CD8+ T cells in the tumor microenvironment modulate the response to endocrine therapy in breast cancer Fabiana Napolitano, Yunguan Wang, Dhivya R. Sudhan, Paula I. Gonzalez-Ericsson, Luigi Formisano, Nisha Unni, Shahbano Shakeel, James Z. Zhu, Khushi Ahuja, Lei Guo, María Rosario Chica-Parrado, Yuki Matsunaga, Pamela Luna, Chang-Ching A. Lin, Yasuaki Uemoto, Kyung-Min Lee, Hongli Ma, Nathaniel J. Evans, Alberto Servetto, Saurabh Mendiratta, Spencer D. Barnes, Roberto Bianco, Yisheng V. Fang, Lin Xu, Jeon Lee, Tao Wang, Justin M. Balko, Gordon B. Mills, Marilyne Labrie, Ariella B. Hanker, Carlos L. Arteaga Journal of Clinical Investigation, 2026 The role of the tumor immune microenvironment (TIME) in modulating responses to antiestrogen therapy in hormone receptor-positive (HR+) breast cancers remains unclear. We analyzed pre- and on-treatment biopsies from patients with HR+ breast cancer treated with letrozole to induce estrogen deprivation (ED). Stromal tumor-infiltrating lymphocytes, assessed by H&E staining, and immune-related gene sets, including IFN-γ signaling genes, measured by RNA-Seq, were increased in ED-resistant tumors. Cyclic immunofluorescence and spatial transcriptomics revealed an abundance of CD8+ T cells and enhanced antigen processing and immune gene signatures in ED-resistant tumors. In this group, the expression of CXCL9, CXCL10, and CXCL11 - chemokine genes involved in CD8+ T cell recruitment - and the CXCR3 receptor were upregulated both before and after letrozole treatment. CXCL11 levels were higher in conditioned media from HR+ breast cancer cells cocultured with CD8+ T cells. Both recombinant CXCL11 and coculture with CD8+ T cells promoted MCF7 and T47D cell growth in estrogen-free conditions. Finally, deletion combined with silencing of the CXCL11 receptors CXCR3 and CXCR7 in MCF7 cells impaired proliferation in response to exogenous CXCL11 and to coculture with CD8+ T cells in estrogen-free conditions. These findings suggest that CD8+ T cell-associated CXCL11 in the TIME modulated the response of HR+ breast cancer cells to estrogen suppression.
CD8+ T cells in the tumor microenvironment modulate the response to endocrine therapy in breast cancer Sarah R. DiNapoli, Katharine M. Wright, Brian J. Mog, Alexander H. Pearlman, Tushar D. Nichakawade, Nikita Marcou, Emily Han-Chung Hsiue, Michael S. Hwang, Jacqueline Douglass, Qiang Liu, Evangeline Watson, Marco Dal Molin, Joshua D. Cohen, Maria Popoli, Suman Paul, Maximilian F. Konig, Nicolas Wyhs, P. Aitana Azurmendi, Stephanie Glavaris, Jiaxin Ge, Tolulope O. Awosika, Jin Liu, Kathleen L. Gabrielson, Sandra B. Gabelli, Drew M. Pardoll, Chetan Bettegowda, Nickolas Papadopoulos, Kenneth W. Kinzler, Shibin Zhou, Bert Vogelstein Journal of Clinical Investigation, 2026 Mutation-associated neoantigens (MANAs) are highly cancer-specific targets for immunotherapy where peptides derived from intracellular mutant proteins are presented on the cell surface via HLA molecules. T cell-engaging bispecific antibodies and CAR T cells can target MANAs to eliminate cancer cells via T cell activation. However, the low antigen density of MANAs on the cell surface can limit therapeutic efficacy. Here, we investigated whether increasing the affinity of the H2 single-chain variable fragment (scFv) targeting the p53 R175H MANA (HMTEVVRHC presented on HLA-A*02:01) improves its therapeutic effect. We identified higher-affinity H2 variants via phage biopanning and a thiocyanate elution method. Increasing bispecific antibody affinity to the low nanomolar range increased cancer cell killing and tumor control in mouse xenograft models without sacrificing antigen specificity. We next asked how increasing scFv affinity impacts CAR T cell function - a matter of debate. We appended each variant scFv to a CD28z CAR, CD3γ, or the T cell receptor. In striking contrast to the bispecific antibody results, increasing CAR affinity decreased function in each CAR format due to lower T cell activation upon interaction with target cancer cells. These results have important implications for the design of future immunotherapeutic approaches targeting low-density antigens.
