PPM1D gene amplification and overexpression in breast cancer: A qRT-PCR and chromogenic in situ hybridization study

Modern Pathology

Volumn 23, Issue 10, 2010, Pages 1334-1345

  Lambros, Maryou B ^a   Natrajan, Rachael ^a   Geyer, Felipe C ^a   Lopez Garcia, Maria A ^a,b   Dedes, Konstantin J ^a   Savage, Kay ^a   Lacroix Triki, Magali ^a,c   Jones, Robin L ^d   Lord, Christopher J ^a   Linardopoulos, Spiros ^a   Ashworth, Alan ^a   Reis Filho, Jorge S ^a  

^a INSTITUTE OF CANCER RESEARCH   (United Kingdom)

^b HOSPITAL UNIVERSITARIO VIRGEN DEL ROCÍO   (Spain)

^c INSTITUT CLAUDIUS REGAUD   (France)

^d ROYAL MARSDEN HOSPITAL   (United Kingdom)

Author keywords

Breast cancer; Chromogenic in situ hybridization; P53; Prognosis; Real time reverse transcriptase PCR; Therapeutic target

Indexed keywords

ANTINEOPLASTIC AGENT; CYTOKERATIN 17; CYTOKERATIN 5; CYTOKERATIN 6; EPIDERMAL GROWTH FACTOR RECEPTOR; EPIDERMAL GROWTH FACTOR RECEPTOR 2; MESSENGER RNA; PHOSPHATASE; PROTEIN PHOSPHATASE MAGNESIUM DEPENDENT 1DELTA; TAMOXIFEN; UNCLASSIFIED DRUG;

ADJUVANT THERAPY; ARTICLE; BREAST CANCER; CANCER ADJUVANT THERAPY; CANCER CHEMOTHERAPY; CANCER SURGERY; CANCER SURVIVAL; CHROMOGENIC IN SITU HYBRIDIZATION; CLINICAL FEATURE; GENE AMPLIFICATION; GENE OVEREXPRESSION; HUMAN; HUMAN TISSUE; IN SITU HYBRIDIZATION; MAJOR CLINICAL STUDY; MASTECTOMY; PRIORITY JOURNAL; QUANTITATIVE REAL TIME POLYMERASE CHAIN REACTION; REAL TIME POLYMERASE CHAIN REACTION;

EID: 77957578978     PISSN: 08933952     EISSN: 15300285     Source Type: Journal    
DOI: 10.1038/modpathol.2010.121     Document Type: Article

References (43)

