| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Regular Articles |
Departments of Pathology [A-M. C-J., H. v. B., E. W. M., V. T. B. H. M. S., C. J. C.] and Human and Clinical Genetics [A-M. C-J.], Leiden University Medical Center, 2300 RC Leiden, the Netherlands; Department of Cytogenetics and Molecular Genetics, Adelaide Women and Children’s Hospital, North Adelaide, SA 5006 South Australia, Australia [D. F. C., J. C., J. A. P., C. S.]; Department of Haematology and Genetic Pathology, Flinders Medical Center, Flinders University of South Australia, Adelaide, SA 5001 South Australia, Australia [R. S., S. G., B. M.]; Division of Medical and Molecular Genetics, United Medical and Dental School, Guy’s Hospital, London, WC2R 2LS United Kingdom [N. V. M., C. G. M.]; and Hedley Atkins/Imperial Cancer Research Fund Breast Pathology Laboratory, Guy’s Hospital, London, WC2R 2LS United Kingdom [W. H. H., R. M., D. B.]
Loss of heterozygosity (LOH) at the long arm of chromosome 16 occurs in at least half of all breast tumors and is considered to target one or more tumor suppressor genes. Despite extensive studies by us and by others, a clear consensus of the boundaries of the smallest region of overlap (SRO) could not be identified. To find more solid evidence for SROs, we tested a large series of 712 breast tumors for LOH at 16q using a dense map of polymorphic markers. Strict criteria for LOH and retention were applied, and results that did not meet these criteria were excluded from the analysis. We compared LOH results obtained from samples with different DNA isolation methods, i.e., from microdissected tissue versus total tissue blocks. In the latter group, 16% of the cases were excluded because of noninterpretable LOH results. The selection of polymorphic markers is clearly influencing the LOH pattern because a chromosomal region seems more frequently involved in LOH when many markers from this region are used. The LOH detection method, i.e., radioactive versus fluorescence detection, has no marked effect on the results. Increasing the threshold window for retention of heterozygosity resulted in significantly more cases with complex LOH, i.e., several alternating regions of loss and retention, than seen in tumors with a small window for retention. Tumors with complex LOH do not provide evidence for clear-cut SROs that are repeatedly found in other samples. On disregarding these complex cases, we could identify three different SROs, two at band 16q24.3 and one at 16q22.1. In all three tumor series, we found cases with single LOH regions that designated the distal region at 16q24.3 and the region at 16q22.1. Comparing histological data on these tumors did not result in the identification of a particular subtype with LOH at 16q or a specific region involved in LOH. Only the rare mucinous tumors had no 16q LOH at all. Furthermore, a positive estrogen content is prevalent in tumors with 16q LOH, but not in tumors with LOH at 16q24.3 only.
This article has been cited by other articles:
|
|
 |
|
  G. Berx and F. van Roy Involvement of Members of the Cadherin Superfamily in Cancer Cold Spring Harb Perspect Biol, December 1, 2009; 1(6): a003129 - a003129. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kumar, K. M. Cheney, R. McKirdy, P. M. Neilsen, R. B. Schulz, J. Lee, J. Cohen, G. W. Booker, and D. F. Callen CBFA2T3-ZNF652 Corepressor Complex Regulates Transcription of the E-box Gene HEB J. Biol. Chem., July 4, 2008; 283(27): 19026 - 19038. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A.H.S. Gylling, T.T. Nieminen, W.M. Abdel-Rahman, K. Nuorva, M. Juhola, E.I. Joensuu, H.J. Jarvinen, J.-P. Mecklin, M. Aarnio, and P.T. Peltomaki Differential cancer predisposition in Lynch syndrome: insights from molecular analysis of brain and urinary tract tumors Carcinogenesis, July 1, 2008; 29(7): 1351 - 1359. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Plourde, C. Manhes, G. Leblanc, F. Durocher, M. Dumont, O. Sinilnikova, I. BRCAs, and J. Simard Mutation analysis and characterization of HSD17B2 sequence variants in breast cancer cases from French Canadian families with high risk of breast and ovarian cancer J. Mol. Endocrinol., April 1, 2008; 40(4): 161 - 172. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Gylling, W M Abdel-Rahman, M Juhola, K Nuorva, E Hautala, H J Jarvinen, J-P Mecklin, M Aarnio, and P Peltomaki Is gastric cancer part of the tumour spectrum of hereditary non-polyposis colorectal cancer? A molecular genetic study Gut, July 1, 2007; 56(7): 926 - 933. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Gratias, H. Rieder, R. Ullmann, L. Klein-Hitpass, S. Schneider, R. Boloni, M. Kappler, and D. R. Lohmann Allelic Loss in a Minimal Region on Chromosome 16q24 Is Associated with Vitreous Seeding of Retinoblastoma Cancer Res., January 1, 2007; 67(1): 408 - 416. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. T. Engelmark, E. L. Ivansson, J. J. Magnusson, I. M. Gustavsson, A. H. Beskow, P. K.E. Magnusson, and U. B. Gyllensten Identification of susceptibility loci for cervical carcinoma by genome scan of affected sib-pairs Hum. Mol. Genet., November 15, 2006; 15(22): 3351 - 3360. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kumar, J. Manning, H. E. Spendlove, G. Kremmidiotis, R. McKirdy, J. Lee, D. N. Millband, K. M. Cheney, M. R. Stampfer, P. P. Dwivedi, et al. ZNF652, A Novel Zinc Finger Protein, Interacts with the Putative Breast Tumor Suppressor CBFA2T3 to Repress Transcription Mol. Cancer Res., September 1, 2006; 4(9): 655 - 665. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. A. Oldenburg, K. Kroeze-Jansema, H. Meijers-Heijboer, C. J. van Asperen, N. Hoogerbrugge, I. van Leeuwen, H. F.A. Vasen, A.-M. Cleton-Jansen, J. Kraan, J. J. Houwing-Duistermaat, et al. Characterization of Familial Non-BRCA1/2 Breast Tumors by Loss of Heterozygosity and Immunophenotyping. Clin. Cancer Res., March 15, 2006; 12(6): 1693 - 1700. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Xie, J. L. Freudenheim, S. S. Cummings, B. Singh, H. He, S. E. McCann, K. B. Moysich, and P. G. Shields Accurate genotyping from paraffin-embedded normal tissue adjacent to breast cancer Carcinogenesis, February 1, 2006; 27(2): 307 - 310. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Kumar, P. M. Neilsen, J. Crawford, R. McKirdy, J. Lee, J. A. Powell, Z. Saif, J. M. Martin, M. Lombaerts, C. J. Cornelisse, et al. FBXO31 Is the Chromosome 16q24.3 Senescence Gene, a Candidate Breast Tumor Suppressor, and a Component of an SCF Complex Cancer Res., December 15, 2005; 65(24): 11304 - 11313. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. van Puijenbroek, J. W. F. Dierssen, P. Stanssens, R. van Eijk, A. M. Cleton-Jansen, T. van Wezel, and H. Morreau Mass Spectrometry-Based Loss of Heterozygosity Analysis of Single-Nucleotide Polymorphism Loci in Paraffin Embedded Tumors Using the MassEXTEND Assay: Single-Nucleotide Polymorphism Loss of Heterozygosity Analysis of the Protein Tyrosine Phosphatase Receptor Type J in Familial Colorectal Cancer J. Mol. Diagn., November 1, 2005; 7(5): 623 - 630. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Rampalli, L. Pavithra, A. Bhatt, T. K. Kundu, and S. Chattopadhyay Tumor Suppressor SMAR1 Mediates Cyclin D1 Repression by Recruitment of the SIN3/Histone Deacetylase 1 Complex Mol. Cell. Biol., October 1, 2005; 25(19): 8415 - 8429. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Jalota, K. Singh, L. Pavithra, R. Kaul-Ghanekar, S. Jameel, and S. Chattopadhyay Tumor Suppressor SMAR1 Activates and Stabilizes p53 through Its Arginine-Serine-rich Motif J. Biol. Chem., April 22, 2005; 280(16): 16019 - 16029. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R A Oldenburg, W H de Vos tot Nederveen Cappel, M van Puijenbroek, A van den Ouweland, E Bakker, G Griffioen, P Devilee, C J Cornelisse, H Meijers-Heijboer, H F A Vasen, et al. Extending the p16-Leiden tumour spectrum by respiratory tract tumours J. Med. Genet., March 1, 2004; 41(3): e31 - 31. [Full Text] [PDF]
|
|
|
|
|
|
R. A. Oldenburg, K. Kroeze-Jansema, J. Kraan, H. Morreau, J. G. M. Klijn, N. Hoogerbrugge, M. J. L. Ligtenberg, C. J. van Asperen, H. F. A. Vasen, C. Meijers, et al. The CHEK2*1100delC Variant Acts as a Breast Cancer Risk Modifier in Non-BRCA1/BRCA2 Multiple-Case Families Cancer Res., December 1, 2003; 63(23): 8153 - 8157. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Riou, R. Saffroy, J. Comoy, M. Gross-Goupil, J.-P. Thiery, J.-F. Emile, D. Azoulay, D. Piatier-Tonneau, A. Lemoine, and B. Debuire Investigation in Liver Tissues and Cell Lines of the Transcription of 13 Genes Mapping to the 16q24 Region That Are Frequently Deleted in Hepatocellular Carcinoma Clin. Cancer Res., October 1, 2002; 8(10): 3178 - 3186. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Kochetkova, O. L. D. McKenzie, A. J. Bais, J. M. Martin, G. A. Secker, R. Seshadri, J. A. Powell, S. J. Hinze, A. E. Gardner, H. E. Spendlove, et al. CBFA2T3 (MTG16) Is a Putative Breast Tumor Suppressor Gene from the Breast Cancer Loss of Heterozygosity Region at 16q24.3 Cancer Res., August 15, 2002; 62(16): 4599 - 4604. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. Cui, H. Feiner, and H. Li Multiplex Loss of Heterozygosity Analysis by Using Single or Very Few Cells J. Mol. Diagn., August 1, 2002; 4(3): 172 - 177. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Wong, J. M. F. Lee, T. C. M. Lau, S. T. Fan, and I. O. L. Ng Clinicopathological Significance of Loss of Heterozygosity on Chromosome 13q in Hepatocellular Carcinoma Clin. Cancer Res., July 1, 2002; 8(7): 2266 - 2272. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Gunnarsson, B. M. Olsson, and O. Stal Abnormal Expression of 17{beta}-Hydroxysteroid Dehydrogenases in Breast Cancer Predicts Late Recurrence Cancer Res., December 1, 2001; 61(23): 8448 - 8451. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |
