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  • 1
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    A second update on mapping the human genetic architecture of COVID-19
    Springer Science and Business Media LLC ; 2023
    In:  Nature Vol. 621, No. 7977 ( 2023-09-07), p. E7-E26
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 621, No. 7977 ( 2023-09-07), p. E7-E26
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/s41586-023-06355-3
    RVK:
    TA 1000
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    UA 1000
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
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  • 2
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    Mapping the human genetic architecture of COVID-19
    Springer Science and Business Media LLC ; 2021
    In:  Nature Vol. 600, No. 7889 ( 2021-12-16), p. 472-477
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 600, No. 7889 ( 2021-12-16), p. 472-477
    Abstract: The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-19 1,2 , host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases 3–7 . They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease.
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/s41586-021-03767-x
    RVK:
    TA 1000
    RVK:
    UA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
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  • 3
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    Clinical Characteristics and Outcomes of COVID-19 in Pediatric and Early Adolescent and Young Adult Hematopoietic Stem Cell Transplant Recipients: A Cohort Study
    Elsevier BV ; 2022
    In:  Transplantation and Cellular Therapy Vol. 28, No. 10 ( 2022-10), p. 696.e1-696.e7
    Details
    In: Transplantation and Cellular Therapy, Elsevier BV, Vol. 28, No. 10 ( 2022-10), p. 696.e1-696.e7
    Type of Medium: Online Resource
    ISSN: 2666-6367
    URL: Article
    DOI: 10.1016/j.jtct.2022.06.026
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
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  • 4
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    Patterns of Cutaneous Malignancy Risk Among Survivors of Non-Hodgkin Lymphoma Subtypes
    American Society of Hematology ; 2016
    In:  Blood Vol. 128, No. 22 ( 2016-12-02), p. 4771-4771
    Details
    In: Blood, American Society of Hematology, Vol. 128, No. 22 ( 2016-12-02), p. 4771-4771
    Abstract: Introduction. Advances in treatment have improved prognosis after diagnosis with non-Hodgkin lymphoma (NHL) and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL). Understanding factors that impact long-term morbidity and mortality of lymphoma survivors is therefore of increasing clinical importance. Elevated risk for developing cutaneous melanoma after lymphoma is well-established, but the potential extension of this association for rarer NHL subtypes and other types of cutaneous malignancies is unknown. Methods. We identified a cohort of 129,850 non-HIV infected adults (age ³20 years) who were initially diagnosed with one of the seven most common types of lymphoma (Table 1) during 2000-2013 and who survived ³1 year, as reported to 17 United States population-based cancer registries from the Surveillance, Epidemiology, and End Results program. Standardized incidence ratios (SIRs) and corresponding 95% confidence intervals (95% CI) quantified risks for second primary melanoma, Merkel cell carcinoma, and sebaceous carcinoma, comparing the observed number of cases to that expected in the general population based on age-, race-, sex- and calendar period-specific incidence rates. Results. Melanoma occurred in 258 survivors of CLL/SLL, nearly two-fold more often than expected in the general population (SIR=1.94, 95% CI=1.71-2.20). Risk also was significantly elevated among survivors of follicular lymphoma (N=108, SIR=1.32, 95% CI=1.08-1.32) and peripheral T-cell lymphoma (N=22, SIR=1.68, 95% CI=1.05-2.54), whereas SIRs were non-significantly greater than unity after other NHL subtypes except marginal zone lymphoma (N=37, SIR=1.06, 95% CI=0.74-1.46). Merkel cell carcinoma and sebaceous carcinomas were much rarer but were associated with substantially higher risks compared with melanoma. Merkel cell carcinoma also occurred most commonly after CLL/SLL (N=20, SIR=3.90, 95%CI=2.38-6.02) with significantly elevated SIRs after follicular lymphoma (N=8, SIR=2.99, 95%CI=1.29-5.89) and mantle cell lymphoma (N=7, SIR=16.04, 95% CI=6.45-33.04). In contrast, the risk patterns differed for sebaceous carcinoma, with elevated risks