Thymoma is a rare malignancy of unknown etiology.
The author examined patterns in thymoma incidence in the US general population using data from Surveillance, Epidemiology, and End Results (SEER) ...cancer registries. Prior studies concerning the risk of additional malignancies in thymoma patients were reviewed.
Based on cancer registry data, the overall incidence of thymoma in the US is 0.13 per 100,000 person-years. Thymoma is exceedingly uncommon in children and young adults, rises in incidence in middle age, and peaks in the seventh decade of life. Thymoma incidence is especially high among Asians and Pacific Islanders in the US. While several studies based at single treatment centers have suggested that thymoma patients have a broadly increased risk for other malignancies, follow up data from US cancer registries support a more limited spectrum of cancer risk. In particular, thymoma patients have a subsequently elevated risk for developing B-cell non-Hodgkin's lymphoma. Based on limited data, thymoma patients may also have an elevated risk for developing soft tissue sarcomas.
Thymoma is a rare malignancy. The excess risk for non-Hodgkin's lymphoma is consistent with an effect of immune disturbance arising from the thymoma or its treatment. While descriptive epidemiologic data may yield clues to the etiology of thymoma, large multi-center case-control studies will be required to formally evaluate environmental and genetic risk factors.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The neutrophil-to-lymphocyte ratio (NLR) in peripheral blood reflects the balance between systemic inflammation and immunity and is emerging as a prognostic biomarker in many diseases, but its ...predictive role for mortality in the general population has not been investigated. We analyzed 1999-2014 National Health and Nutrition Examination Survey mortality-linked data, followed up until 2015. In participants aged > 30 with measurements of differential white blood cell counts, NLR was calculated and categorized into quartiles. Associations of increased NLR with overall or cause-specific mortality were assessed with Cox proportional hazard regression models, adjusted for potential confounders. Increased NLR was associated with overall mortality (hazard ratio HR 1.14, 95% confidence interval CI 1.10-1.17, per quartile NLR) and mortality due to heart disease (1.17, 1.06-1.29), chronic lower respiratory disease (1.24, 1.04-1.47), influenza/pneumonia (1.26, 1.03-1.54) and kidney disease (1.26, 1.03-1.54). NLR was associated with cancer mortality only in the first follow-up year (HR 1.48, 95% CI 1.11-1.98). The association with chronic lower respiratory disease mortality was stronger in individuals with prevalent lung diseases (HR 1.46, 95% CI 1.14-1.88, P
= 0.01), while NLR showed positive associations with mortality from heart disease (1.21, 1.07-1.38) and cerebrovascular disease (1.30, 1.04-1.63) only among individuals without these conditions at baseline. NLR is associated with mortality overall and due to certain causes in the general population. Associations over short follow-up intervals and among individuals with conditions at baseline suggest effects of disordered inflammation and immunity on progression of those conditions, while other associations may reflect contributions to disease etiology.
Full text
Available for:
IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
The advent in the last several years of effective immunotherapy for cancer has renewed interest in the role of the immune system in controlling cancer. The idea that the immune system can help ...control cancer has a long history. Solid organ transplant recipients (SOTRs) as well as human immunodeficiency virus (HIV)–infected people are affected by cell‐mediated immune dysfunction. Epidemiologic studies of these populations reveal a pattern characterized by a strongly increased incidence of virus‐related cancers (eg, Kaposi sarcoma, non‐Hodgkin lymphoma, and anogenital cancers). In addition, recent epidemiologic studies have evaluated cancer‐specific mortality among SOTRs and HIV‐infected people following a cancer diagnosis. For a wider range of cancers—not limited to those caused by viruses, and including melanoma and cancers of the colorectum, lung, and breast— these immunosuppressed cancer patients have higher cancer‐specific mortality than other cancer patients. This latter group of cancers somewhat mirrors those for which immunotherapy with checkpoint inhibitors is approved. These epidemiologic observations suggest that there are 2 distinct immune selection processes in humans: immunosurveillance directed against premalignant cells before cancer diagnosis (most relevant for preventing virus‐related cancers), and “immunocontainment” directed against established cancers. These processes thus appear relevant for different groups of malignancies and may have different mechanisms.
The author summarizes epidemiologic studies of solid organ transplant recipients and HIV‐infected people, supporting an important role for the immune system in preventing and controlling cancer.
Full text
Available for:
BFBNIB, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Chronic HCV infection is associated with several extrahepatic manifestations (EHMs). Data on the effect of sustained virological response (SVR) on the risk of EHMs are limited.
We conducted a ...retrospective cohort study using data of patients from the US Veterans Affairs HCV Clinical Case Registry who had a positive HCV RNA test (10/1999-08/2009). Patients receiving interferon-based antiviral therapy (AVT) were identified. SVR was defined as negative HCV RNA at least 12 weeks after end of AVT. Risks of eight incident EHMs were evaluated in Cox regression models.
