Bernd Frank


Affiliation: German Cancer Research Center
Country: Germany


  1. Frank B, Hemminki K, Meindl A, Wappenschmidt B, Sutter C, Kiechle M, et al. BRIP1 (BACH1) variants and familial breast cancer risk: a case-control study. BMC Cancer. 2007;7:83 pubmed
    ..We found no effect of the putatively functional BRIP1 variants -64G>A and Pro919Ser on the risk of familial BC. ..
  2. Frank B, Rigas S, Bermejo J, Wiestler M, Wagner K, Hemminki K, et al. The CASP8 -652 6N del promoter polymorphism and breast cancer risk: a multicenter study. Breast Cancer Res Treat. 2008;111:139-44 pubmed
    ..The combined per allele odds ratio (OR) was 0.97 (95% confidence interval (CI), 95% CI = 0.93-1.02). The present result indicates that the CASP8 -652 6N del variant has no significant effect on BC risk in Europeans. ..
  3. Frank B, Hemminki K, Wirtenberger M, Bermejo J, Bugert P, Klaes R, et al. The rare ERBB2 variant Ile654Val is associated with an increased familial breast cancer risk. Carcinogenesis. 2005;26:643-7 pubmed
    ..We hypothesize that ERBB2 Val654 represents an oncogenic variant which might, in addition, influence clinical outcome and predict a worse prognosis. ..
  4. Frank B, Muller H, Weck M, Klopp N, Illig T, Raum E, et al. DNA repair gene polymorphisms and risk of chronic atrophic gastritis: a case-control study. BMC Cancer. 2011;11:440 pubmed publisher
  5. Frank B, Hoffmeister M, Klopp N, Illig T, Chang Claude J, Brenner H. Single nucleotide polymorphisms in Wnt signaling and cell death pathway genes and susceptibility to colorectal cancer. Carcinogenesis. 2010;31:1381-6 pubmed publisher
    ..However, our results provide evidence that CRC subsets may be affected. If confirmed, this knowledge may be used to assess individual susceptibility and to target potential measures of cancer prevention. ..
  6. Frank B, Hemminki K, Shanmugam K, Meindl A, Klaes R, Schmutzler R, et al. Association of death receptor 4 haplotype 626C-683C with an increased breast cancer risk. Carcinogenesis. 2005;26:1975-7 pubmed
    ..84, 95% confidence interval (CI) = 0.65-1.08, P = 0.18 and OR = 0.89, 95% CI = 0.72-1.12, P = 0.30]. However, haplotype analysis revealed a 3.5-fold risk for carriers of the 626C-683C haplotype (OR = 3.52, 95% CI = 1.45-8.52, P = 0.003). ..
  7. Frank B, Hemminki K, Bermejo J, Klaes R, Bugert P, Wappenschmidt B, et al. TP53-binding protein variants and breast cancer risk: a case-control study. Breast Cancer Res. 2005;7:R502-5 pubmed
    ..Investigating a larger study cohort might elucidate the influence of the 6bp deletion 1347_1352delTATCCC. Studying the functional effect and the impact of this variant on the risk of other cancers may be revealing. ..
  8. Frank B, Hemminki K, Wappenschmidt B, Meindl A, Klaes R, Schmutzler R, et al. Association of the CASP10 V410I variant with reduced familial breast cancer risk and interaction with the CASP8 D302H variant. Carcinogenesis. 2006;27:606-9 pubmed
    ..35, P(trend) = 0.007), pointing to the interaction between the CASP10 and CASP8 polymorphisms in breast carcinogenesis. ..
  9. Frank B, Hemminki K, Meindl A, Wappenschmidt B, Klaes R, Schmutzler R, et al. Association of the ARLTS1 Cys148Arg variant with familial breast cancer risk. Int J Cancer. 2006;118:2505-8 pubmed
    ..10-1.99, p=0.009; ptrend=0.003). On the basis of the small number of 46 cases, we additionally showed an association between the Trp149Stop mutation and an increased risk of bilateral BC (OR=4.11, 95% CI=1.27-13.31, p=0.011). ..

More Information


  1. Frank B, Hemminki K, Brenner H, Hoffmeister M, Chang Claude J, Burwinkel B. ARLTS1 variants and risk of colorectal cancer. Cancer Lett. 2006;244:172-5 pubmed
    ..However, we showed a non-significant increased risk of familial CRC for both variants (OR=1.40 and 1.45), indicating a possible role of ARLTS1 in familial CRC. ..
  2. Frank B, Meyer P, Boettger M, Hemminki K, Stapelmann H, Gast A, et al. ARLTS1 variants and melanoma risk. Int J Cancer. 2006;119:1736-7 pubmed
    ..43, 95% CI = 1.05-1.95, p = 0.02). An additional risk enhancement, though statistically non-significant, was observed in individuals with multiple melanomas (OR = 2.33, 95% CI = 0.87-6.26, p = 0.08). ..
  3. Frank B, Shanmugam K, Beckmann L, Hemminki K, Brenner H, Hoffmeister M, et al. Death receptor 4 variants and colorectal cancer risk. Cancer Epidemiol Biomarkers Prev. 2006;15:2002-5 pubmed
    ..37; 95% CI, 0.98-5.76). The score statistic yielded an empirical P of 0.03 of the haplotype-specific test for 626C-683C based on 20,000 simulations, suggesting that DR4 626C-683C may affect colorectal cancer predisposition. ..
  4. Frank B, Bermejo J, Hemminki K, Sutter C, Wappenschmidt B, Meindl A, et al. Copy number variant in the candidate tumor suppressor gene MTUS1 and familial breast cancer risk. Carcinogenesis. 2007;28:1442-5 pubmed
    ..37-0.90, P = 0.01 and OR = 0.41, 95% CI = 0.23-0.74, P = 0.003), supporting its role in human cancer. To our knowledge, the present study is the first to determine the impact of a CNV in a tumor suppressor gene on cancer risk. ..
  5. Frank B, Hoffmeister M, Klopp N, Illig T, Chang Claude J, Brenner H. Colorectal cancer and polymorphisms in DNA repair genes WRN, RMI1 and BLM. Carcinogenesis. 2010;31:442-5 pubmed publisher
    ..Although none of them showed a significant association with CRC, the association of BLM P868L with rectal cancer risk requires further investigation. ..
  6. Frank B, Hoeft B, Hoffmeister M, Linseisen J, Breitling L, Chang Claude J, et al. Association of hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD) variants and colorectal cancer risk. Carcinogenesis. 2011;32:190-6 pubmed publisher
    ..82, 95% CI = 0.70, 0.95, P = 0.01) as well as among smokers (OR = 0.74, 95% CI = 0.61, 0.90, P = 0.003). Yet, our data do not support the previously reported associations of HPGD tagSNPs and risk of CRC. ..
  7. Frank B, Weck M, Muller H, Klopp N, Illig T, Raum E, et al. Polymorphisms in MUC1, MUC2, MUC5B and MUC6 genes are not associated with the risk of chronic atrophic gastritis. Eur J Cancer. 2012;48:114-20 pubmed publisher
    ..None of the analysed SNPs was associated with CAG. However, large studies are needed to disclose or exclude potential weak associations of these SNPs with CAG risk. ..