Nidogen-1 suppresses cell proliferation, migration, and glycolysis via integrin β1-mediated HIF-1α downregulation in triple-negative breast cancer Joo-hyung Lee, Seogho Son, Yunhyo Ko, Hogeun Lim, Minhyeok Lee, Min-gyeong Kang, Hyungjoo Kim, Kyung-min Lee, Incheol Shin Scientific Reports, 2025 Nidogen-1 (NID1) is a secreted glycoprotein widely distributed in basement membranes. NID1 interacts with extracellular matrix proteins such as collagen and laminin and has been implicated in the progression of various cancers. However, study on the role of NID1 in breast cancer is scarce and inconsistent. In this work, we found that the expression of NID1 is significantly lower in breast cancer tissue than in normal tissue. In addition, NID1 expression correlated negatively with a poor prognosis for breast cancer patients. Based on those findings, we speculated that NID1 might act as a cancer suppressor in breast cancer. To investigate the role of NID1 in breast cancer, we constructed NID1-overexpressing cell lines. NID1 overexpression decreased breast cancer cell proliferation, migration, and in vivo tumor growth. Moreover, glucose metabolism, which is known to enhance cancer cell proliferation and migration, was also decreased by NID1 overexpression. Mechanistically, NID1 overexpression downregulated hypoxia-inducible factor-1α (HIF-1α) expression at the transcription level. Furthermore, we found that NID1 reduced integrin β1 stability and downregulated the transcription of HIF-1α through the FAK/Src/NF-κB p65 signaling axis, which is downstream of integrin β1. Together, the results of this study demonstrate the tumor suppressive role of NID1 in triple-negative breast cancer.
PRMT5 is an actionable therapeutic target in CDK4/6 inhibitor-resistant ER+/RB-deficient breast cancer Chang-Ching Lin, Tsung-Cheng Chang, Yunguan Wang, Lei Guo, Yunpeng Gao, Emmanuel Bikorimana, Andrew Lemoff, Yisheng V. Fang, He Zhang, Yanfeng Zhang, Dan Ye, Isabel Soria-Bretones, Alberto Servetto, Kyung-min Lee, Xuemei Luo, Joseph J. Otto, Hiroaki Akamatsu, Fabiana Napolitano, Ram Mani, David W. Cescon, Lin Xu, Yang Xie, Joshua T. Mendell, Ariella B. Hanker, Carlos L. Arteaga Nature Communications, 2024 CDK4/6 inhibitors (CDK4/6i) have improved survival of patients with estrogen receptor-positive (ER+) breast cancer. However, patients treated with CDK4/6i eventually develop drug resistance and progress. RB1 loss-of-function alterations confer resistance to CDK4/6i, but the optimal therapy for these patients is unclear. Through a genome-wide CRISPR screen, we identify protein arginine methyltransferase 5 (PRMT5) as a molecular vulnerability in ER+/ RB1 -knockout breast cancer cells. Inhibition of PRMT5 blocks the G1-to-S transition in the cell cycle independent of RB, leading to growth arrest in RB1 -knockout cells. Proteomics analysis uncovers fused in sarcoma (FUS) as a downstream effector of PRMT5. Inhibition of PRMT5 results in dissociation of FUS from RNA polymerase II, leading to hyperphosphorylation of serine 2 in RNA polymerase II, intron retention, and subsequent downregulation of proteins involved in DNA synthesis. Furthermore, treatment with the PRMT5 inhibitor pemrametostat and a selective ER degrader fulvestrant synergistically inhibits growth of ER+/RB-deficient cell-derived and patient-derived xenografts. These findings highlight dual ER and PRMT5 blockade as a potential therapeutic strategy to overcome resistance to CDK4/6i in ER+/RB-deficient breast cancer.
