Bruce Armstrong

Publications of Bruce Armstrong

• Optimizing the frequency of follow-up visits for patients treated for localized primary cutaneous melanoma.

  Authors: Robin M Turner, Katy J L Bell, Rachael L Morton, Andrew Hayen, Anne Brecht Francken, Kirsten Howard, Bruce Armstrong, John F Thompson, Les Irwig

  Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 11/2011; 29(35):4641-6.

  To develop more evidence-based guidelines for the frequency of patient follow-up after treatment of localized (American Joint Committee on Cancer [AJCC] stage I or II) melanoma. We used data fromTo develop more evidence-based guidelines for the frequency of patient follow-up after treatment of localized (American Joint Committee on Cancer [AJCC] stage I or II) melanoma. We used data from Melanoma Institute Australia on an inception cohort of 3,081 consecutive patients first diagnosed with stage I or II melanoma between January 1985 and December 2009. Kaplan-Meier curves and Cox models were used to characterize the time course and predictors for recurrence and new primaries. We modeled the delay in diagnosis of recurrence or new primary as well as the number of monitoring visits required using two monitoring schedules: first, according to 2008 Australian and New Zealand guidelines and, second, with fewer visits, especially for those at lowest risk of recurrence. For every 1,000 patients beginning follow-up, 229 developed recurrence and 61 developed new primary within 10 years. There was only a small difference in modeled delay in diagnosis (extra 44.9 and 9.6 patients per 1,000 for recurrence and new primary, respectively, with delay greater than 2 months) using a schedule that requires far fewer visits (3,000 fewer visits per 1,000 patients) than recommended by current guidelines. AJCC substage was the most important predictor of recurrence, whereas age and date of primary diagnosis were important predictors of developing new primary. By providing less intensive monitoring, more efficient follow-up strategies are possible. Fewer visits with a more focused approach may address the needs of patients and clinicians to detect recurrent or new melanoma.

• GWAS of follicular lymphoma reveals allelic heterogeneity at 6p21.32 and suggests shared genetic susceptibility with diffuse large B-cell lymphoma.

  Authors: Karin E Smedby, Jia Nee Foo, Christine F Skibola, Hatef Darabi, Lucia Conde, Henrik Hjalgrim, Vikrant Kumar, Ellen T Chang, Nathaniel Rothman, James R Cerhan [......] Stephen J Chanock, Leonid Padyukov, Lars Alfredsson, Lars Klareskog, Bengt Glimelius, Mads Melbye, Edison T Liu, Hans-Olov Adami, Keith Humphreys, Jianjun Liu

  PLoS genetics. 04/2011; 7(4):e1001378.

  Non-Hodgkin lymphoma (NHL) represents a diverse group of hematological malignancies, of which follicular lymphoma (FL) is a prevalent subtype. A previous genome-wide association study has establishedNon-Hodgkin lymphoma (NHL) represents a diverse group of hematological malignancies, of which follicular lymphoma (FL) is a prevalent subtype. A previous genome-wide association study has established a marker, rs10484561 in the human leukocyte antigen (HLA) class II region on 6p21.32 associated with increased FL risk. Here, in a three-stage genome-wide association study, starting with a genome-wide scan of 379 FL cases and 791 controls followed by validation in 1,049 cases and 5,790 controls, we identified a second independent FL-associated locus on 6p21.32, rs2647012 (OR(combined)  = 0.64, P(combined)  = 2 × 10(-21)) located 962 bp away from rs10484561 (r(2)<0.1 in controls). After mutual adjustment, the associations at the two SNPs remained genome-wide significant (rs2647012:OR(adjusted)  = 0.70, P(adjusted)  =  4 × 10(-12); rs10484561:OR(adjusted)  = 1.64, P(adjusted)  = 5 × 10(-15)). Haplotype and coalescence analyses indicated that rs2647012 arose on an evolutionarily distinct haplotype from that of rs10484561 and tags a novel allele with an opposite (protective) effect on FL risk. Moreover, in a follow-up analysis of the top 6 FL-associated SNPs in 4,449 cases of other NHL subtypes, rs10484561 was associated with risk of diffuse large B-cell lymphoma (OR(combined)  = 1.36, P(combined)  =  1.4 × 10(-7)). Our results reveal the presence of allelic heterogeneity within the HLA class II region influencing FL susceptibility and indicate a possible shared genetic etiology with diffuse large B-cell lymphoma. These findings suggest that the HLA class II region plays a complex yet important role in NHL.

• Genetic variation in Th1/Th2 pathway genes and risk of non-Hodgkin lymphoma: a pooled analysis of three population-based case-control studies.