Of the 160 875 HCV-infected veterans, 31 143 (19.4%) received AVT, of whom 10 575 (33.9%) experienced SVR. EHM risk was reduced in the SVR group compared with untreated patients for mixed cryoglobulinaemia (adjusted HR (aHR)=0.61; 95% CI 0.39 to 0.94), glomerulonephritis (aHR=0.62; 95% CI 0.48 to 0.79), porphyria cutanea tarda (PCT) (aHR=0.41; 95% CI 0.20 to 0.83), non-Hodgkin's lymphoma (NHL) (aHR=0.64; 95% CI 0.43 to 0.95), diabetes (aHR=0.82; 95% CI 0.76 to 0.88) and stroke (aHR=0.84; 95% CI 0.74 to 0.94), but not for lichen planus (aHR=1.11; 95% CI 0.78 to 1.56) or coronary heart disease (aHR=1.12; 95% CI 0.81 to 1.56). Risk reductions were also observed when patients with SVR were compared with treated patients without SVR for mixed cryoglobulinaemia, glomerulonephritis, PCT and diabetes. Significant reductions in the magnitude of aHRs towards the null with increasing time to initiation of AVT after HCV diagnosis were observed for glomerulonephritis, NHL and stroke.
Risks of several EHMs of HCV infection are reduced after AVT with SVR. However, early initiation of AVT may be required to reduce the risk of glomerulonephritis, NHL and stroke.
Abstract
Background
Sepsis is an important cause of mortality among older adults in the United States. The association between sepsis and subsequent risk of cancer is poorly understood.
Methods
Using ...the Surveillance, Epidemiology, and End Results (SEER)-Medicare linked database, we conducted a case-control study in US adults. We included 1801156 cases with a first cancer diagnosis in SEER during 1992–2013 (ages 66–115 years) and 200000 cancer-free controls from a 5% random sample of Medicare beneficiaries. Sepsis was identified using inpatient Medicare claims. Associations with sepsis were estimated using logistic regression.
Results
After correction for multiple comparisons, sepsis was significantly associated with increased risk for cancers of the colon (adjusted odds ratio aOR = 1.12), rectum (1.13), liver (1.47), lung (1.17), and cervix (1.52), as well as acute myeloid leukemia (AML, 1.19), chronic myeloid leukemia (1.54), and myelodysplastic syndrome (1.30). Inverse associations were observed for cancers of the breast (aOR = 0.86), prostate (0.75), kidney (0.90), and thyroid (0.68) and for melanoma (0.83), diffuse large B-cell lymphoma (0.89), and follicular lymphoma (0.65). Sepsis was significantly associated with the following 9 types of cancer in the period >5 years following sepsis diagnosis: thyroid, prostate, colon, rectum, lung, and liver and follicular lymphoma, melanoma, and AML.
Conclusions
Sepsis is associated with increased or decreased risks for a small group of cancers. Factors that may explain these associations include etiologic effects. Other associations may reflect the presence of precursor conditions or patterns in ascertainment of cancer and screening.
Based on a national database of elderly individuals, we found that sepsis is a significantly associated risk for 15 types of cancer, which supports sepsis as having long-term health consequences and that some effects may impact the development of cancer.
Summary Background Hepatitis B virus (HBV) infection is common throughout Asia and Africa. Whether chronic HBV infection increases risk of non-Hodgkin lymphoma (NHL) is unclear. We aimed to assess ...the association between chronic HBV infection and subsequent development of NHL in a South Korean cohort. Methods The Korean Cancer Prevention Study is a cohort study of South Korean workers and their dependants enrolled during 1992–95. From this cohort, we excluded individuals who died before Jan 1, 1993, who had cancer at or before the initial visit, who had missing information about weight, height, alanine aminotransferase or aspartate aminotransferase concentrations, or alcohol use, or who had evidence of HIV or HCV infection. Of 1 284 586 eligible participants, 603 585 had baseline data for serum hepatitis B surface antigen (HBsAg) status and were included in our study. We regarded HBsAg positivity at baseline as evidence of chronic HBV infection. Participants were followed up from baseline until Dec 31, 2006. We used national databases of inpatient and outpatient diagnoses and mortality records to ascertain occurrence of haematological malignancies. We assessed incidence of NHL overall and of NHL subtypes, malignant immunoproliferation, Hodgkin's lymphoma, multiple myeloma, and various leukaemias. We used Cox regression to evaluate associations with HBsAg status, adjusting for sex, age, and enrolment year. Findings 53 045 (9%) of 603 585 participants tested positive for HBsAg at baseline. Subsequently, 133 HBsAg-positive and 905 HBsAg-negative individuals developed NHL. HBsAg-positive participants had an increased risk of NHL overall compared with those who were HBsAg-negative (incidence 19·4 vs 12·3 per 100 000 person-years; hazard ratio HR 1·74, 95% CI 1·45–2·09, adjusted for sex, age at baseline, and enrolment year). Among NHL subtypes, HBsAg positivity was associated with increased risk