Combined inhibition of CDK4/6 and AKT is highly effective against the luminal androgen receptor (LAR) subtype of triple negative breast cancer María Rosario Chica-Parrado, Gun Min Kim, Yasuaki Uemoto, Fabiana Napolitano, Chang-Ching Lin, Dan Ye, Emmanuel Bikorimana, Yisheng Fang, Kyung-min Lee, Saurabh Mendiratta, Ariella B. Hanker, Carlos L. Arteaga Cancer Letters, 2024 Luminal Androgen Receptor (LAR) triple-negative breast cancers (TNBC) express androgen receptors (AR), exhibit high frequency of PIK3CA mutations and intact RB. Herein, we investigated combined blockade of the CDK4/6 and PI3K signaling with palbociclib, alpelisib, and capivasertib, which inhibit CDK4/6, PI3Kα, and AKT1-3, respectively. The combination of palbociclib/capivasertib, but not palbociclib/alpelisib, synergistically inhibited proliferation of MDA-MB-453 and MFM-223 LAR cells [synergy score 7.34 (p = 5.81x10 −11 ) and 4.78 (p = 0.012), respectively]. The AR antagonist enzalutamide was inactive against MDA-MB-453, MFM-223, and CAL148 cells and did not enhance the efficacy of either combination. Palbociclib/capivasertib inhibited growth of LAR patient-derived xenografts more potently than palbociclib/alpelisib. Treatment of LAR cells with palbociclib suppressed phosphorylated-RB and resulted in adaptive phosphorylation/activation of S473 pAKT and AKT substrates GSK3β, PRAS40, and FoxO3a. Capivasertib blocked palbociclib-induced phosphorylation of AKT substrates more potently than alpelisib. Treatment with PI3Kβ inhibitors did not block phosphorylation of AKT substrates, suggesting that PI3Kβ did not mediate the adaptive response to CDK4/6 inhibition. Phosphokinase arrays of MDA-MB-453 cells treated with palbociclib showed time-dependent upregulation of PDGFRβ, GSK3β, STAT3, and STAT6. RNA silencing of PDGFRβ in palbociclib-treated MDA-MB-453 and MFM-223 cells blocked the upregulation of S473 pAKT, suggesting that the adaptive response to CDK4/6 blockade involves PDGFRβ signaling. Finally, treatment with palbociclib and the PDGFR inhibitor CP637451 arrested growth of MDA-MB-453 and MFM-223 cells to the same degree as palbociclib/capivasertib. These findings support testing the combination of CDK4/6 and AKT inhibitors in patients with LAR TNBC, and further investigation of PDGFR antagonists in this breast cancer subtype. • The combination of CDK4/6and AKT inhibitors (CDK4/6i, AKTi) results in synergistic inhibition of cell proliferation in Luminal Androgen Receptor (LAR) subtype triple-negative breast cancer cells. • CDK4/6i and AKTi effectively inhibit tumor growth in LAR TNBC patient-derived and cell-derived xenografts. • CDK4/6 blockade induces adaptive activation of AKT in LAR preclinical models, which is more effectively suppressed by an AKTi than a PI3K inhibitor. • PDGFRβ plays a compensatory role by activating AKT after treatment with CDK4/6i.
CYR61 confers chemoresistance by upregulating survivin expression in triple-negative breast cancer Hyungjoo Kim, Seogho Son, Yunhyo Ko, Hogeun Lim, Joohyung Lee, Kyung-Min Lee, Incheol Shin Carcinogenesis, 2024 Cysteine-rich angiogenic inducer 61 (CYR61) is a protein from the CCN family of matricellular proteins that play diverse regulatory roles in the extracellular matrix. CYR61 is involved in cell adhesion, migration, proliferation, differentiation, apoptosis, and senescence. Here, we show that CYR61 induces chemoresistance in triple-negative breast cancer (TNBC). We observed that CYR61 is overexpressed in TNBC patients, and CYR61 expression correlates negatively with the survival of patients who receive chemotherapy. CYR61 knockdown reduced cell migration, sphere formation and the cancer stem cell (CSC) population and increased the chemosensitivity of TNBC cells. Mechanistically, CYR61 activated Wnt/β-catenin signaling and increased survivin expression, which are associated with chemoresistance, the epithelial–mesenchymal transition, and CSC-like phenotypes. Altogether, our study demonstrates a novel function of CYR61 in chemotherapy resistance in breast cancer.