  Authors: Qing Lan, Sophia S Wang, Idan Menashe, Bruce Armstrong, Yawei Zhang, Patricia Hartge, Mark P Purdue, Theodore R Holford, Lindsay M Morton, Anne Kricker [......] Meredith Yeager, Claire M Vajdic, Maryjean Schenk, Brian Leaderer, Jeff Yuenger, Richard K Severson, Nilanjan Chatterjee, Stephen J Chanock, Tongzhang Zheng, Nathaniel Rothman

  British journal of haematology. 03/2011; 153(3):341-50.

  The balance between T-helper 1 (Th1) and T-helper 2 (Th2) activity is critical in lymphoid cell development and differentiation. Immune dysfunction underlies lymphomagenesis, so an alteration in theThe balance between T-helper 1 (Th1) and T-helper 2 (Th2) activity is critical in lymphoid cell development and differentiation. Immune dysfunction underlies lymphomagenesis, so an alteration in the regulation of key Th1/Th2 cytokines may lead to the development of non-Hodgkin lymphoma (NHL). To study the impact of polymorphisms in Th1/Th2 cytokines on NHL risk, we analyzed 145 tag single nucleotide polymorphisms (SNPs) in 17 Th1/Th2 cytokine and related genes in three population-based case-control studies (1946 cases and 1808 controls). Logistic regression was used to compute odds ratios (OR) for NHL and four major NHL subtypes in relation to tag SNP genotypes and haplotypes. A gene-based analysis adjusting for the number of tag SNPs genotyped in each gene showed significant associations with risk of NHL combined and one or more NHL subtypes for Th1 (IL12A and IL12RB1) and Th2 (IL4, IL10RB, and IL18) genes. The strongest association was for rs485497 in IL12A, which plays a central role in bridging the cellular and humoral pathways of innate resistance and antigen-specific adaptive immune responses (allele risk OR= 1·17; P(trend)= 0·00099). This SNP was also associated specifically with risk of follicular lymphoma (allele risk OR= 1·26; P(trend)= 0·0012). These findings suggest that genetic variation in Th1/Th2 cytokine genes may contribute to lymphomagenesis.

• A pooled analysis of three studies evaluating genetic variation in innate immunity genes and non-Hodgkin lymphoma risk.

  Authors: H Dean Hosgood, Mark P Purdue, Sophia S Wang, Tongzhang Zheng, Lindsay M Morton, Qing Lan, Idan Menashe, Yawei Zhang, James R Cerhan, Andrew Grulich [......] Scott Davis, Brian Leaderer, Anne Kricker, Maryjean Schenk, Shelia H Zahm, Nilanjan Chatterjee, Stephen J Chanock, Nathaniel Rothman, Patricia Hartge, Bruce Armstrong

  British journal of haematology. 01/2011; 152(6):721-6.

  Genetic variation in immune-related genes may play a role in the development of non-Hodgkin lymphoma (NHL). To test the hypothesis that innate immunity polymorphisms may be associated with NHL risk,Genetic variation in immune-related genes may play a role in the development of non-Hodgkin lymphoma (NHL). To test the hypothesis that innate immunity polymorphisms may be associated with NHL risk, we genotyped 144 tag single nucleotide polymorphisms (tagSNPs) capturing common genetic variation within 12 innate immunity gene regions in three independent population-based case-control studies (1946 cases and 1808 controls). Gene-based analyses found IL1RN to be associated with NHL risk (minP = 0·03); specifically, IL1RN rs2637988 was associated with an increased risk of NHL (per-allele odds ratio = 1·15, 95% confidence interval = 1·05-1·27; P(trend) = 0·003), which was consistent across study, subtype, and gender. FCGR2A was also associated with a decreased risk of the follicular lymphoma NHL subtype (minP = 0·03). Our findings suggest that genetic variation in IL1RN and FCGR2A may play a role in lymphomagenesis. Given that conflicting results have been reported regarding the association between IL1RN SNPs and NHL risk, a larger number of innate immunity genes with sufficient genomic coverage should be evaluated systematically across many studies.

• Polymorphisms in DNA repair genes and risk of non-Hodgkin lymphoma in a pooled analysis of three studies.

  Authors: Min Shen, Idan Menashe, Lindsay M Morton, Yawei Zhang, Bruce Armstrong, Sophia S Wang, Qing Lan, Patricia Hartge, Mark P Purdue, James R Cerhan [......] Claire M Vajdic, Scott Davis, Brian Leaderer, Anne Kricker, Richard K Severson, Shelia H Zahm, Nilanjan Chatterjee, Nathaniel Rothman, Stephen J Chanock, Tongzhang Zheng

  British journal of haematology. 11/2010; 151(3):239-44.