after CLL/SLL (N=10, SIR=5.04, 95% CI=2.42-9.27), DLBCL (N=7, SIR=5.13, 95% CI=2.06-10.57), marginal zone lymphoma (N=4, SIR=7.67, 95% CI=2.09-19.63), and lymphoplasmacytic lymphoma/Waldenstršm macroglobulinemia (N=3, SIR=14.15, 95% CI=2.92-41.35). Conclusions. Survivors of specific lymphoma subtypes have differential risks of developing a range of subsequent cutaneous malignancies. CLL/SLL is the lymphoma subtype most closely associated with cutaneous malignancy risk, whereas DLBCL survivors only have strongly elevated risk for sebaceous carcinoma. Further studies should investigate potential roles for immune dysfunction, infection, and genetic susceptibility in the etiology of cutaneous malignancies developing after NHL. Survivors and clinicians should consider the importance of regular full skin examinations to maximize opportunities for early detection of cutaneous malignancies to reduce morbidity. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V128.22.4771.4771
    RVK:
    XA 33000
    RVK:
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2016
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  • 5
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    Risk of Second Primary Bone and Soft–Tissue Sarcomas Among Young Adulthood Cancer Survivors
    Oxford University Press (OUP) ; 2019
    In:  JNCI Cancer Spectrum Vol. 3, No. 3 ( 2019-09-01)
    Details
    In: JNCI Cancer Spectrum, Oxford University Press (OUP), Vol. 3, No. 3 ( 2019-09-01)
    Abstract: Excess sarcoma risks after childhood cancer are well established, but risks among young adulthood cancer survivors are poorly understood. Using US population-based cancer registry data, we compared bone and soft-tissue sarcoma risk vs the general population among 186 351 individuals who were diagnosed with nonsarcoma first primary malignancies at ages 20–39 years from 1975 to 2014 (follow-up through 2015) and survived at least 1 year. Bone sarcomas were rare (n = 50), but risk was statistically significantly elevated overall (2.9-fold) and greater than fivefold after Hodgkin lymphoma, non-Hodgkin lymphoma, and central nervous system tumors. Soft-tissue sarcomas were more common (n = 284) and risks were statistically significantly elevated approximately twofold overall and after melanoma and carcinomas of the breast, thyroid, and testis, and greater than fourfold after Hodgkin lymphoma and central nervous system tumors. Risks varied markedly by subtype, with the highest risks (greater than fourfold) for osteosarcoma and the soft-tissue subtypes of rhabdomyosarcoma and blood vessel and nerve sheath sarcomas. These data demonstrate elevated risk for sarcoma after a range of young adulthood cancers.
    Type of Medium: Online Resource
    ISSN: 2515-5091
    URL: Article
    DOI: 10.1093/jncics/pkz043
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
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  • 6
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    Abstract LB-236: Risk of tMDS/AML after chemotherapy for first primary lymphoid malignancy, 2000-2013
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. LB-236-LB-236
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. LB-236-LB-236
    Abstract: Previous studies have demonstrated elevated risks for tMDS/AML after chemotherapy for non-Hodgkin lymphoma, Hodgkin lymphoma, and plasma cell neoplasms, but current treatment practices have changed considerably. We utilized large-scale, population-based cancer registry data from the United States to quantify for the first time tMDS/AML risks after chemotherapy for lymphoid malignancies in the current treatment era, including analysis for specific non-Hodgkin lymphoma subtypes. In 17 registries, we identified 121,840 adults without HIV infection who survived ≥1 year following a first primary lymphoid malignancy diagnosis during 2000-2013 and were initially treated with chemotherapy. tMDS/AML risk was compared with that expected in the general population using SIRs. tMDS/AML risk was significantly increased 5- to 9-fold after chemotherapy for the most common lymphoid malignancies, including DLBCL, plasma cell neoplasms, follicular lymphoma, Hodgkin lymphoma, and CLL/SLL (Table 1). Approximately 5-fold increased risks were observed after chemotherapy for marginal zone lymphoma, LPL/WM, and other/unspecified lymphomas. In contrast, risks were strikingly elevated ( & gt;10-fold) after chemotherapy for precursor leukemia/lymphoma, Burkitt lymphoma/leukemia, peripheral T-cell lymphoma, and mantle cell lymphoma. Only chemotherapy for hairy