Special Issue: Resistance to Targeted Therapies in Human Cancer Tae-Won Lee, Hee-Joo Choi, Kyung-Min Lee, Jeong-Yeon Lee Biomedicines, 2023 Cancer is the second leading cause of death worldwide, accounting for approximately 10 million deaths in 2020 [...]
CCN3/NOV promotes metastasis and tumor progression via GPNMB-induced EGFR activation in triple-negative breast cancer Seogho Son, Hyungjoo Kim, Hogeun Lim, Joo-hyung Lee, Kyung-min Lee, Incheol Shin Cell Death and Disease, 2023 Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. TNBC patients typically exhibit unfavorable outcomes due to its rapid growth and metastatic potential. Here, we found overexpression of CCN3 in TNBC patients. We identified that CCN3 knockdown diminished cancer stem cell formation, metastasis, and tumor growth in vitro and in vivo. Mechanistically, ablation of CCN3 reduced activity of the EGFR/MAPK pathway. Transcriptome profiling revealed that CCN3 induces glycoprotein nonmetastatic melanoma protein B (GPNMB) expression, which in turn activates the EGFR pathway. An interrogation of the TCGA dataset further supported the transcriptional regulation of GPNMB by CCN3. Finally, we showed that CCN3 activates Wnt signaling through a ligand-dependent or -independent mechanism, which increases microphthalmia-associated transcription factor (MITF) protein, a transcription factor inducing GPNMB expression. Together, our findings demonstrate the oncogenic role of CCN3 in TNBC, and we propose CCN3 as a putative therapeutic target for TNBC.
Epigenetic Repression of STING by MYC Promotes Immune Evasion and Resistance to Immune Checkpoint Inhibitors in Triple-Negative Breast Cancer Kyung-min Lee, Chang-Ching Lin, Alberto Servetto, Joonbeom Bae, Vishal Kandagatla, Dan Ye, GunMin Kim, Dhivya R. Sudhan, Saurabh Mendiratta, Paula I. González Ericsson, Justin M. Balko, Jeon Lee, Spencer Barnes, Venkat S. Malladi, Siamak Tabrizi, Sangeetha M. Reddy, Seoyun Yum, Ching-Wei Chang, Katherine E. Hutchinson, Susan E. Yost, Yuan Yuan, Zhijian J. Chen, Yang-Xin Fu, Ariella B. Hanker, Carlos L. Arteaga Cancer Immunology Research, 2022
Nuclear FGFR1 regulates gene transcription and promotes antiestrogen resistance in ERþ breast cancer Alberto Servetto, Rahul Kollipara, Luigi Formisano, Chang-Ching Lin, Kyung-Min Lee, Dhivya R. Sudhan, Paula I. Gonzalez-Ericsson, Sumanta Chatterjee, Angel Guerrero-Zotano, Saurabh Mendiratta, Hiroaki Akamatsu, Nicholas James, Roberto Bianco, Ariella B. Hanker, Ralf Kittler, Carlos L. Arteaga Clinical Cancer Research, 2021
A versatile oblique plane microscope for large-scale and high-resolution imaging of subcellular dynamics Etai Sapoznik, Bo-Jui Chang, Jaewon Huh, Robert J Ju, Evgenia V Azarova, Theresa Pohlkamp, Erik S Welf, David Broadbent, Alexandre F Carisey, Samantha J Stehbens, Kyung-Min Lee, Arnaldo Marín, Ariella B Hanker, Jens C Schmidt, Carlos L Arteaga, Bin Yang, Yoshihiko Kobayashi, Purushothama Rao Tata, Rory Kruithoff, Konstantin Doubrovinski, Douglas P Shepherd, Alfred Millett-Sikking, Andrew G York, Kevin M Dean, Reto P Fiolka Elife, 2020
Hyperactivation of TORC1 Drives Resistance to the Pan-HER Tyrosine Kinase Inhibitor Neratinib in HER2-Mutant Cancers Dhivya R. Sudhan, Angel Guerrero-Zotano, Helen Won, Paula González Ericsson, Alberto Servetto, Mariela Huerta-Rosario, Dan Ye, Kyung-min Lee, Luigi Formisano, Yan Guo, Qi Liu, Lisa N. Kinch, Monica Red Brewer, Teresa Dugger, James Koch, Michael J. Wick, Richard E. Cutler, Alshad S. Lalani, Richard Bryce, Alan Auerbach, Ariella B. Hanker, Carlos L. Arteaga Cancer Cell, 2020
Aberrant FGFR signaling mediates resistance to CDK4/6 inhibitors in ER+ breast cancer Luigi Formisano, Yao Lu, Alberto Servetto, Ariella B. Hanker, Valerie M. Jansen, Joshua A. Bauer, Dhivya R. Sudhan, Angel L. Guerrero-Zotano, Sarah Croessmann, Yan Guo, Paula Gonzalez Ericsson, Kyung-min Lee, Mellissa J. Nixon, Luis J. Schwarz, Melinda E. Sanders, Teresa C. Dugger, Marcelo Rocha Cruz, Amir Behdad, Massimo Cristofanilli, Aditya Bardia, Joyce O’Shaughnessy, Rebecca J. Nagy, Richard B. Lanman, Nadia Solovieff, Wei He, Michelle Miller, Fei Su, Yu Shyr, Ingrid A. Mayer, Justin M. Balko, Carlos L. Arteaga Nature Communications, 2019
Discovery of Potent Myeloid Cell Leukemia-1 (Mcl-1) Inhibitors That Demonstrate in Vivo Activity in Mouse Xenograft Models of Human Cancer Taekyu Lee, Plamen P. Christov, Subrata Shaw, James C. Tarr, Bin Zhao, Nagarathanam Veerasamy, Kyu Ok Jeon, Jonathan J. Mills, Zhiguo Bian, John L. Sensintaffar, Allison L. Arnold, Stuart A. Fogarty, Evan Perry, Haley E. Ramsey, Rebecca S. Cook, Melinda Hollingshead, Myrtle Davis Millin, Kyung-min Lee, Brian Koss, Amit Budhraja, Joseph T. Opferman, Kwangho Kim, Carlos L. Arteaga, William J. Moore, Edward T. Olejniczak, Michael R. Savona, Stephen W. Fesik Journal of Medicinal Chemistry, 2019
ERþ Breast cancers resistant to prolonged neoadjuvant letrozole exhibit an e2f4 transcriptional program sensitive to cdk4/6 inhibitors Angel L. Guerrero-Zotano, Thomas P. Stricker, Luigi Formisano, Katherine E. Hutchinson, Daniel G. Stover, Kyung-Min Lee, Luis J. Schwarz, Jennifer M. Giltnane, Monica V. Estrada, Valerie M. Jansen, Alberto Servetto, Joaquín Gavilá, J. Alejandro Perez-Fidalgo, Ana Lluch, Antonio Llombart-Cussac, Mohamed Amine Bayar, Stefan Michiels, Fabrice André, Mónica Arnedos, Vicente Guillem, Amparo Ruiz-Simon, Carlos L. Arteaga Clinical Cancer Research, 2018
CD8 + T cells in the tumor microenvironment modulate the response to endocrine therapy in breast cancer F Napolitano, Y Wang, DR Sudhan, PI Gonzalez-Ericsson, L Formisano, ... The Journal of Clinical Investigation 136 (3) , 2026 2026 Citations: 2
Combined inhibition of CDK4/6 and AKT is highly effective against the luminal androgen receptor (LAR) subtype of triple negative breast cancer (vol 604, 217219, 2024) MR Chica-Parrado, GM Kim, Y Uemoto, F Napolitano, CC Lin, D Ye, ... CANCER LETTERS 630 , 2025 2025
Corrigendum to “Combined inhibition of CDK4/6 and AKT is highly effective against the luminal androgen receptor (LAR) subtype of triple negative breast cancer”(Cancer Letters … MR Chica-Parrado, GM Kim, Y Uemoto, F Napolitano, CC Lin, D Ye, ... Cancer Letters 630, 217891 , 2025 2025