  Genetic variations in DNA repair genes are thought to play an important role in the pathogenesis and development of non-Hodgkin lymphoma (NHL). To further explore this hypothesis, we genotyped 319Genetic variations in DNA repair genes are thought to play an important role in the pathogenesis and development of non-Hodgkin lymphoma (NHL). To further explore this hypothesis, we genotyped 319 tag single nucleotide polymorphisms (SNPs) in 27 DNA repair gene regions in 1946 cases and 1808 controls pooled from three population-based case-control studies of NHL in the US and Australia. Relative risks of NHL and NHL subtypes in relation to SNP genotypes were assessed using logistic regression. Associations of gene regions and pathways with NHL or NHL subtypes were explored using the minP and tail-strength statistics, respectively. Overall, genetic polymorphisms within the DNA repair pathway were associated with NHL (P = 0·005). Similar associations were seen with the double-strand break repair (P = 0·02) and nucleotide excision repair (P = 0·04) pathways. Five SNPs (BLM rs441399, RAD50 rs2237060, FAM82A2 rs2304583, ERCC3 rs4150506, and XRCC4 rs13178127) were particularly noteworthy because their gene regions were significantly associated with NHL or NHL subtypes (minP ≤ 0·05), or because of high level of statistical significance (P ≤ 0·005) and consistent findings across the three studies. These results support the hypothesis that common genetic polymorphisms in human DNA repair genes may modify the risk of NHL.

• Genome-wide association study of follicular lymphoma identifies a risk locus at 6p21.32.

  Authors: Lucia Conde, Eran Halperin, Nicholas K Akers, Kevin M Brown, Karin E Smedby, Nathaniel Rothman, Alexandra Nieters, Susan L Slager, Angela Brooks-Wilson, Luz Agana [......] Laura Z Rassenti, Logan G Spector, Sara S Strom, Celine M Vachon, J Brice Weinberg, Elizabeth A Holly, Stephen Chanock, Martyn T Smith, Paige M Bracci, Christine F Skibola

  Nature genetics. 08/2010; 42(8):661-4.

  To identify susceptibility loci for non-Hodgkin lymphoma subtypes, we conducted a three-stage genome-wide association study. We identified two variants associated with follicular lymphoma at 6p21.32To identify susceptibility loci for non-Hodgkin lymphoma subtypes, we conducted a three-stage genome-wide association study. We identified two variants associated with follicular lymphoma at 6p21.32 (rs10484561, combined P = 1.12 x 10(-29) and rs7755224, combined P = 2.00 x 10(-19); r(2) = 1.0), supporting the idea that major histocompatibility complex genetic variation influences follicular lymphoma susceptibility. We also found confirmatory evidence of a previously reported association between chronic lymphocytic leukemia/small lymphocytic lymphoma and rs735665 (combined P = 4.24 x 10(-9)).

• Relationships between epidermal growth factor receptor expression and human papillomavirus status as markers of prognosis in oropharyngeal cancer.

  Authors: Angela Hong, Timothy Dobbins, C Soon Lee, Deanna Jones, Elise Jackson, Jonathan Clark, Bruce Armstrong, Gerald Harnett, Christopher Milross, Christopher O'Brien, Barbara Rose

  European journal of cancer (Oxford, England : 1990). 07/2010; 46(11):2088-96.

  This study examines the prognostic significance of epidermal growth factor receptor (EGFR) expression in relation to human papillomavirus (HPV) status in oropharyngeal squamous cell carcinomaThis study examines the prognostic significance of epidermal growth factor receptor (EGFR) expression in relation to human papillomavirus (HPV) status in oropharyngeal squamous cell carcinoma (SCC). Pathological diagnosis of 270 oropharyngeal SCCs was verified by the study pathologist; clinical details were extracted from institutional databases. Recurrence in any form or death from any cause was recorded for a median of 2.5 (range: 0-19.3) years after diagnosis. HPV status was determined by HPV E6-targeted multiplex real-time PCR/p16 immunohistochemistry; EGFR expression was evaluated by semiquantitative immunohistochemistry. Determinants of recurrence and mortality hazards were modelled using Cox regression with censoring at dates of last follow-up. Thirty-seven percent of cancers were HPV-positive (91% type 16). HPV was a predictor of loco-regional recurrence, event-free and overall survival after adjustment for clinicopathological variables and EGFR. Patients with EGFR-positive cancers were 5-fold more likely to have loco-regional failure relative to those with EGFR-negative cancers. Patients with HPV-negative/EGFR-positive cancers had an adjusted 13-fold increased risk of having a loco-regional failure, an almost 4-fold increased risk of having an event and more than a 4-fold increased risk of dying of any cause relative to those with HPV-positive/EGFR-negative cancers. There was weak evidence that the effects of EGFR on outcome were limited to patients with HPV-negative cancers. HPV and EGFR are independent prognostic markers in oropharyngeal SCC. Combining testing for HPV and EGFR appears to provide additional prognostic information.