cell leukemia was not associated with increased tMDS/AML risk (SIR=1.4), albeit based on small numbers. tMDS/AML risks were higher & lt;5 years after diagnosis compared with ≥5 years for Hodgkin lymphoma, precursor leukemia/lymphoma, Burkitt lymphoma/leukemia, and peripheral T-cell lymphoma. In contrast risks were persistently elevated ≥5 years after diagnosis for other lymphoid malignancies. In summary, tMDS/AML risk remains elevated in the modern era following chemotherapy for nearly all lymphoid malignancies. With ongoing introduction of new treatment approaches, continued consideration of risks and benefits of specific agents (and combinations), doses, and duration of therapy is critical. By time since lymphoid neoplasm diagnosisOverall1.0-4.9 years≥5 yearsFirst primary lymphoid malignancyTotal (N)Mean age at diagnosis (y)NSIR(95%CI)NSIR(95%CI)NSIR(95%CI)Hodgkin lymphoma16,74840.3659.0(6.9, 11.4)4310.7(7.8, 14.5)226.8(4.3, 10.3)CLL/SLL8,47864.31129.4(7.7, 11.3)729.2(7.2, 11.6)409.8(7.0, 13.3)DLBCL31,69259.72045.6(4.8, 6.4)1265.6(4.7, 6.7)785.5(4.4, 6.9)Follicular lymphoma15,65659.51457.8(6.6, 9.2)867.9(6.3, 9.8)597.7(5.8, 9.9)Marginal zone lymphoma4,22362.8295.5(3.7, 7.8)195.7(3.4, 8.9)105.1(2.4, 9.4)Plasma cell neoplasms22,75363.21176.1(5.0, 7.3)795.4(4.3, 6.8)388.2(5.8, 11.2)Precursor leukemia/lymphoma3,53042.73237.3(25.5, 52.7)2852.6(35.0, 76.1)412.3(3.3, 31.4)Mantle cell lymphoma3,52163.44010.1(7.3, 13.8)279.9(6.5, 14.4)1310.7(5.7, 18.3)LPL/WM1,95466.0134.3(2.3, 7.3)105.0(2.4, 9.2)32.8(0.6, 8.2)Peripheral T-cell lymphoma3,15655.73012.7(8.6, 18.1)2315.5(9.8, 23.2)78.0(3.2, 16.5)Burkitt lymphoma/leukemia1,18048.41924.3(14.6, 37.9)1328.6(15.2, 48.9)618.3(6.7, 39.8)Hairy cell leukemia1,70554.631.4(0.3, 4.2)~~Other, unspecified7,24462.0535.7(4.3, 7.4)386.6(4.7, 9.1)154.2(2.3, 6.9) Abbreviations: chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL); confidence interval (CI); diffuse large B-cell lymphoma (DLBCL); lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (LPL/WM); standardized incidence ratio (SIR); Surveillance, Epidemiology, and End Results (SEER); treatment-related myelodysplastic syndrome/acute myeloid leukemia (tMDS/AML). Citation Format: Lindsay M. Morton, Graca M. Dores, Megan M. Herr, Martha S. Linet, Margaret A. Tucker, Rochelle E. Curtis. Risk of tMDS/AML after chemotherapy for first primary lymphoid malignancy, 2000-2013 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-236. doi:10.1158/1538-7445.AM2017-LB-236
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-LB-236
    RVK:
    XA 36000
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    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 7
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    Redox Associated Gene Expression Predicts For Responses To The Pro-Oxidant Molecule Imexon In Relapsed and Refractory B-Cell Non-Hodgkin Lymphoma: Results Of a Multi-Center Phase II Study
    American Society of Hematology ; 2013
    In:  Blood Vol. 122, No. 21 ( 2013-11-15), p. 89-89
    Details
    In: Blood, American Society of Hematology, Vol. 122, No. 21 ( 2013-11-15), p. 89-89
    Abstract: Imexon is a 1-carboxamido-2-cyan-aziridine isomer investigated as an anti-cancer agent given its pro-oxidant properties. By binding reduced sulfhydryls leading to the accumulation of reactive oxygen species, imexon interferes with the endoplasmic reticulum and mitochondrial reduction-oxidation (redox) balance, inhibiting protein translation and cell growth and inducing apoptosis. Pre-clinical studies demonstrated activity across an array of tumor cells in vitro and increased activity amongst B-cell non-Hodgkin lymphomas (NHL). A partial response in a follicular lymphoma (FL) patient was observed in a previous phase I study. This phase II trial was initiated to further investigate the clinical activity of imexon in patients with relapsed or refractory NHL. Methods Histologically confirmed NHL, 〉 1 prior therapy, age≥18, ECOG performance status 0–2, measurable disease, signed informed consent, creatinine and bilirubin 〈 2.0 x IULN as well as G6PD 〉 IULN were required. Patients were treated with imexon 1000 mg/m2 IV daily on days 1-5 of a 21 day cycle for up to 1 year. Messenger RNA analysis was performed on pre-treatment tumor specimens, evaluating 22 genes important for antioxidant enzyme expression, 16 genes previously associated with outcome in NHL as well as 4 immune cell surface markers. Included were 13 genes used to generate a redox signature score, previously demonstrated to correlate with NHL prognosis (Tome, Blood 