Abstract PS12-02: CXCL11 in the tumor immune microenvironment modulates resistance to endocrine therapy in hormone receptor-positive breast cancer F Napolitano, Y Wang, DR Sudhan, PI González-Ericsson, L Formisano, ... Clinical Cancer Research 31 (12_Supplement), PS12-02-PS12-02 , 2025 2025
Combined inhibition of CDK4/6 and AKT is highly effective against the luminal androgen receptor (LAR) subtype of triple negative breast cancer MR Chica-Parrado, GM Kim, Y Uemoto, F Napolitano, CC Lin, D Ye, ... Cancer letters 604, 217219 , 2024 2024 Citations: 11
Abstract PS03-04: Tumor immune microenvironment modulates resistance to estrogen suppression in ER+ breast cancer F Napolitano, Y Wang, D Sudhan, P Gonzalez-Ericsson, L Formisano, ... Cancer Research 84 (9_Supplement), PS03-04-PS03-04 , 2024 2024
Combined inhibition of CDK4/6 and AKT is highly active against the luminal androgen receptor (LAR) subtype of triple negative breast cancer (TNBC) R Chica-Parrado, GM Kim, Y Uemoto, D Ye, F Napolitano, CC Lin, ... Cancer Research 84 (6_Supplement), 7592-7592 , 2024 2024
PRMT5 is an actionable therapeutic target in CDK4/6 inhibitor-resistant ER+/RB-deficient breast cancer CC Lin, TC Chang, Y Wang, L Guo, Y Gao, E Bikorimana, A Lemoff, ... Nature communications 15 (1), 2287 , 2024 2024 Citations: 46
Protein arginine methyltransferase 5 (PRMT5) is an actionable therapeutic target in CDK4/6 inhibitor-resistant ER+/RB-deficient breast cancer CC Lin, TC Chang, Y Wang, L Guo, Y Gao, E Bikorimana, A Lemoff, ... Research Square, rs. 3. rs-2966905 , 2023 2023 Citations: 1
Combined inhibition of CDK4/6 and AKT is highly active against the luminal androgen receptor (LAR) subtype of triple negative breast cancer (TNBC) M del Rosario Chica-Parrado, GM Kin, CC Lin, K Lee, F Napolitano, D Ye, ... Cancer Research 83 (7_Supplement), 5483-5483 , 2023 2023 Citations: 1
Immune cells infiltration and activation are higher in breast cancers resistant to antiestrogen therapy F Napolitano, DR Sudhan, Y Wang, PI González-Ericsson, L Formisano, ... Cancer Research 83 (7_Supplement), 3445-3445 , 2023 2023
Resistance to Targeted Therapies in Human Cancer TW Lee, HJ Choi, KM Lee, JY Lee Biomedicines 11 (2), 414 , 2023 2023 Citations: 1
Epigenetic repression of STING by MYC promotes immune evasion and resistance to immune checkpoint inhibitors in triple-negative breast cancer K Lee, CC Lin, A Servetto, J Bae, V Kandagatla, D Ye, GM Kim, ... Cancer Immunology Research 10 (7), 829-843 , 2022 2022 Citations: 73
Immune checkpoint blockades in triple-negative breast cancer: current state and molecular mechanisms of resistance H Kim, JM Choi, K Lee Biomedicines 10 (5), 1130 , 2022 2022 Citations: 22
Combined inhibition of CDK4/6 and AKT is effective in Rb-intact triple-negative breast cancer of the luminal androgen receptor (LAR) subtype GM Kim, K Lee, D Sudhan, A Lin, A Marin, S Chatterjee, D Ye, ... CANCER RESEARCH 82 (4) , 2022 2022
Abstract GS3-09: Loss of ASXL1 tumor suppressor promotes resistance to CDK4/6 inhibitors in ER+ breast cancer DR Sudhan, S Chatterjee, J Kim, Y Wang, V Kandagatla, D Ye, CC Lin, ... Cancer Research 82 (4_Supplement), GS3-09-GS3-09 , 2022 2022 Citations: 1
Abstract P5-17-09: A genome-wide CRISPR screen identifies PRMT5 as a novel therapeutic target in ER+/ RB1 -deficient breast cancer CC Lin, TC Chang, A Servetto, K Lee, H Zhang, Y Wang, D Ye, ... Cancer Research 82 (4_Supplement), P5-17-09-P5-17-09 , 2022 2022
Abstract PD3-07: Combined inhibition of CDK4/6 and AKT is effective in Rb-intact triple-negative breast cancer of the luminal androgen receptor (LAR) subtype GM Kim, K Lee, D Sudhan, A Lin, A Marin, S Chatterjee, D Ye, ... Cancer Research 82 (4_Supplement), PD3-07-PD3-07 , 2022 2022
Co-occurring gain-of-function mutations in HER2 and HER3 modulate HER2/HER3 activation, oncogenesis, and HER2 inhibitor sensitivity AB Hanker, BP Brown, J Meiler, A Marin, HS Jayanthan, D Ye, CC Lin, ... Cancer cell 39 (8), 1099-1114. e8 , 2021 2021 Citations: 104
Nuclear FGFR1 Regulates Gene Transcription and Promotes Antiestrogen Resistance in ER + Breast Cancer A Servetto, R Kollipara, L Formisano, CC Lin, KM Lee, DR Sudhan, ... Clinical Cancer Research 27 (15), 4379-4396 , 2021 2021 Citations: 70
MOST CITED SCHOLAR PUBLICATIONS
MYC and MCL1 cooperatively promote chemotherapy-resistant breast cancer stem cells via regulation of mitochondrial oxidative phosphorylation K Lee, JM Giltnane, JM Balko, LJ Schwarz, AL Guerrero-Zotano, ... Cell metabolism 26 (4), 633-647. e7 , 2017 2017 Citations: 713
Aberrant FGFR signaling mediates resistance to CDK4/6 inhibitors in ER+ breast cancer L Formisano, Y Lu, A Servetto, AB Hanker, VM Jansen, JA Bauer, ... Nature communications 10 (1), 1373 , 2019 2019 Citations: 417
Kinome-wide RNA interference screen reveals a role for PDK1 in acquired resistance to CDK4/6 inhibition in ER-positive breast cancer VM Jansen, NE Bhola, JA Bauer, L Formisano, KM Lee, KE Hutchinson, ... Cancer research 77 (9), 2488-2499 , 2017 2017 Citations: 253
A versatile oblique plane microscope for large-scale and high-resolution imaging of subcellular dynamics E Sapoznik, BJ Chang, J Huh, RJ Ju, EV Azarova, T Pohlkamp, ES Welf, ... Elife 9, e57681 , 2020 2020 Citations: 229
CD44 regulates cell proliferation, migration, and invasion via modulation of c-Src transcription in human breast cancer cells KS Nam, S Oh, K Lee, S Yoo, I Shin Cellular signalling 27 (9), 1882-1894 , 2015 2015 Citations: 159
ECM1 regulates tumor metastasis and CSC-like property through stabilization of β-catenin KM Lee, K Nam, S Oh, J Lim, RK Kim, D Shim, JH Choi, SJ Lee, JH Yu, ... Oncogene 34 (50), 6055-6065 , 2015 2015 Citations: 119
Co-occurring gain-of-function mutations in HER2 and HER3 modulate HER2/HER3 activation, oncogenesis, and HER2 inhibitor sensitivity AB Hanker, BP Brown, J Meiler, A Marin, HS Jayanthan, D Ye, CC Lin, ... Cancer cell 39 (8), 1099-1114. e8 , 2021 2021 Citations: 104