1. Fiscella M, Zhang H, Fan S, et al.Wip1, a novel human protein phosphatase that is induced in response to ionizing radiation in a p53-dependent manner. Proc Natl Acad Sci USA 1997;94:6048-6053.
2. Bulavin DV, Demidov ON, Saito S, et al. Amplification of PPM1D in human tumors abrogates p53 tumorsuppressor activity. Nat Genet 2002;31:210-215.
3. Bulavin DV, Phillips C, Nannenga B, et al. Inactivation of the Wip1 phosphatase inhibits mammary tumorigenesis through p38 MAPK-mediated activation of the p16(Ink4a)-p19(Arf) pathway. Nat Genet 2004;36: 343-350.
4. Hu X, Stern HM, Ge L, et al. Genetic alterations and oncogenic pathways associated with breast cancer subtypes. Mol Cancer Res 2009;7:511-522.
5. Li J, Yang Y, Peng Y, et al. Oncogenic properties of PPM1D located within a breast cancer amplification epicenter at 17q23. Nat Genet 2002;31:133-134.
6. Loukopoulos P, Shibata T, Katoh H, et al. Genome-wide array-based comparative genomic hybridization analysis of pancreatic adenocarcinoma: identification of genetic indicators that predict patient outcome. Cancer Sci 2007;98:392-400.
7. Saito-Ohara F, Imoto I, Inoue J, et al. PPM1D is a potential target for 17q gain in neuroblastoma. Cancer Res 2003;63:1876-1883.
8. Tan DS, Lambros MB, Rayter S, et al. PPM1D is a potential therapeutic target in ovarian clear cell carcinomas. Clin Cancer Res 2009;15:2269-2280.
9. Natrajan R, Lambros MB, Rodriguez-Pinilla SM, et al. Tiling path genomic profiling of grade 3 invasive ductal breast cancers. Clin Cancer Res 2009;15: 2711-2722.
10. Natrajan R, Weigelt B, Mackay A, et al. An integrative genomic and transcriptomic analysis reveals molecular pathways and networks regulated by copy number aberrations in basal-like, HER2 and luminal cancers. Breast Cancer Res Treat 2010;121:575-589.
11. Lu X, Nguyen TA, Moon SH, et al. The type 2C phosphatase Wip1: an oncogenic regulator of tumor suppressor and DNA damage response pathways. Cancer Metastasis Rev 2008;27:123-135.
12. Zhang X, Lin L, Guo H, et al. Phosphorylation and degradation of MdmX is inhibited by Wip1 phosphatase in the DNA damage response. Cancer Res 2009;69:7960-7968.
13. Lu X, Ma O, Nguyen TA, et al. The Wip1 phosphatase acts as a gatekeeper in the p53-Mdm2 autoregulatory loop. Cancer Cell 2007;12:342-354.
14. Fujimoto H, Onishi N, Kato N, et al. Regulation of the antioncogenic Chk2 kinase by the oncogenic Wip1 phosphatase. Cell Death Differ 2006;13: 1170-1180.
15. Lu X, Nguyen TA, Appella E, et al. Homeostatic regulation of base excision repair by a p53-induced phosphatase: linking stress response pathways with DNA repair proteins. Cell Cycle 2004;3:1363-1366.
16. Moon SH, Lin L, Zhang X, et al. Wildtype p53-induced phosphatase 1 dephosphorylates histone variant {gamma}-H2AX and suppresses DNA double strand break repair. J Biol Chem 2010;285:12935-12947.
17. Macurek L, Lindqvist A, Voets O, et al. Wip1 phosphatase is associated with chromatin and dephosphorylates gammaH2AX to promote checkpoint inhibition. Oncogene 2010;29:2281-2291.
18. Harrison M, Li J, Degenhardt Y, et al. Wip1-deficient mice are resistant to common cancer genes. Trends Mol Med 2004;10:359-361.
19. Lu X, Nannenga B, Donehower LA. PPM1D dephosphorylates Chk1 and p53 and abrogates cell cycle checkpoints. Genes Dev 2005;19:1162-1174.
20. Lu X, Bocangel D, Nannenga B, et al. The p53-induced oncogenic phosphatase PPM1D interacts with uracil DNA glycosylase and suppresses base excision repair. Mol Cell 2004;15:621-634.
21. Proia DA, Nannenga BW, Donehower LA, et al. Dual roles for the phosphatase PPM1D in regulating progesterone receptor function. J Biol Chem 2006;281: 7089-7101.
22. Perkins ND. Integrating cell-signalling pathways with NF-kappaB and IKK function. Nat Rev Mol Cell Biol 2007;8:49-62.
23. Chew J, Biswas S, Shreeram S, et al. WIP1 phosphatase is a negative regulator of NF-kappaB signalling. Nat Cell Biol 2009;11:659-666.