• Tumor necrosis factor (TNF) and lymphotoxin-alpha (LTA) polymorphisms and risk of non-Hodgkin lymphoma in the InterLymph Consortium.

  Authors: Christine F Skibola, Paige M Bracci, Alexandra Nieters, Angela Brooks-Wilson, Silvia de Sanjosé, Ann Maree Hughes, James R Cerhan, Danica R Skibola, Mark Purdue, Eleanor Kane [......] Alex Smith, Renee Shiao, Anne J Novak, Marc Maynadie, Stephen J Chanock, Anthony Staines, Theodore R Holford, Elizabeth A Holly, Nathaniel Rothman, Sophia S Wang

  American journal of epidemiology. 02/2010; 171(3):267-76.

  In an International Lymphoma Epidemiology Consortium pooled analysis, polymorphisms in 2 immune-system-related genes, tumor necrosis factor (TNF) and interleukin-10 (IL10), were associated withIn an International Lymphoma Epidemiology Consortium pooled analysis, polymorphisms in 2 immune-system-related genes, tumor necrosis factor (TNF) and interleukin-10 (IL10), were associated with non-Hodgkin lymphoma (NHL) risk. Here, 8,847 participants were added to previous data (patients diagnosed from 1989 to 2005 in 14 case-control studies; 7,999 cases, 8,452 controls) for testing of polymorphisms in the TNF -308G>A (rs1800629), lymphotoxin-alpha (LTA) 252A>G (rs909253), IL10 -3575T>A (rs1800890, rs1800896), and nucleotide-binding oligomerization domain containing 2 (NOD2) 3020insC (rs2066847) genes. Odds ratios were estimated for non-Hispanic whites and several ethnic subgroups using 2-sided tests. Consistent with previous findings, odds ratios were increased for "new" participant TNF -308A carriers (NHL: per-allele odds ratio (OR(allelic)) = 1.10, P(trend) = 0.001; diffuse large B-cell lymphoma (DLBCL): OR(allelic) = 1.23, P(trend) = 0.004). In the combined population, odds ratios were increased for TNF -308A carriers (NHL: OR(allelic) = 1.13, P(trend) = 0.0001; DLBCL: OR(allelic) = 1.25, P(trend) = 3.7 x 10(-6); marginal zone lymphoma: OR(allelic) = 1.35, P(trend) = 0.004) and LTA 252G carriers (DLBCL: OR(allelic) = 1.12, P(trend) = 0.006; mycosis fungoides: OR(allelic) = 1.44, P(trend) = 0.015). The LTA 252A>G/TNF -308G>A haplotype containing the LTA/TNF variant alleles was strongly associated with DLBCL (P = 2.9 x 10(-8)). Results suggested associations between IL10 -3575T>A and DLBCL (P(trend) = 0.02) and IL10 -1082A>G and mantle cell lymphoma (P(trend) = 0.04). These findings strengthen previous results for DLBCL and the LTA 252A>G/TNF -308A locus and provide robust evidence that these TNF/LTA gene variants, or others in linkage disequilibrium, are involved in NHL etiology.

• Estimates of overdiagnosis of invasive breast cancer associated with screening mammography.

  Authors: Stephen Morrell, Alexandra Barratt, Les Irwig, Kirsten Howard, Corné Biesheuvel, Bruce Armstrong

  Cancer causes & control : CCC. 11/2009;

  PURPOSE: To estimate the extent of overdiagnosis of invasive breast cancer associated with screening in New South Wales, Australia, a population with a well-established mammography screening programPURPOSE: To estimate the extent of overdiagnosis of invasive breast cancer associated with screening in New South Wales, Australia, a population with a well-established mammography screening program which has achieved full geographic coverage. METHODS: We calculated overdiagnosis as the observed annual incidence of invasive breast cancer in NSW in 1999-2001 (a screened population) minus the expected annual incidence in this population at the same time, as a percentage of the expected incidence. We estimated expected incidence without screening in 1999-2001 from the incidence of invasive breast cancer in: (1) women in unscreened age groups (interpolation method); and (2) women in all age groups prior to the implementation of screening (extrapolation method). We then adjusted these estimates for trends in major risk factors for breast cancer that may have coincided with the introduction of mammography screening: increasing obesity, use of hormone replacement therapy (HRT) and nulliparity. Finally, we adjusted for lead time to produce estimates of expected incidence in 1999-2001. These were compared with the observed incidence in 1999-2001 to calculate overdiagnosis of breast cancer associated with screening. RESULTS: Overdiagnosis of invasive breast cancer among 50-69 year NSW women was estimated to be 42 and 30% using the interpolation and extrapolation methods, respectively. CONCLUSION: Overdiagnosis of invasive breast cancer attributable to mammography screening appears to be substantial. Our estimates are similar to recent estimates from other screening programmes. Overdiagnosis merits greater attention in research and in clinical and public health policy making.

• Non-Hodgkin lymphoma and occupational radiation exposure assessed using local data.

  Authors: Ken K Karipidis, Geza Benke, Malcolm R Sim, Lin Fritschi, Claire Vajdic, Anne Kricker, Bruce Armstrong

  Occupational medicine (Oxford, England). 08/2009;

  BACKGROUND: Our previous investigation of occupational exposure to ionizing radiation using a Finnish job-exposure matrix (JEM) showed no association with non-Hodgkin lymphoma (NHL) in aBACKGROUND: Our previous investigation of occupational exposure to ionizing radiation using a Finnish job-exposure matrix (JEM) showed no association with non-Hodgkin lymphoma (NHL) in a population-based case-control study in Australia. AIMS: To determine whether occupational exposure to ionizing radiation assessed using an Australian JEM is associated with NHL. METHODS: We analysed 694 NHL cases, first diagnosed between 1 January 2000 and 31 August 2001 and 694 controls from south-eastern Australia, matched by age, sex and region of residence. A detailed occupational history was obtained using a lifetime calendar and a telephone interview. Exposure to radiation was assessed using the ionizing radiation component of an Australian JEM. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated from logistic regression models that included the matching variables as covariates. RESULTS: The OR for workers ever exposed to ionizing radiation was 0.86 (95% CI = 0.52-1.40). Dividing the subjects into tertiles of exposure also found ORs that were close to or below the null for each exposure group. CONCLUSIONS: The application of an Australian JEM did not provide evidence for an association between NHL and occupational exposure to ionizing radiation and is consistent with previous analyses.

• Genetic variation in caspase genes and risk of non-Hodgkin lymphoma: a pooled analysis of three population-based case-control studies.

  Authors: Qing Lan, Lindsay M Morton, Bruce Armstrong, Patricia Hartge, Idan Menashe, Tongzhang Zheng, Mark P Purdue, James R Cerhan, Yawei Zhang, Andrew Grulich [......] Claire M Vajdic, Scott Davis, Brian Leaderer, Anne Kricker, Maryjean Schenk, Shelia H Zahm, Nilanjan Chatterjee, Stephen J Chanock, Nathaniel Rothman, Sophia S Wang

  Blood. 06/2009;

  Caspases play a critical role in regulation of apoptosis, cell differentiation, inflammation, and innate immunity, and several are mutated or have altered expression in non-Hodgkin lymphoma (NHL). ToCaspases play a critical role in regulation of apoptosis, cell differentiation, inflammation, and innate immunity, and several are mutated or have altered expression in non-Hodgkin lymphoma (NHL). To study the impact of genetic variation in caspases on NHL risk, we analyzed tag single nucleotide polymorphisms (SNPs) in 12 caspase and related genes in three population-based case-control studies (1,946 cases and 1,808 controls). Gene-based analysis, adjusting for the number of tag SNPs genotyped in each gene, showed significant associations for CASP8, CASP9, and CASP1. SNP-based analysis showed that CASP8 rs6736233 (odds ratio (OR)CG=1.21; ORCC=2.13; p-trend=0.011); CASP9 rs4661636 (ORCT=0.89; ORTT=0.77; p-trend=0.014); and CASP1 rs1785882 (ORAT=1.12; ORAA=1.30; p-trend=0.0054) were significantly associated with NHL risk and consistent across studies. It is noteworthy that genetic variants in CASP8 were associated with risk of all major NHL subtypes. Our findings suggest that genetic variation in caspases may play an important role in lymphomagenesis.

• Risk of Non-Hodgkin Lymphoma Associated with Germline Variation in Genes that Regulate the Cell Cycle, Apoptosis, and Lymphocyte Development.

  Authors: Lindsay M Morton, Mark P Purdue, Tongzhang Zheng, Sophia S Wang, Bruce Armstrong, Yawei Zhang, Idan Menashe, Nilanjan Chatterjee, Scott Davis, Qing Lan [......] Anne Kricker, James R Cerhan, Brian Leaderer, Andrew Grulich, Meredith Yeager, Wendy Cozen, Shelia Hoar Zahm, Stephen J Chanock, Nathaniel Rothman, Patricia Hartge

  Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 05/2009; 18(4):1259-70.