Regulation of cell proliferation and migration by keratin19-induced nuclear import of early growth response-1 in breast cancer cells J Ju, W Yang, K Lee, S Oh, KS Nam, S Shim, SY Shin, MC Gye, IS Chu, ... Clinical cancer research 19 (16), 4335-4346 , 2013 2013 Citations: 94
Elacestrant (RAD1901) exhibits anti-tumor activity in multiple ER+ breast cancer models resistant to CDK4/6 inhibitors HK Patel, N Tao, KM Lee, M Huerta, H Arlt, T Mullarkey, S Troy, ... Breast Cancer Research 21 (1), 146 , 2019 2019 Citations: 86
Extracellular matrix protein 1 regulates cell proliferation and trastuzumab resistance through activation of epidermal growth factor signaling K Lee, K Nam, S Oh, J Lim, YP Kim, JW Lee, JH Yu, SH Ahn, SB Kim, ... Breast Cancer Research 16 (6), 479 , 2014 2014 Citations: 80
Discovery of potent myeloid cell leukemia-1 (Mcl-1) inhibitors that demonstrate in vivo activity in mouse xenograft models of human cancer T Lee, PP Christov, S Shaw, JC Tarr, B Zhao, N Veerasamy, KO Jeon, ... Journal of medicinal chemistry 62 (8), 3971-3988 , 2019 2019 Citations: 74
Epigenetic repression of STING by MYC promotes immune evasion and resistance to immune checkpoint inhibitors in triple-negative breast cancer K Lee, CC Lin, A Servetto, J Bae, V Kandagatla, D Ye, GM Kim, ... Cancer Immunology Research 10 (7), 829-843 , 2022 2022 Citations: 73
Nuclear FGFR1 Regulates Gene Transcription and Promotes Antiestrogen Resistance in ER + Breast Cancer A Servetto, R Kollipara, L Formisano, CC Lin, KM Lee, DR Sudhan, ... Clinical Cancer Research 27 (15), 4379-4396 , 2021 2021 Citations: 70
CD24 enhances DNA damage-induced apoptosis by modulating NF-κB signaling in CD44-expressing breast cancer cells J Ju, K Jang, K Lee, M Kim, J Kim, JY Yi, DY Noh, I Shin Carcinogenesis 32 (10), 1474-1483 , 2011 2011 Citations: 60
Hyperactivation of TORC1 drives resistance to the pan-HER tyrosine kinase inhibitor neratinib in HER2-mutant cancers DR Sudhan, A Guerrero-Zotano, H Won, PG Ericsson, A Servetto, ... Cancer cell 37 (2), 183-199. e5 , 2020 2020 Citations: 59
Cytokeratin19 induced by HER2/ERK binds and stabilizes HER2 on cell membranes JH Ju, S Oh, KM Lee, W Yang, KS Nam, HG Moon, DY Noh, CG Kim, ... Cell Death & Differentiation 22 (4), 665-676 , 2015 2015 Citations: 55
Proline rich 11 ( PRR11 ) overexpression amplifies PI3K signaling and promotes antiestrogen resistance in breast cancer K Lee, AL Guerrero-Zotano, A Servetto, DR Sudhan, CC Lin, L Formisano, ... Nature communications 11 (1), 5488 , 2020 2020 Citations: 54
ECM1 promotes the Warburg effect through EGF-mediated activation of PKM2 K Lee, K Nam, S Oh, J Lim, T Lee, I Shin Cellular signalling 27 (2), 228-235 , 2015 2015 Citations: 52
Protein kinase B/Akt1 inhibits autophagy by down-regulating UVRAG expression W Yang, J Ju, K Lee, KS Nam, S Oh, I Shin Experimental cell research 319 (3), 122-133 , 2013 2013 Citations: 51
PRMT5 is an actionable therapeutic target in CDK4/6 inhibitor-resistant ER+/RB-deficient breast cancer CC Lin, TC Chang, Y Wang, L Guo, Y Gao, E Bikorimana, A Lemoff, ... Nature communications 15 (1), 2287 , 2024 2024 Citations: 46