24. Lowe JM, Cha H, Yang Q, et al. Nuclear factor-kappaB (NF-kappaB) is a novel positive transcriptional regulator of the oncogenicWip1 phosphatase. J Biol Chem 2010;285:5249-5257.
25. Rayter S, Elliott R, Travers J, et al. A chemical inhibitor of PPM1D that selectively kills cells overexpressing PPM1D. Oncogene 2008;27:1036-1044.
26. Elston CW, Ellis IO. Pathological prognostic factors in breast cancer. I. The value of histological grade in breast cancer: experience from a large study with longterm follow-up. Histopathology 1991;19:403-410.
27. Singletary SE, Connolly JL. Breast cancer staging: working with the sixth edition of the AJCC Cancer Staging Manual. CA Cancer J Clin 2006;56:37-47; quiz 50-51.
28. Lambros MB, Simpson PT, Jones C, et al. Unlocking pathology archives for molecular genetic studies: a reliable method to generate probes for chromogenic and fluorescent in situ hybridization. Lab Invest 2006;86:398-408.
29. Arriola E, Marchio C, Tan DS, et al. Genomic analysis of the HER2/TOP2A amplicon in breast cancer and breast cancer cell lines. Lab Invest 2008;88:491-503.
30. Reis-Filho JS, Savage K, Lambros MB, et al. Cyclin D1 protein overexpression and CCND1 amplification in breast carcinomas: an immunohistochemical and chromogenic in situ hybridisation analysis. Mod Pathol 2006;19:999-1009.
31. Dedes KJ, Lopez-Garcia MA, Geyer FC, et al. Cortactin gene amplification and expression in breast cancer: a chromogenic in situ hybridisation and immunohistochemical study. Breast Cancer Res Treat 2010; doi:10.1007/s10549-010- 0816-0; e-pub ahead of print.
32. Tan DS, Marchio C, Jones RL, et al. Triple negative breast cancer: molecular profiling and prognostic impact in adjuvant anthracycline-treated patients. Breast Cancer Res Treat 2008;111:27-44.
33. Abdel-Fatah TM, Powe DG, Agboola J, et al. The biological, clinical and prognostic implications of p53 transcriptional pathways in breast cancers. J Pathol 2010;220:419-434.
34. Mahler-Araujo B, Savage K, Parry S, et al. Reduction of E-cadherin expression is associated with non-lobular breast carcinomas of basal-like and triple negative phenotype. J Clin Pathol 2008;61: 615-620.
35. Parry S, Savage K, Marchio C, et al. Nestin is expressed in basal-like and triple negative breast cancers. J Clin Pathol 2008;61:1045-1050.
36. Nielsen TO, Hsu FD, Jensen K, et al. Immunohistochemical and clinical characterization of the basal-like subtype of invasive breast carcinoma. Clin Cancer Res 2004;10:5367-5374.
37. Rossner Jr P, Gammon MD, Zhang YJ, et al. Mutations in p53, p53 protein overexpression and breast cancer survival. J Cell Mol Med 2009;13:3847-3857.
38. Blancato J, Singh B, Liu A, et al. Correlation of amplification and overexpression of the c-myc oncogene in high-grade breast cancer: FISH, in situ hybridisation and immunohistochemical analyses. Br J Cancer 2004;90:1612-1619.
39. Reis-Filho JS, Pinheiro C, Lambros MB, et al. EGFR amplification and lack of activating mutations in metaplastic breast carcinomas. J Pathol 2006;209: 445-453.
40. Slamon DJ, Press MF. Alterations in the TOP2A and HER2 genes: association with adjuvant anthracycline sensitivity in human breast cancers. J Natl Cancer Inst 2009;101:615-618.
41. Hicks J, Krasnitz A, Lakshmi B, et al. Novel patterns of genome rearrangement and their association with survival in breast cancer. Genome Res 2006;16: 1465-1479.
42. Natrajan R, Lambros MB, Geyer FC, et al. Loss of 16q in high grade breast cancer is associated with estrogen receptor status: evidence for progression in tumors with a luminal phenotype? Genes Chromosomes Cancer 2009;48:351-365.
43. Belova GI, Demidov ON, Fornace Jr AJ, et al. Chemical inhibition of Wip1 phosphatase contributes to suppression of tumorigenesis. Cancer Biol Ther 2005;4: 1154-1158.