2005). Results Twenty-two NHL patients [9 FL, 5 diffuse large B cell (DLBCL), 3 mantle cell, 2 transformed follicular, 2 chronic lymphocytic leukemia and 1 Burkitt] with a median age of 64 (range 43-92) completed a median of 2.5 (range 1-13) cycles of therapy. With a median number of 4 prior therapies, 9 patients had undergone a prior stem cell transplant, 10 had stage IV disease and 6 were refractory to prior therapy. Twenty patients were evaluable for response, 2 pts discontinued therapy during cycle 1 due to progressive disease and grade 5 sepsis respectively. Of the 20 evaluable patients, the overall response rate was 30% (6/20) with another 35% achieving stable disease. Responses were observed in 4 FL and 2 DLBCL pts. After a median follow-up of 7 months, the median progression free survival (PFS) was 2.4 mos (range, 0.6 to 19.1 mos) with a median PFS of 6.7 mos (range, 1.2 to 9.0 mos) in FL patients. The median overall survival has not been reached. Grade 3 and 4 toxicities consisted of anemia (7 pts), thrombocytopenia (2 pts), neutropenia (2 pts), sepsis (2 pts), vomiting (2 pts), pneumonia (2 pts), fatigue (2 pts), dehydration (2 pts) as well as hypokalemia, hyperuricemia, transient ischemic attack, increased creatinine, rash and urinary tract infection in 1 pt each. 13 pts had available pre-treatment tumor biopsies, 2 of which attained a partial response with therapy. Patients with a higher redox score were more likely to achieve an objective response (p=0.03). Further, individual genes most predictive of response included CD68, GPX1 and SOD2. Conclusions This is the first trial to demonstrate that targeting the cellular redox environment is a viable therapeutic strategy in NHL and may be particularly effective in FL. The side effect profile may lend imexon to rational combination studies. Lymphomas reliant on antioxidant defense enzymes for proliferation and survival may be more susceptible to redox directed therapy. Evaluation of antioxidant related gene expression as a predictive biomarker is warranted in future investigations of imexon and similar targeted agents. (NCT01314014) Disclosures: Barr: Seattle Genetics: Consultancy; Celgene: Consultancy. Off Label Use: Imexon; being investigated for use in Non-Hodgkin lymphoma. Schwartz:HTG Molecular Diagnostics: Employment. Dorr:Amplimed Corporation: Employment.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V122.21.89.89
    RVK:
    XA 33000
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    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2013
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  • 8
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    Abstract 1894: Early adulthood sun exposure, vitamin D related gene variants, and risk of non-Hodgkin lymphoma
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1894-1894
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1894-1894
    Abstract: Background. Several recent studies have reported an inverse relationship between sun exposure and non-Hodgkin (NHL) risk. One hypothesis is that vitamin D mediates this effect. We evaluated the association of sun exposure at various ages and common variants in vitamin D related genes with risk of NHL and its major subtypes. Methods. Newly diagnosed NHL cases (N=1023) and frequency matched controls (N=1254) were enrolled in a clinic-based case-control study conducted at the Mayo Clinic. Thirty-eight single nucleotide polymorphisms (SNPs) from 5 candidate genes relevant to vitamin D metabolism and sun sensitivity (IRF4, RXR, VDR, CYP24A1, CYP27B1) were genotyped. Participants also completed a detailed questionnaire, including self-reported sun exposure at ages 13-21, 22-40, and 41+ years. Odds ratios (OR), 95% confidence intervals (CI), and tests for trend and effect modification were estimated using unconditional logistic regression adjusted for age and gender. ORs are reported for the highest vs. lowest exposure category or as the ordinal OR for SNPs. Results. The mean age of diagnosis/enrollment was 61 years for cases and 60 years for controls. The most common subtypes were chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; 34%), follicular (FL; 24%), and diffuse large B-cell (DLBCL; 18%) lymphomas. There was a significant decrease in NHL risk with increased sun exposure at ages 13-21 years (OR=0.66, 95% CI 0.44-1.00; ptrend=0.04), which attenuated with increasing age at exposure. Exploratory analysis by NHL subtype indicated a trend toward a protective effect of sun exposure at ages 13-21 years for each of the major subtypes, though