of diffuse large B-cell lymphoma (n=325, incidence 6·86 vs 3·79 per 100 000 person-years; adjusted HR 2·01, 1·48–2·75) and other or unknown subtypes (n=591, incidence 10·5 vs 7·07 per 100 000 person-years; adjusted HR 1·65, 1·29–2·11), compared with HBsAg negativity. Increased risk was also recorded for malignant immunoproliferation (n=14, incidence 0·44 vs 0·15 per 100 000 person-years; adjusted HR 3·79, 1·05–13·7). Risk of these malignancies was consistently raised in HBsAg-positive participants throughout 14 years of follow-up. HBsAg positivity was not associated with follicular or T-cell NHL, Hodgkin's lymphoma, multiple myeloma, or various leukaemias. Interpretation During extended follow-up, HBsAg-positive individuals had an increased risk of NHL, suggesting that chronic HBV infection promotes lymphomagenesis. Funding Korean Seoul City Research and the National Research and Development Program for Cancer Control, Ministry for Health, Welfare and Family Affairs, Republic of Korea; US National Cancer Institute.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Abstract
Background
The optimal clinical management of oral precancer remains uncertain. We investigated the natural history of oral leukoplakia, the most common oral precancerous lesion, to estimate ...the relative and absolute risks of progression to cancer, the predictive accuracy of a clinician’s decision to biopsy a leukoplakia vis-à-vis progression, and histopathologic predictors of progression.
Methods
We conducted a retrospective cohort study (1996–2012) of patients with oral leukoplakia (n = 4886), identified using electronic medical records within Kaiser Permanente Northern California. Among patients with leukoplakia who received a biopsy (n = 1888), we conducted a case-cohort study to investigate histopathologic predictors of progression. Analyses included indirect standardization and unweighted or weighted Cox regression.
Results
Compared with the overall Kaiser Permanente Northern California population, oral cancer incidence was substantially elevated in oral leukoplakia patients (standardized incidence ratio = 40.8, 95% confidence interval CI = 34.8 to 47.6; n = 161 cancers over 22 582 person-years). Biopsied leukoplakias had a higher oral cancer risk compared with those that were not biopsied (adjusted hazard ratio = 2.38, 95% CI = 1.73 to 3.28). However, to identify a prevalent or incident oral cancer, the biopsy decision had low sensitivity (59.6%), low specificity (62.1%), and moderate positive–predictive value (5.1%). Risk of progression to oral cancer statistically significantly increased with the grade of dysplasia; 5-year competing risk-adjusted absolute risks were: leukoplakia overall = 3.3%, 95% CI = 2.7% to 3.9%; no dysplasia = 2.2%, 95% CI = 1.5% to 3.1%; mild-dysplasia = 11.9%, 95% CI = 7.1% to 18.1%; moderate-dysplasia = 8.7%, 95% CI = 3.2% to 17.9%; and severe dysplasia = 32.2%, 95% CI = 8.1%–60.0%. Yet 39.6% of cancers arose from biopsied leukoplakias without dysplasia.
Conclusions
The modest accuracy of the decision to biopsy a leukoplakia vis-à-vis presence or eventual development of oral cancer highlights the need for routine biopsy of all leukoplakias regardless of visual or clinical impression. Leukoplakia patients, particularly those with dysplasia, need to be closely monitored for signs of early cancer.
Hepatitis B virus (HBV) infection causes hepatocellular carcinoma (HCC). Associations with other cancers are not established. We systematically assessed associations between HBV infection and cancers ...in the US elderly population. We conducted a case–control study using the Surveillance, Epidemiology, and End Results (SEER)‐Medicare database in US adults aged ≥66 years. Cases (N = 1,825,316) were people with first cancers diagnosed in SEER registries (1993–2013). Controls (N = 200,000) were randomly selected, cancer‐free individuals who were frequency‐matched to cases on age, sex, race and calendar year. Associations with HBV infection (ascertained by Medicare claims) were assessed by logistic regression. HBV prevalence was higher in cases than controls (0.6% vs. 0.5%). HBV was positively associated with cancers of the stomach (adjusted odds ratio aOR = 1.19; 95% confidence intervals CI = 1.03–1.37), anus (1.66; 1.17–2.33), liver (10.6; 9.66–11.6), intrahepatic bile ducts (1.67; 1.18–2.37), nasopharynx (2.08; 1.33–3.25), as well as myelodysplastic syndrome (1.26; 1.07–1.49) and diffuse large B‐cell lymphoma (DLBCL) (1.24; 1.06–1.46). Inverse associations were observed with female breast (aOR = 0.86; 95%CI = 0.76–0.98) and prostate (0.81; 0.73–0.91) cancers and chronic lymphocytic leukemia (0.77; 0.62–0.96). Associations were maintained in sensitivity analyses conducted in people without claims for cirrhosis or hepatitis C or human immunodeficiency virus infections. HBV infection is associated with increased risk of cancers other than HCC, such as bile duct cancers and DLBCL. The biological mechanisms by which HBV may lead to these cancers need to be explored.
