiation had greatest difference (-0.66, 95% CI -0.99, -0.34) to their controls. Patients with HL and Wilms tumor performed similarly or even better than their controls in all academic subjects. Grades for physical education were impaired in Wilms tumor patients (-0.20; 95% CI -0.33, -0.06). Impairment of school report grades was observed in patients with NHL. The difference to controls was greatest in mathematics. The patients with HL and Wilms tumor, who had not received any central nervous system directed therapy, achieved equally good grades as their controls in all the academic subjects.     

Hodgkin’s and Non-Hodgkin’s Lymphomas in an Indian Rural Medical Institution: Comparative Clinicopathologic Analysis

In this prospective, hospital-based two year study, we comparatively evaluated clinicopathologic featuresof Hodgkin’s lymphoma (HL, n = 48) and Non-Hodgkin’s lymphoma (NHL, n = 76) in an Indian rural medicalinstitution. A lower median age of onset (28.1 versus 39.9 years) and and higher male to female ratio (3.8:1versus 3.2:1) were noted for HL compared to NHL. The commonest symptom was neck swelling (58.3% versus65.8%) while peripheral lymphadenopathy was the commonest sign (83.3% versus 94.7%). The commonestlymph-node group involved was cervical (79.2% versus 79.0%). Bone marrow involvement was lower in HL(8.33% versus 18.4%). The commonest histological subtype was mixed cellularity (45.8%) in HL and diffusemixed variant (31.6%) in NHL. Most cases presented at advanced stage (54.2% in HL, 71.1 % in NHL). Hencea distinct clinicopathologic profile was noted in HL and NHL that are comparable to other Indian studies butdifferent from Western studies. Recognition of such characteristic features should assist in providing appropriatediagnosis and suitable management in rural communities having limited access to sophisticated medical services.     

Cancer risk in people infected with human immunodeficiency virus in the United States

Data are limited regarding cancer risk in human immunodeficiency virus (HIV)-infected persons with modest immunosuppression, before the onset of acquired immunodeficiency syndrome (AIDS). For some cancers, risk may be affected by highly active antiretroviral therapy (HAART) widely available since 1996. We linked HIV/AIDS and cancer registries in Colorado, Florida and New Jersey. Standardized incidence ratios (SIRs) compared cancer risk in HIV-infected persons (initially AIDS-free) during the 5-year period after registration with the general population. Poisson regression was used to compare incidence across subgroups, adjusting for demographic factors. Among 57,350 HIV-infected persons registered during 1991-2002 (median CD4 count 491 cells/mm(3)), 871 cancers occurred during follow-up. Risk was elevated for Kaposi sarcoma (KS, SIR 1,300 [n = 173 cases]), non-Hodgkin lymphoma (NHL, 7.3 [n = 203]), cervical cancer (2.9 [n = 28]) and several non-AIDS-defining malignancies, including Hodgkin lymphoma (5.6 [n = 36]) and cancers of the lung (2.6 [n = 109]) and liver (2.7 [n = 14]). KS and NHL incidence declined over time but nonetheless remained elevated in 1996-2002. Incidence increased in 1996-2002 compared to 1991-1995 for Hodgkin lymphoma (relative risk 2.7, 95%CI 1.0-7.1) and liver cancer (relative risk infinite, one-sided 95%CI 1.1-infinity). Non-AIDS-defining cancers comprised 31.4% of cancers in 1991-1995, versus 58.0% in 1996-2002. For KS and NHL, risk was inversely related to CD4 count, but these associations attenuated after 1996. We conclude that KS and NHL incidence declined markedly in recent years, likely reflecting HAART-related improvements in immunity, while incidence of some non-AIDS-defining cancers increased. These trends have led to a shift in the spectrum of cancer among HIV-infected persons.     

Liver cancer and non-Hodgkin lymphoma in hepatitis C virus-infected patients: results from the DANVIR cohort study

Hepatitis C virus (HCV)-infection can cause hepatocellular carcinoma (HCC) and most likely non-Hodgkin lymphoma (NHL). No studies have compared the risk of these cancers between patients with chronic and cleared HCV-infection. The aim of this study was to estimate the 10-year risk of HCC and NHL in HCV-infected patients and to compare the risk of these cancers between HCV-infected patients and the general population in Denmark and between patients with chronic and cleared HCV-infection. Nationwide cohorts were used: 11,975 HCV-infected patients in the DANVIR cohort and 71,850 individuals from an age- and gender-matched general population cohort. Within DANVIR, 4,158 patients with chronic HCV-infection and 2,427 patients with cleared HCV-infection were studied. The 10-year risks of HCC and NHL in HCV-infected patients were 1.0% [95% confidence interval (CI): 0.8-1.3%] and 0.1% (95% CI: 0.1-0.2%), respectively. Compared to the general population, HCV-infected patients had a 62.91-fold increased risk of HCC (95% CI: 28.99-136.52), a 29.97-fold increased risk of NHL during the first year of follow-up (95% CI: 6.08-147.84), and a 1.26-fold increased risk of NHL after the first year (95% CI: 0.36-4.41). Chronic HCV-infection was associated with a 4.71-fold increased risk of HCC (95% CI: 1.67-13.32) compared to cleared HCV-infection; 5 and 0 events of NHL occurred in patients with chronic and cleared HCV-infection, respectively. HCC-risk is increased substantially in HCV-infected patients compared to the general population. Chronic as opposed to cleared HCV-infection increases the risk of HCC and perhaps NHL.