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Items: 1 to 20 of 97

1.

A comparative genomic approach for identifying synthetic lethal interactions in human cancer.

Deshpande R, Asiedu MK, Klebig M, Sutor S, Kuzmin E, Nelson J, Piotrowski J, Shin SH, Yoshida M, Costanzo M, Boone C, Wigle DA, Myers CL.

Cancer Res. 2013 Oct 15;73(20):6128-36. doi: 10.1158/0008-5472.CAN-12-3956.

2.

Imprinted CDKN1C is a tumor suppressor in rhabdoid tumor and activated by restoration of SMARCB1 and histone deacetylase inhibitors.

Algar EM, Muscat A, Dagar V, Rickert C, Chow CW, Biegel JA, Ekert PG, Saffery R, Craig J, Johnstone RW, Ashley DM.

PLoS One. 2009;4(2):e4482. doi: 10.1371/journal.pone.0004482.

3.

Use of clinical next-generation sequencing to identify melanomas harboring SMARCB1 mutations.

Stockman DL, Curry JL, Torres-Cabala CA, Watson IR, Siroy AE, Bassett RL, Zou L, Patel KP, Luthra R, Davies MA, Wargo JA, Routbort MA, Broaddus RR, Prieto VG, Lazar AJ, Tetzlaff MT.

J Cutan Pathol. 2015 May;42(5):308-17. doi: 10.1111/cup.12481.

PMID:
25754356
4.

An evolutionarily conserved synthetic lethal interaction network identifies FEN1 as a broad-spectrum target for anticancer therapeutic development.

van Pel DM, Barrett IJ, Shimizu Y, Sajesh BV, Guppy BJ, Pfeifer T, McManus KJ, Hieter P.

PLoS Genet. 2013;9(1):e1003254. doi: 10.1371/journal.pgen.1003254. Erratum in: PLoS Genet. 2013 Feb;9(2). doi: 10.1371/annotation/a26cb527-ec18-46ec-a63f-c69d0983add6.

5.

The genomic landscape of epithelioid sarcoma cell lines and tumours.

Jamshidi F, Bashashati A, Shumansky K, Dickson B, Gokgoz N, Wunder JS, Andrulis IL, Lazar AJ, Shah SP, Huntsman DG, Nielsen TO.

J Pathol. 2016 Jan;238(1):63-73. doi: 10.1002/path.4636.

PMID:
26365879
6.

Saccharomyces cerevisiae genetics predicts candidate therapeutic genetic interactions at the mammalian replication fork.

van Pel DM, Stirling PC, Minaker SW, Sipahimalani P, Hieter P.

G3 (Bethesda). 2013 Feb;3(2):273-82. doi: 10.1534/g3.112.004754.

7.

Exploration of synthetic lethal interactions as cancer drug targets.

Kuiken HJ, Beijersbergen RL.

Future Oncol. 2010 Nov;6(11):1789-802. doi: 10.2217/fon.10.131. Review.

PMID:
21142664
8.

Genome-wide approach to identify second gene targets for malignant rhabdoid tumors using high-density oligonucleotide microarrays.

Takita J, Chen Y, Kato M, Ohki K, Sato Y, Ohta S, Sugita K, Nishimura R, Hoshino N, Seki M, Sanada M, Oka A, Hayashi Y, Ogawa S.

Cancer Sci. 2014 Mar;105(3):258-64. doi: 10.1111/cas.12352.

9.

Synthetic lethality and cancer: cohesin and PARP at the replication fork.

O'Neil NJ, van Pel DM, Hieter P.

Trends Genet. 2013 May;29(5):290-7. doi: 10.1016/j.tig.2012.12.004. Review.

10.

Expression of SMARCB1 modulates steroid sensitivity in human lymphoblastoid cells: identification of a promoter SNP that alters PARP1 binding and SMARCB1 expression.

Pottier N, Cheok MH, Yang W, Assem M, Tracey L, Obenauer JC, Panetta JC, Relling MV, Evans WE.

Hum Mol Genet. 2007 Oct 1;16(19):2261-71.

PMID:
17616514
11.

Inferring synthetic lethal interactions from mutual exclusivity of genetic events in cancer.

Srihari S, Singla J, Wong L, Ragan MA.

Biol Direct. 2015 Oct 1;10:57. doi: 10.1186/s13062-015-0086-1.

12.

SMARCB1 protein and mRNA loss is not caused by promoter and histone hypermethylation in epithelioid sarcoma.

Papp G, Changchien YC, Péterfia B, Pecsenka L, Krausz T, Stricker TP, Khoor A, Donner L, Sápi Z.

Mod Pathol. 2013 Mar;26(3):393-403. doi: 10.1038/modpathol.2012.190.

13.

SMARCB1-deficient Vulvar Neoplasms: A Clinicopathologic, Immunohistochemical, and Molecular Genetic Study of 14 Cases.

Folpe AL, Schoolmeester JK, McCluggage WG, Sullivan LM, Castagna K, Ahrens WA, Oliva E, Biegel JA, Nielsen GP.

Am J Surg Pathol. 2015 Jun;39(6):836-49. doi: 10.1097/PAS.0000000000000397.

PMID:
25651469
14.

RNA-based analysis of two SMARCB1 mutations associated with familial schwannomatosis with meningiomas.

Melean G, Velasco A, Hernández-Imaz E, Rodríguez-Álvarez FJ, Martín Y, Valero A, Hernández-Chico C.

Neurogenetics. 2012 Aug;13(3):267-74. doi: 10.1007/s10048-012-0335-8.

PMID:
22752724
15.

SMARCB1/INI1 genetic inactivation is responsible for tumorigenic properties of epithelioid sarcoma cell line VAESBJ.

Brenca M, Rossi S, Lorenzetto E, Piccinin E, Piccinin S, Rossi FM, Giuliano A, Dei Tos AP, Maestro R, Modena P.

Mol Cancer Ther. 2013 Jun;12(6):1060-72. doi: 10.1158/1535-7163.MCT-13-0005.

16.

Inactivating mutations in SWI/SNF chromatin remodeling genes in human cancer.

Oike T, Ogiwara H, Nakano T, Yokota J, Kohno T.

Jpn J Clin Oncol. 2013 Sep;43(9):849-55. doi: 10.1093/jjco/hyt101.

PMID:
23904343
17.

Differential microRNA expression profiles between malignant rhabdoid tumor and epithelioid sarcoma: miR193a-5p is suggested to downregulate SMARCB1 mRNA expression.

Kohashi K, Yamamoto H, Kumagai R, Yamada Y, Hotokebuchi Y, Taguchi T, Iwamoto Y, Oda Y.

Mod Pathol. 2014 Jun;27(6):832-9. doi: 10.1038/modpathol.2013.213.

18.

SMARCB1/INI1 tumor suppressor gene is frequently inactivated in epithelioid sarcomas.

Modena P, Lualdi E, Facchinetti F, Galli L, Teixeira MR, Pilotti S, Sozzi G.

Cancer Res. 2005 May 15;65(10):4012-9.

19.

Epithelioid sarcoma is associated with a high percentage of SMARCB1 deletions.

Sullivan LM, Folpe AL, Pawel BR, Judkins AR, Biegel JA.

Mod Pathol. 2013 Mar;26(3):385-92. doi: 10.1038/modpathol.2012.175.

20.

Multi-omic measurement of mutually exclusive loss-of-function enriches for candidate synthetic lethal gene pairs.

Wappett M, Dulak A, Yang ZR, Al-Watban A, Bradford JR, Dry JR.

BMC Genomics. 2016 Jan 19;17:65. doi: 10.1186/s12864-016-2375-1.

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