  Chromosomal translocations are the hallmark genetic aberration in non-Hodgkin lymphoma (NHL), with specific translocations often selectively associated with specific NHL subtypes. Because manyChromosomal translocations are the hallmark genetic aberration in non-Hodgkin lymphoma (NHL), with specific translocations often selectively associated with specific NHL subtypes. Because many NHL-associated translocations involve cell cycle, apoptosis, and lymphocyte development regulatory genes, we evaluated NHL risk associated with common genetic variation in 20 candidate genes in these pathways. Genotyping of 203 tag single nucleotide polymorphisms (SNP) was conducted in 1,946 NHL cases and 1,808 controls pooled from 3 independent population-based case-control studies. We used logistic regression to compute odds ratios (OR) and 95% confidence intervals (CI) for NHL and four major NHL subtypes in relation to tag SNP genotypes and haplotypes. We observed the most striking associations for tag SNPs in the proapoptotic gene BCL2L11 (BIM) and BCL7A, which is involved in a rare NHL-associated translocation. Variants in BCL2L11 were strongly related to follicular lymphoma only, particularly rs3789068 (OR(AG), 1.41; 95% CI, 1.10-1.81; OR(GG), 1.65; 95% CI, 1.25-2.19; P(trend) = 0.0004). Variants in BCL7A were strongly related to diffuse large B-cell lymphoma only, particularly rs1880030 (OR(AG), 1.34; 95% CI, 1.08-1.68; OR(AA), 1.60; 95% CI, 1.22-2.08; P(trend) = 0.0004). The associations for both variants were similar in all three studies and supported by haplotype analyses. We also observed notable associations for variants in BCL6, CCND1, and MYC. Our results support the role of common genetic variation in cell cycle, apoptosis, and lymphocyte development regulatory genes in lymphomagenesis, and suggest that effects may vary by NHL subtype. Replication of our findings and further study to identify functional SNPs are warranted. (Cancer Epidemiol Biomarkers Prev 2009;18(4):1259-70).

• Effects of life event stress and social support on the odds of a >/=2 cm breast cancer.

  Authors: Anne Kricker, Melanie Price, Phyllis Butow, Chris Goumas, Jane Armes, Bruce Armstrong

  Cancer causes & control : CCC. 11/2008;

  OBJECTIVE: To examine the contribution of life event and social support factors to diagnosis with a >/=2 cm breast cancer. METHODS: We studied 1,459 Australian women aged 40-69 diagnosed in 2002-2003OBJECTIVE: To examine the contribution of life event and social support factors to diagnosis with a >/=2 cm breast cancer. METHODS: We studied 1,459 Australian women aged 40-69 diagnosed in 2002-2003 with a first primary invasive breast cancer 1.1 cm or larger. We measured stressful life events, perceived stress levels, and social support in the year before diagnosis and collected information on other potential risk factors and confounders. RESULTS: The odds of a >/=2 cm breast cancer relative to a 1.1-1.9 cm breast cancer were reduced in women who reported tension or change in an intimate relationship in the year before diagnosis (OR = 0.71 95% CI 0.54-0.92; p = 0.009); the reduction was greatest in women living with a partner (OR = 0.64 95% CI 0.47-0.88; p = 0.006) and was largely unaffected by adjustment for other variables independently associated with a >/=2 cm breast cancer in our study. There was no evidence that the total number or severity of all studied life events influenced cancer size. Low partner support increased the odds of a >/=2 cm cancer but only in women not living with a partner. CONCLUSION: Intimate relationship stress may reduce risk of a >/=2 cm breast cancer. Suppression by stress of estrogen synthesis and metabolism is a possible mechanism.

• Occupational exposure to ionizing and non-ionizing radiation and risk of non-Hodgkin lymphoma.

  Authors: Ken K Karipidis, Geza Benke, Malcolm R Sim, Timo Kauppinen, Anne Kricker, Ann Maree Hughes, Andrew E Grulich, Claire M Vajdic, John Kaldor, Bruce Armstrong, Lin Fritschi

  International archives of occupational and environmental health. 09/2007; 80(8):663-70.

  OBJECTIVE: To investigate the association between occupational exposure to ionizing, ultraviolet (UV), radiofrequency (RF) and extremely low frequency (ELF) radiation and risk of developingOBJECTIVE: To investigate the association between occupational exposure to ionizing, ultraviolet (UV), radiofrequency (RF) and extremely low frequency (ELF) radiation and risk of developing non-Hodgkin lymphoma (NHL) in a population-based case-control study. METHODS: The study population consisted of 694 NHL cases, first diagnosed between 1 January 2000 and 31 August 2001, and 694 controls from two regions in Australia, matched by age, sex and region of residence. A detailed occupation history was first obtained using a lifetime calendar and a telephone interview. Exposure to radiation was then assessed using a Finnish job-exposure matrix (FINJEM). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated from logistic regression models that included the matching variables as covariates. RESULTS: For ionizing radiation, the ORs were close to unity. For UV and ELF radiation, the highest exposed group of workers had ORs of 1.32 (95% CI=0.96-1.81) and 1.25 (95% CI=0.91-1.72), respectively. For UV radiation there was a positive dose-response when exposure was lagged by 5 and 10 years (P for trend 0.04 for both lag periods). Workers in the upper tertile of exposure for RF radiation had an OR of 3.15 (95% CI=0.63-15.87), but the estimate was based on very small numbers. CONCLUSIONS: Our results do not provide support for an association between NHL and occupational exposure to ionizing or ELF radiation. For UV radiation, our findings are consistent with a weak positive association. Further investigation focusing on UV and RF radiation and NHL is required.

