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1. Inducible nitric oxide synthase (iNOS)-activated Cxcr2 signaling in myeloid cells promotes TGFβ-dependent squamous cell carcinoma lung metastasis

Author

Li, Xing, Ke, Yao, Hernandez, Ariel L, Yu, Jingjing, Bian, Li, Hall, Spencer C, Nolan, Kyle, Wang, Jing H, Young, Christian D, and Wang, Xiao-Jing

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Lung, Cancer, Lung Cancer, Humans, Mice, Animals, Nitric Oxide Synthase Type II, Transforming Growth Factor beta, Carcinoma, Squamous Cell, Carcinoma, Non-Small-Cell Lung, Lung Neoplasms, Myeloid Cells, Nitric Oxide, Oral cancer, Myeloid-derived suppressor cells, L-NIL, Spontaneous lung metastasis model, Smad4 deletion, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Transforming growth factor beta (TGFβ) activity is linked to metastasis in many cancer types, but whether TGFβ activity is necessary for squamous cell carcinoma (SCC) lung metastasis has not been studied. Here we used a lung metastatic SCC model derived from keratin 15 (K15). KrasG12D.Smad4-/- SCC and human SCC specimens to identify metastasis drivers and test therapeutic interventions. We demonstrated that a TGFβ receptor (TGFβR) inhibitor reduced lung metastasis in mouse SCC correlating with reduced CD11b+/Ly6G+ myeloid cells positive for inducible nitric oxide synthase (iNOS). Further, TGFβ activity and iNOS were higher in primary human oral SCCs with metastasis than SCCs without metastasis. Consistently, either depleting myeloid cells with anti-Gr1 antibody or inhibiting iNOS with L-N6-(1-iminoethyl)-l-lysine (L-NIL) reduced SCC lung metastasis. L-NIL treated tumor-bearing mice exhibited reductions in tumor-infiltrating myeloid cells and in plasma Cxcl5 levels, and attenuated primary tumor growth with increased apoptosis and decreased proliferation. Blocking Cxcl5 with an antagonist of its receptor Cxcr2, SB225002, also reduced SCC lung metastasis.

Published
2023

2. Distinct immune microenvironment profiles of therapeutic responders emerge in combined TGFβ/PD-L1 blockade-treated squamous cell carcinoma

Author

Strait, Alexander A, Woolaver, Rachel A, Hall, Spencer C, Young, Christian D, Karam, Sana D, Jimeno, Antonio, Lan, Yan, Raben, David, Wang, Jing H, and Wang, Xiao-Jing

Subjects
Cancer, Animals, B7-H1 Antigen, Carcinoma, Squamous Cell, Female, Mice, Mice, Inbred C57BL, Transforming Growth Factor beta, Tumor Microenvironment
Abstract

Transforming growth factor beta (TGFβ) and programmed death-ligand 1 (PD-L1) are often overproduced in refractory squamous cell carcinoma (SCC). We examined spatial patterns of PD-L1+ cells in mouse and human SCCs and found that PD-L1 was primarily expressed on infiltrating leukocytes. Although combined TGFβ and PD-L1 blockade are undergoing cancer clinical trials, there are no predictive markers for therapeutic responders. To address this, we used both a small molecule TGFβ inhibitor in combination with anti-PD-L1 and a bifunctional fusion protein targeting both TGFβ and PD-L1 to treat mouse SCCs and found TGFβ inhibition enhanced PD-L1 blockade-induced tumor eradication in multiple tumor models. Furthermore, we identified distinct cell populations of responders and non-responders to bintrafusp alfa, with responders showing a shift toward a more immune-permissive microenvironment. The cellular and molecular signatures of responders versus non-responders to combined TGFβ and PD-L1 blockade provide important insights into future personalized immunotherapy in SCC.

Published
2021

3. Cancer Cell CD44 Mediates Macrophage/Monocyte-Driven Regulation of Head and Neck Cancer Stem Cells

Author

Gomez, Karina E, Wu, FangLong, Keysar, Stephen B, Morton, J Jason, Miller, Bettina, Chimed, Tugs-Saikhan, Le, Phuong N, Nieto, Cera, Chowdhury, Farshad N, Tyagi, Anit, Lyons, Traci R, Young, Christian D, Zhou, Hongmei, Somerset, Hilary L, Wang, Xiao-Jing, and Jimeno, Antonio

Subjects
Stem Cell Research - Nonembryonic - Human, Dental/Oral and Craniofacial Disease, Cancer, Stem Cell Research - Nonembryonic - Non-Human, Clinical Research, Rare Diseases, Stem Cell Research, Underpinning research, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Aetiology, Adaptor Proteins, Signal Transducing, Animals, Cell Cycle Proteins, Cell Line, Tumor, Feedback, Physiological, Female, Head and Neck Neoplasms, Humans, Hyaluronan Receptors, Hyaluronic Acid, Male, Mice, Inbred NOD, Monocytes, Neoplastic Stem Cells, Phosphatidylinositol 3-Kinases, SOXB1 Transcription Factors, Squamous Cell Carcinoma of Head and Neck, Tumor Microenvironment, Tumor-Associated Macrophages, Xenograft Model Antitumor Assays, Zinc Finger E-box-Binding Homeobox 1, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Tumor-associated macrophages (TAM) in the tumor microenvironment (TME) cooperate with cancer stem cells (CSC) to maintain stemness. We recently identified cluster of differentiation 44 (CD44) as a surface marker defining head and neck squamous cell carcinoma (HNSCC) CSC. PI3K-4EBP1-SOX2 activation and signaling regulate CSC properties, yet the upstream molecular control of this pathway and the mechanisms underlying cross-talk between TAM and CSC in HNSCC remain largely unknown. Because CD44 is a molecular mediator in the TME, we propose here that TAM-influenced CD44 signaling could mediate stemness via the PI3K-4EBP1-SOX2 pathway, possibly by modulating availability of hyaluronic acid (HA), the main CD44 ligand. HNSCC IHC was used to identify TAM/CSC relationships, and in vitro coculture spheroid models and in vivo mouse models were used to identify the influence of TAMs on CSC function via CD44. Patient HNSCC-derived TAMs were positively and negatively associated with CSC marker expression at noninvasive and invasive edge regions, respectively. TAMs increased availability of HA and increased cancer cell invasion. HA binding to CD44 increased PI3K-4EBP1-SOX2 signaling and the CSC fraction, whereas CD44-VCAM-1 binding promoted invasive signaling by ezrin/PI3K. In vivo, targeting CD44 decreased PI3K-4EBP1-SOX2 signaling, tumor growth, and CSC. TAM depletion in syngeneic and humanized mouse models also diminished growth and CSC numbers. Finally, a CD44 isoform switch regulated epithelial-to-mesenchymal plasticity as standard form of CD44 and CD44v8-10 determined invasive and tumorigenic phenotypes, respectively. We have established a mechanistic link between TAMs and CSCs in HNSCC that is mediated by CD44 intracellular signaling in response to extracellular signals. SIGNIFICANCE: These findings establish a mechanistic link between tumor cell CD44, TAM, and CSC properties at the tumor-stroma interface that can serve as a vital area of focus for target and drug discovery.

Published
2020

4. PARP Inhibition Enhances Radiotherapy of SMAD4-Deficient Human Head and Neck Squamous Cell Carcinomas in Experimental Models

Author

Hernandez, Ariel L, Young, Christian D, Bian, Li, Weigel, Kelsey, Nolan, Kyle, Frederick, Barbara, Han, Gangwen, He, Guanting, Trahan, G Devon, Rudolph, Michael C, Jones, Kenneth L, Oweida, Ayman J, Karam, Sana D, Raben, David, and Wang, Xiao-Jing

Subjects
Cancer, Human Genome, Genetics, Rare Diseases, Dental/Oral and Craniofacial Disease, Animals, Antineoplastic Combined Chemotherapy Protocols, Apoptosis, Cell Proliferation, Cetuximab, Disease Models, Animal, Female, Head and Neck Neoplasms, Humans, Mice, Mice, Nude, Phthalazines, Piperazines, Poly(ADP-ribose) Polymerase Inhibitors, Prognosis, Smad4 Protein, Squamous Cell Carcinoma of Head and Neck, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeSMAD4 loss causes genomic instability and the initiation/progression of head and neck squamous cell carcinoma (HNSCC). Here, we study whether SMAD4 loss sensitizes HNSCCs to olaparib (PARP inhibitor) in combination with radiotherapy (RT).Experimental designWe analyzed HNSCC The Cancer Genome Atlas data for SMAD4 expression in association with FANC/BRCA family gene expression. Human HNSCC cell lines were screened for sensitivity to olaparib. Isogenic HNSCC cell lines were generated to restore or reduce SMAD4 expression and treated with olaparib, radiation, or the combination. HNSCC pretreatment specimens from a phase I trial investigating olaparib were analyzed.ResultsSMAD4 levels correlated with levels of FANC/BRCA genes in HNSCC. HNSCC cell lines with SMAD4 homozygous deletion were sensitive to olaparib. In vivo, olaparib or RT monotherapy reduced tumor volumes in SMAD4-mutant but not SMAD4-positive tumors. Olaparib with RT dual therapy sustained tumor volume reduction in SMAD4-deficient (mutant or knockdown) xenografts, which exhibited increased DNA damage and cell death compared with vehicle-treated tumors. In vitro, olaparib alone or in combination with radiation caused lower clonogenic survival, more DNA damage-associated cell death, and less proliferation in SMAD4-deficient cells than in SMAD4-positive (endogenous SMAD4 or transduced SMAD4) cells. Applicable to clinic, 5 out of 6 SMAD4-negative HNSCCs and 4 out of 8 SMAD4-positive HNSCCs responded to a standard treatment plus olaparib in a phase I clinical trial, and SMAD4 protein levels inversely correlated with DNA damage.ConclusionsSMAD4 levels are causal in determining sensitivity to PARP inhibition in combination with RT in HNSCCs.