What's new?
Hepatitis B virus (HBV) infection is a known cause of hepatocellular carcinoma, but associations with other cancers remain unclear. The authors used the Surveillance, Epidemiology and End Results (SEER)‐linked Medicare database in the US to assess associations between HBV infection and cancers in the elderly. They found that HBV infection is also associated with other cancers, including of the biliary tract and diffuse large B cell lymphoma, findings that warrant further mechanistic studies.
Full text
Available for:
BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
OBJECTIVE:HIV-infected people have elevated risk for some cancers. Changing incidence of these cancers over time may reflect changes in three factorsHIV population demographic structure (e.g. age ...distribution), general population (background) cancer rates, and HIV-associated relative risks. We assessed the contributions of these factors to time trends for 10 cancers during 1996–2010.
DESIGN:Population-based registry linkage study.
METHODS:We applied Poisson models to data from the U.S. HIV/AIDS Cancer Match Study to estimate annual percentage changes (APCs) in incidence rates of AIDS-defining cancers ADCsKaposi sarcoma, non-Hodgkin lymphoma (NHL), and cervical cancer and seven non-AIDS-defining cancers (NADCs). We evaluated HIV-infected cancer trends with and without adjustment for demographics, trends in background rates, and trends in standardized incidence ratios (SIRs, to capture relative risk).
RESULTS:Cancer rates among HIV-infected people rose over time for anal (APC 3.8%), liver (8.5%), and prostate (9.8%) cancers, but declined for Kaposi sarcoma (1996–2000−29.3%; 2000–2010−7.8%), NHL (1996–2003−15.7%; 2003–2010−5.5%), cervical cancer (−11.1%), Hodgkin lymphoma (−4.0%), and lung cancer (−2.8%). Breast and colorectal cancer incidence did not change over time. Based on comparison to adjusted models, changing demographics contributed to trends for Kaposi sarcoma and breast, colorectal, liver, lung, and prostate cancers (all P < 0.01). Trends in background rates were notable for liver (APC 5.6%) and lung (−3.2%) cancers. SIRs declined for ADCs, Hodgkin lymphoma (APC −3.2%), and lung cancer (−4.4%).
CONCLUSION:Demographic shifts influenced several cancer trends among HIV-infected individuals. Falling relative risks largely explained ADC declines, while background incidence contributed to some NADC trends.
To investigate the impact of human papillomavirus (HPV) on the epidemiology of oral squamous cell carcinomas (OSCCs) in the United States, we assessed differences in patient characteristics, ...incidence, and survival between potentially HPV-related and HPV-unrelated OSCC sites.
Data from nine Surveillance, Epidemiology, and End Results program registries (1973 to 2004) were used to classify OSCCs by anatomic site as potentially HPV-related (n = 17,625) or HPV-unrelated (n = 28,144). Joinpoint regression and age-period-cohort models were used to assess incidence trends. Life-table analyses were used to compare 2-year overall survival for HPV-related and HPV-unrelated OSCCs.
HPV-related OSCCs were diagnosed at younger ages than HPV-unrelated OSCCs (mean ages at diagnosis, 61.0 and 63.8 years, respectively; P < .001). Incidence increased significantly for HPV-related OSCC from 1973 to 2004 (annual percentage change APC = 0.80; P < .001), particularly among white men and at younger ages. By contrast, incidence for HPV-unrelated OSCC was stable through 1982 (APC = 0.82; P = .186) and declined significantly during 1983 to 2004 (APC = -1.85; P < .001). When treated with radiation, improvements in 2-year survival across calendar periods were more pronounced for HPV-related OSCCs (absolute increase in survival from 1973 through 1982 to 1993 through 2004 for localized, regional, and distant stages = 9.9%, 23.1%, and 18.6%, respectively) than HPV-unrelated OSCCs (5.6%, 3.1%, and 9.9%, respectively). During 1993 to 2004, for all stages treated with radiation, patients with HPV-related OSCCs had significantly higher survival rates than those with HPV-unrelated OSCCs.
The proportion of OSCCs that are potentially HPV-related increased in the United States from 1973 to 2004, perhaps as a result of changing sexual behaviors. Recent improvements in survival with radiotherapy may be due in part to a shift in the etiology of OSCCs.
PDF