• Consortia in cancer epidemiology: lessons from InterLymph.

  Authors: Paolo Boffetta, Bruce Armstrong, Martha Linet, Carol Kasten, Wendy Cozen, Patricia Hartge

  Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 03/2007; 16(2):197-9.

• Does sunlight have a beneficial influence on certain cancers?

  Authors: Anne Kricker, Bruce Armstrong

  Progress in biophysics and molecular biology. 10/2006; 92(1):132-9.

  Apperly [1941. The relation of solar radiation to cancer mortality in North America. Cancer Research 1, 191-195] first proposed that increased mortality from cancer in the north than in the south ofApperly [1941. The relation of solar radiation to cancer mortality in North America. Cancer Research 1, 191-195] first proposed that increased mortality from cancer in the north than in the south of the USA might be due to the south to north decrease in ambient solar radiation. This inverse association between ambient solar radiation and cancer mortality has been subsequently reported for cancers of the colon, breast, ovary and prostate. While the evidence that sunlight might be related to lower incidence or more favourable outcomes from cancer came initially from ecological studies, case-control and cohort studies have now shown a similar association of sun exposure with risks of colon, breast and prostate cancers in individuals, and other studies in individuals have found that serum and dietary vitamin D levels are associated with reduced risks of colorectal cancer and, less certainly, prostate cancer. Studies in individuals have recently also suggested an effect of sun exposure to reduce risk of non-Hodgkin lymphoma and to increase survival after a diagnosis of melanoma. Data on variation in survival from cancer by season of diagnosis suggest that sun exposure may also improve outcome from cancers of the breast, colon and prostate and Hodgkin lymphoma.

• Men?s preferences for treatment of early stage prostate cancer: Results from a discrete choice experiment, CHERE Working Paper 2006/14

  Authors: Madeleine King, Rosalie Viney, Ishrat Hossain, David Smith, Sandra Fowler, Elizabeth Savage, Bruce Armstrong

  08/2006;

  Prostate cancer is the most common cancer in men in Australia; each year over 10,000 Australians are diagnosed with this disease. There are a number of treatment options for early stage prostateProstate cancer is the most common cancer in men in Australia; each year over 10,000 Australians are diagnosed with this disease. There are a number of treatment options for early stage prostate cancer (ESPC); radical prostatectomy, external beam radiotherapy, brachytherapy, hormonal therapy and combined therapy. Treatment can cause serious side-effects, including severe sexual and urinary dysfunction, bowel symptoms and fatigue. Furthermore, there is no evidence as yet to demonstrate that any of these treatments confers a survival gain over active surveillance (watchful waiting). While patient preferences should be important determinants in the type of treatment offered, little is known about patients? views of the relative tolerability of side effects and of the survival gains needed to justify these. To investigate this, a discrete choice experiment (DCE) was conducted in a sample of 357 men who had been treated for ESPC and 65 age-matched controls. The sample was stratified by treatment, with approximately equal numbers in each treatment group. The DCE included nine attributes: seven side-effects and two survival attributes (duration and uncertainty). An orthogonal fractional set of 108 scenarios from the full factorial was used to generate three versions of the questionnaire, with 18 scenarios per respondent. Multinomial logit (MNL) and mixed logit (MXL) models were estimated. A random intercept MXL model provided a significantly better fit to the data than the simple MNL model, and adding random coefficients for all attributes dramatically improved model fit. Each side-effect had a statistically significant mean effect on choice, as did survival duration. Most attributes had significant variance parameters, suggesting considerable heterogeneity among respondents in their preferences. To model this heterogeneity, we included men?s health-related quality of life scores following treatment as covariates to see whether their preferences were influenced by their previous treatment experience. This study demonstrate how DCEs can be used to quantify the trade-offs patients make between side-effects and survival gains. The results provide useful insights for clinicians who manage patients with ESPC, highlighting the importance of patient preferences in treatment decisions.

• Evaluating new screening tests for breast cancer.

  Authors: Les Irwig, Nehmat Houssami, Bruce Armstrong, Paul Glasziou

  BMJ (Clinical research ed.). 04/2006; 332(7543):678-9.

• Polymorphisms in nucleotide excision repair genes and risk of multiple primary melanoma: the Genes Environment and Melanoma Study.

