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BAP1 missense mutation c.2054 A>T (p.E685V) completely disrupts normal splicing through creation of a novel 5' splice site in a human mesothelioma cell line

PloS one, 2015-04, Vol.10 (4), p.e0119224

2015

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Immunohistochemical detection of ARID1A in colorectal carcinoma: loss of staining is associated with sporadic microsatellite unstable tumors with medullary histology and high TNM stage

Human pathology, 2014-12, Vol.45 (12), p.2430-2436

2014

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CDH1 Missense Variant c.1679C>G (p.T560R) Completely Disrupts Normal Splicing through Creation of a Novel 5' Splice Site

PloS one, 2016-11, Vol.11 (11), p.e0165654-e0165654

2016

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BAP1 Missense Mutation c.2054 AT

PloS one, 2015-04, Vol.10 (4), p.e0119224

2015

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BAP1 Missense Mutation c.2054 AT Completely Disrupts Normal Splicing through Creation of a Novel 5' Splice Site in a Human Mesothelioma Cell Line

PloS one, 2015-04, Vol.10 (4), p.e0119224

2015

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Secondary mutation in a coding mononucleotide tract in MSH6 causes loss of immunoexpression of MSH6 in colorectal carcinomas with MLH1/PMS2 deficiency

Modern pathology, 2013-01, Vol.26 (1), p.131-138

2013

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Enhanced clinical assessment of hematologic malignancies through routine paired tumor and normal sequencing

Nature communications, 2023-10, Vol.14 (1), p.6895-16, Article 6895

2023

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Abstract A05: BRCA1 promoter hypermethylation loss in recurrent high-grade serous carcinoma

Clinical cancer research, 2016-01, Vol.22 (2_Supplement), p.A05-A05

2016

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CDH1 Missense Variant c.1679CG

PloS one, 2016-11, Vol.11 (11), p.e0165654

2016

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CDH1 Missense Variant c.1679CG Completely Disrupts Normal Splicing through Creation of a Novel 5' Splice Site

PloS one, 2016-11, Vol.11 (11), p.e0165654

2016

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BRCA1 R71K missense mutation contributes to cancer predisposition by increasing alternative transcript levels

Breast cancer research and treatment, 2011-12, Vol.130 (3), p.1051-1056

2011

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Juvenile polyposis syndrome presenting with familial gastric cancer and massive gastric polyposis

Journal of clinical oncology, 2012-09, Vol.30 (25), p.e229-e232

2012

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BAP1 Missense Mutation c.2054 A>T (p.E685V) Completely Disrupts Normal Splicing through Creation of a Novel 5' Splice Site in a Human Mesothelioma Cell Line: e0119224

PloS one, 2015-04, Vol.10 (4)

2015

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Corrigendum to “The germline CDH1 c.48 G > C substitution contributes to cancer predisposition through generation of a pro-invasive mutation” [Mutat. Res. 770 (2014) 106–111]

Mutation research, 2015-04, Vol.774, p.59-59

2015

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The germline CDH1 c.48 G>C substitution contributes to cancer predisposition through generation of a pro-invasive mutation

Mutation research, 2014-12, Vol.770, p.106-111

2014

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cDNA analysis demonstrates that the BRCA2 intronic variant IVS4-12del5 is a deleterious mutation

Mutation research, 2009-04, Vol.663 (1), p.84-89

2009

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BAP1 missense mutation c.2054 A>T (p.E685V) completely disrupts normal splicing through creation of a novel 5' splice site in a human mesothelioma cell line

Immunohistochemical detection of ARID1A in colorectal carcinoma: loss of staining is associated with sporadic microsatellite unstable tumors with medullary histology and high TNM stage

CDH1 Missense Variant c.1679C>G (p.T560R) Completely Disrupts Normal Splicing through Creation of a Novel 5' Splice Site

BAP1 Missense Mutation c.2054 AT

BAP1 Missense Mutation c.2054 AT Completely Disrupts Normal Splicing through Creation of a Novel 5' Splice Site in a Human Mesothelioma Cell Line

Secondary mutation in a coding mononucleotide tract in MSH6 causes loss of immunoexpression of MSH6 in colorectal carcinomas with MLH1/PMS2 deficiency

Enhanced clinical assessment of hematologic malignancies through routine paired tumor and normal sequencing

Abstract A05: BRCA1 promoter hypermethylation loss in recurrent high-grade serous carcinoma

CDH1 Missense Variant c.1679CG

CDH1 Missense Variant c.1679CG Completely Disrupts Normal Splicing through Creation of a Novel 5' Splice Site

BRCA1 R71K missense mutation contributes to cancer predisposition by increasing alternative transcript levels

Juvenile polyposis syndrome presenting with familial gastric cancer and massive gastric polyposis

BAP1 Missense Mutation c.2054 A>T (p.E685V) Completely Disrupts Normal Splicing through Creation of a Novel 5' Splice Site in a Human Mesothelioma Cell Line: e0119224

Corrigendum to “The germline CDH1 c.48 G > C substitution contributes to cancer predisposition through generation of a pro-invasive mutation” [Mutat. Res. 770 (2014) 106–111]

The germline CDH1 c.48 G>C substitution contributes to cancer predisposition through generation of a pro-invasive mutation

cDNA analysis demonstrates that the BRCA2 intronic variant IVS4-12del5 is a deleterious mutation

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