these estimates did not reach statistical significance. Of the 38 SNPs evaluated, there was a significant association for 3 SNPs in VDR and 1 SNP in CYP24A1: rs3819545 (OR=1.24, 95% CI 1.10-1.40, p=0.0004), rs2239186 (OR=1.22, 95% CI 1.05-1.41, p=0.009), and rs886441 (OR=0.82, 95% CI 0.70-0.96, p=0.02) for VDR and rs2762939 (OR=0.85, 95% CI 0.75-0.98, p=0.02) for CYP24A1. Both the VDR and CYP24A1 associations were observed for CLL/SLL, FL, but were attenuated for DLBCL. There was no evidence of any significant effect modification of sun exposure at ages 13-21 years by genotype in these four SNPs for NHL overall, or for NHL subtypes. Conclusions. We observed an inverse association between the frequency of sun exposure at ages 13-21 years and NHL risk, which attenuated for sun exposure at older ages, suggesting that early life exposure may be more relevant. While genetic variation in VDR and CYP24A1 were associated with NHL risk, there was no evidence for an interaction of sun exposure with these genes, suggesting that a sun association may not act through the vitamin D metabolism pathway. This would be consistent with a lack of association of circulating vitamin D with NHL risk recently published from the Cohort Consortium pooling project. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1894. doi:10.1158/1538-7445.AM2011-1894
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-1894
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 9
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    Early life sun exposure, vitamin D-related gene variants, and risk of non-Hodgkin lymphoma
    Springer Science and Business Media LLC ; 2012
    In:  Cancer Causes & Control Vol. 23, No. 7 ( 2012-7), p. 1017-1029
    Details
    In: Cancer Causes & Control, Springer Science and Business Media LLC, Vol. 23, No. 7 ( 2012-7), p. 1017-1029
    Type of Medium: Online Resource
    ISSN: 0957-5243 , 1573-7225
    URL: Article
    DOI: 10.1007/s10552-012-9967-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2012
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  • 10
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    Risk for malignancies of infectious etiology among adult survivors of specific non-Hodgkin lymphoma subtypes
    American Society of Hematology ; 2019
    In:  Blood Advances Vol. 3, No. 13 ( 2019-07-09), p. 1961-1969
    Details
    In: Blood Advances, American Society of Hematology, Vol. 3, No. 13 ( 2019-07-09), p. 1961-1969
    Abstract: Infectious agents have been identified in the etiology of certain non-Hodgkin lymphoma (NHL) subtypes and solid tumors. The impact of this shared etiology on risk for second cancers in NHL survivors has not been comprehensively studied. We used US population–based cancer registry data to quantify risk of solid malignancies associated with infectious etiology among 127 044 adult 1-year survivors of the 4 most common NHL subtypes diagnosed during 2000 to 2014 (mean follow-up, 4.5-5.2 years). Compared with the general population, elevated risks for liver, stomach, and anal cancers were observed among diffuse large B-cell lymphoma (DLBCL) survivors (standardized incidence ratio [SIR], 1.85; 95% confidence interval [CI] , 1.46-2.31; SIR, 1.51; 95% CI, 1.16-1.94; SIR, 3.71; 95% CI, 2.52-5.27, respectively) and marginal zone lymphoma (MZL; SIR, 1.98; 95% CI, 1.34-2.83; SIR, 2.78; 95% CI, 2.02-3.74; SIR, 2.36; 95% CI, 1.02-4.64, respectively) but not follicular lymphoma or chronic lymphocytic leukemia/small lymphocytic lymphoma. Anal cancer risk was particularly elevated among DLBCL survivors with HIV (SIR, 68.34; 95% CI, 37.36-114.66) vs those without (SIR, 2.09; 95% CI, 1.22-3.34). The observed patterns are consistent with shared associations between these cancers and hepatitis C virus, Helicobacter pylori, and HIV, respectively. In contrast, risks for cervical and oropharyngeal/tonsil cancers were not elevated among survivors of any NHL subtype, possibly because of the lack of NHL association with human papillomavirus or population-wide screening practices (for cervical cancer). In summary, patterns of elevated second cancer risk differed by NHL subtype. Our results suggest shared infectious etiology has implications for subsequent cancer risks among DLBCL and MZL survivors, which may help inform surveillance for these survivors.
    Type of Medium: Online Resource
    ISSN: 2473-9529 , 2473-9537
    URL: Article
    DOI: 10.1182/bloodadvances.2019030924
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2019
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