  Authors: Robert C Millikan, Amanda Hummer, Colin Begg, Jon Player, Allan René de Cotret, Scott Winkel, Harvey Mohrenweiser, Nancy Thomas, Bruce Armstrong, Anne Kricker [......] Stephen B Gruber, Hoda Anton-Culver, Roberto Zanetti, Richard P Gallagher, Terence Dwyer, Timothy R Rebbeck, Klaus Busam, Lynn From, Urvi Mujumdar, Marianne Berwick

  Carcinogenesis. 04/2006; 27(3):610-8.

  Polymorphisms in six genes involved in nucleotide excision repair of DNA were examined in a large population-based case-control study of melanoma. Genotyping was conducted for 2485 patients with aPolymorphisms in six genes involved in nucleotide excision repair of DNA were examined in a large population-based case-control study of melanoma. Genotyping was conducted for 2485 patients with a single primary melanoma (controls) and 1238 patients with second or higher order primary melanomas (cases). Patients were ascertained from nine geographic regions in Australia, Canada, Italy and the United States. Positive associations were observed for XPD 312 Asn/Asn versus Asp/Asp [odds ratio (OR) = 1.5, 95% confidence interval (CI) 1.2-1.9] and XPD 751 Gln/Gln versus Lys/Lys (OR = 1.4, 95% CI 1.1-1.7) genotypes and melanoma. The combined XPD Asn (A) 312 + Gln (C) 751 haplotype was significantly more frequent in cases (32%) compared with controls (29%) (P = 0.003) and risk of melanoma increased significantly with one and two copies of the haplotype (ORs 1.2, 95% CI 1.0-1.4, and 1.6, 95% CI 1.2-2.0, trend P = 0.002). No significant associations were observed for HR23B codon 249, XPG codon 1104, XPC codon 939, XPF codon 415, XPF nt 2063, ERCC6 codon 1213 or ERCC6 codon 1230. ORs for XPD and XPC genotypes were stronger for melanoma diagnosed at an early age, but tests for interaction were not statistically significant. The results provide further evidence for a role of XPD in the etiology of melanoma.

• Genetic variation in TNF and IL10 and risk of non-Hodgkin lymphoma: a report from the InterLymph Consortium.

  Authors: Nathaniel Rothman, Christine F Skibola, Sophia S Wang, Gareth Morgan, Qing Lan, Martyn T Smith, John J Spinelli, Eleanor Willett, Silvia de Sanjose, Pierluigi Cocco [......] Agnes Lai, Charlotte Spink, Scott Davis, Ramon Bosch, Aldo Scarpa, Yawei Zhang, Richard K Severson, Meredith Yeager, Stephen Chanock, Alexandra Nieters

  The lancet oncology. 01/2006; 7(1):27-38.

  BACKGROUND: Common genetic variants in immune and inflammatory response genes can affect the risk of developing non-Hodgkin lymphoma. We aimed to test this hypothesis using previously unpublishedBACKGROUND: Common genetic variants in immune and inflammatory response genes can affect the risk of developing non-Hodgkin lymphoma. We aimed to test this hypothesis using previously unpublished data from eight European, Canadian, and US case-control studies of the International Lymphoma Epidemiology Consortium (InterLymph). METHODS: We selected 12 single-nucleotide polymorphisms for analysis, on the basis of previous functional or association data, in nine genes that have important roles in lymphoid development, Th1/Th2 balance, and proinflammatory or anti-inflammatory pathways (IL1A, IL1RN, IL1B, IL2, IL6, IL10, TNF, LTA, and CARD15). Genotype data for one or more single-nucleotide polymorphisms were available for 3586 cases of non-Hodgkin lymphoma and for 4018 controls, and were assessed in a pooled analysis by use of a random-effects logistic regression model. FINDINGS: The tumour necrosis factor (TNF) -308G-->A polymorphism was associated with increased risk of non-Hodgkin lymphoma (p for trend=0.005), particularly for diffuse large B-cell lymphoma, the main histological subtype (odds ratio 1.29 [95% CI 1.10-1.51] for GA and 1.65 [1.16-2.34] for AA, p for trend <0.0001), but not for follicular lymphoma. The interleukin 10 (IL10) -3575T-->A polymorphism was also associated with increased risk of non-Hodgkin lymphoma (p for trend=0.02), again particularly for diffuse large B-cell lymphoma (p for trend=0.006). For individuals homozygous for the TNF -308A allele and carrying at least one IL10 -3575A allele, risk of diffuse large B-cell lymphoma doubled (2.13 [1.37-3.32], p=0.00083). INTERPRETATION: Common polymorphisms in TNF and IL10, key cytokines for the inflammatory response and Th1/Th2 balance, could be susceptibility loci for non-Hodgkin lymphoma. Moreover, our results underscore the importance of consortia for investigating the genetic basis of chronic diseases like cancer.