J. Garay

发表

Androgen receptor as a targeted therapy for breast cancer.

B. Park, Joseph P Garay, Ben H Park, 2012, American journal of cancer research.

Knockin of mutant PIK3CA activates multiple oncogenic pathways

B. Park, K. Bachman, H. Konishi, 2009, Proceedings of the National Academy of Sciences.

Mutation of a single allele of the cancer susceptibility gene BRCA1 leads to genomic instability in human breast epithelial cells

Hiroyuki Konishi, David Cosgrove, Yuko Konishi, 2011, Proceedings of the National Academy of Sciences.

A PCR-based high-throughput screen with multiround sample pooling: application to somatic cell gene targeting

B. Park, H. Konishi, B. Karakas, 2007, Nature Protocols.

B Cells and T Follicular Helper Cells Mediate Response to Checkpoint Inhibitors in High Mutation Burden Mouse Models of Breast Cancer

David L. Marron, C. Perou, Xiaping He, 2019, Cell.

The growth response to androgen receptor signaling in ERα-negative human breast cells is dependent on p21 and mediated by MAPK activation

A. Weeraratna, P. Argani, A. D. De Marzo, 2012, Breast Cancer Research.

MultiK: an automated tool to determine optimal cluster numbers in single-cell RNA sequencing data

C. Perou, J. Marron, A. Thennavan, 2021, Genome biology.

Sex assignment in gestational trophoblastic neoplasia.

J. Garay, E. Surwit, K. Fortier, 1984, American journal of obstetrics and gynecology.

Ki-67 is required for maintenance of cancer stem cells but not cell proliferation

P. Argani, J. Hicks, A. D. De Marzo, 2016, Oncotarget.

Omics and therapy – A basis for precision medicine

J. Gray, Joseph P. Garay, Joe W. Gray, 2012, Molecular oncology.

PIK3CA mutations and EGFR overexpression predict for lithium sensitivity in human breast epithelial cells

B. Park, H. Konishi, M. Mohseni, 2011, Cancer biology & therapy.

TMSB 4 Y is a Candidate Tumor Suppressor on the Y Chromosome and is Deleted in Male Breast Cancer

P. Argani, B. Park, A. Meeker, 2016 .

TMSB4Y is a candidate tumor suppressor on the Y chromosome and is deleted in male breast cancer

P. Argani, B. Park, A. Meeker, 2015, Oncotarget.

Knock-in of mutant K-ras in nontumorigenic human epithelial cells as a new model for studying K-ras mediated transformation.

B. Park, K. Bachman, H. Konishi, 2007, Cancer research.

CRISPR‐based knock‐in mutagenesis of the pioneer transcription factor FOXA1: optimization of strategies for multi‐allelic proteins in cancer cells

Hector L. Franco, Shen Li, J. Garay, 2020, bioRxiv.

Knock in of the AKT1 E17K mutation in human breast epithelial cells does not recapitulate oncogenic PIK3CA mutations

B. Vogelstein, K. Polyak, D. Gorkin, 2010, Oncogene.

The multiple myeloma associated MMSET gene contributes to cellular adhesion, clonogenic growth, and tumorigenicity.

R. Arceci, B. Park, H. Konishi, 2008, Blood.

MACROD2 overexpression mediates estrogen independent growth and tamoxifen resistance in breast cancers

R. Scharpf, P. Argani, A. Cimino-Mathews, 2014, Proceedings of the National Academy of Sciences.

Review Article Androgen receptor as a targeted therapy for breast cancer

B. Park, J. Garay, 2012 .

FGFR4 regulates tumor subtype differentiation in luminal breast cancer and metastatic disease.

Sara R. Selitsky, David L. Marron, C. Fan, 2020, The Journal of clinical investigation.

Sensitivity to targeted therapy differs between HER2-amplified breast cancer cells harboring kinase and helical domain mutations in PIK3CA

Laura M. Heiser, K. Chin, J. Gray, 2021, Breast Cancer Research.

Tamoxifen-stimulated growth of breast cancer due to p21 loss

P. Argani, A. D. De Marzo, B. Park, 2008, Proceedings of the National Academy of Sciences.

The growth response to androgen receptor signaling in ERα-negative human breast cells is dependent on p21 and mediated by MAPK activation

A. Weeraratna, P. Argani, A. D. De Marzo, 2012, Breast Cancer Research.

Single copies of mutant KRAS and mutant PIK3CA cooperate in immortalized human epithelial cells to induce tumor formation.

P. Argani, B. Park, H. Konishi, 2013, Cancer research.

Molecular and Cellular Pathobiology Single Copies of Mutant KRAS and Mutant PIK 3 CA Cooperate in Immortalized Human Epithelial Cells to Induce Tumor Formation

P. Argani, B. Park, H. Konishi, 2013 .

TMSB4Y is a candidate tumor suppressor on the Y chromosome and is deleted in male breast cancer

P. Argani, B. Park, A. Meeker, 2015, Oncotarget.