Published
2020

6. Lessons learned from SMAD4 loss in squamous cell carcinomas

Author

Hernandez, Ariel L, Young, Christian D, Wang, Jing H, and Wang, Xiao‐Jing

Subjects
Cancer, Genetics, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Animals, Biomarkers, Tumor, Carcinoma, Squamous Cell, DNA Repair, Epithelial Cells, Genes, Tumor Suppressor, Humans, Signal Transduction, Smad4 Protein, Tumor Microenvironment, prevalence, SCCs, SMAD4 loss, tumor initiation, tumor progression, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

SMAD4 is a potent tumor suppressor and a central mediator of the TGFß signaling pathway. SMAD4 genetic loss is frequent in squamous cell carcinomas (SCCs). Reports of SMAD4 expression in SCCs vary significantly possibly due to inter-tumor heterogeneity or technical reasons. SMAD4 loss is an initiation event for SCCs. In tumor epithelial cells, SMAD4 loss causes increased proliferation, decreased apoptosis, and "Brca-like" genomic instability associated with DNA repair defects. SMAD4 loss also plays a role in the expansion of cancer stem cells. Epithelial SMAD4 loss causes overexpression of TGFß that is released into the tumor microenvironment and contributes to SCC progression through proinflammatory and immune evasive mechanisms. SMAD4 loss, while not a direct therapeutic target, is associated with multiple targetable pathways that require further therapeutic studies. Altogether, SMAD4 loss is a potential biomarker in SCCs that should be further studied for its values in prognostic and therapeutic predictions. Such information will potentially guide future biomarker-driven clinical trial designs and improve SCC patient outcomes.

Published
2019

9. Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M, Giltnane, Jennifer M, Wang, Kai, Schwarz, Luis J, Young, Christian D, Cook, Rebecca S, Owens, Phillip, Sanders, Melinda E, Kuba, Maria G, Sánchez, Violeta, Kurupi, Richard, Moore, Preston D, Pinto, Joseph A, Doimi, Franco D, Gómez, Henry, Horiuchi, Dai, Goga, Andrei, Lehmann, Brian D, Bauer, Joshua A, Pietenpol, Jennifer A, Ross, Jeffrey S, Palmer, Gary A, Yelensky, Roman, Cronin, Maureen, Miller, Vincent A, Stephens, Phillip J, and Arteaga, Carlos L

Subjects
Biotechnology, Human Genome, Breast Cancer, Clinical Research, Genetics, Cancer, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Antineoplastic Combined Chemotherapy Protocols, Cell Line, Tumor, Cluster Analysis, DNA Copy Number Variations, Drug Resistance, Neoplasm, Female, Gene Amplification, Gene Expression Profiling, Genes, myc, Humans, Ki-67 Antigen, Myeloid Cell Leukemia Sequence 1 Protein, Neoadjuvant Therapy, Neoplasm, Residual, Prognosis, Treatment Outcome, Triple Negative Breast Neoplasms, Oncology and Carcinogenesis
Abstract

UnlabelledNeoadjuvant chemotherapy (NAC) induces a pathologic complete response (pCR) in approximately 30% of patients with triple-negative breast cancers (TNBC). In patients lacking a pCR, NAC selects a subpopulation of chemotherapy-resistant tumor cells. To understand the molecular underpinnings driving treatment-resistant TNBCs, we performed comprehensive molecular analyses on the residual disease of 74 clinically defined TNBCs after NAC, including next-generation sequencing (NGS) on 20 matched pretreatment biopsies. Combined NGS and digital RNA expression analysis identified diverse molecular lesions and pathway activation in drug-resistant tumor cells. Ninety percent of the tumors contained a genetic alteration potentially treatable with a currently available targeted therapy. Thus, profiling residual TNBCs after NAC identifies targetable molecular lesions in the chemotherapy-resistant component of the tumor, which may mirror micrometastases destined to recur clinically. These data can guide biomarker-driven adjuvant studies targeting these micrometastases to improve the outcome of patients with TNBC who do not respond completely to NAC.SignificanceThis study demonstrates the spectrum of genomic alterations present in residual TNBC after NAC. Because TNBCs that do not achieve a CR after NAC are likely to recur as metastatic disease at variable times after surgery, these alterations may guide the selection of targeted therapies immediately after mastectomy before these metastases become evident.

Published
2014

12. Data from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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13. Supplementary Data Figure 5 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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14. Supplementary Data Tables from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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15. Supplementary Data Figure 6 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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16. Supplementary Data Figure 7 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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17. Supplementary Data Figure 2 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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18. Supplementary Data Figure 4 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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19. Supplementary Data Figure Legends from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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20. Supplementary Data Figure 3 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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21. Supplementary Data Figure 1 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets

Author

Balko, Justin M., primary, Giltnane, Jennifer M., primary, Wang, Kai, primary, Schwarz, Luis J., primary, Young, Christian D., primary, Cook, Rebecca S., primary, Owens, Phillip, primary, Sanders, Melinda E., primary, Kuba, Maria G., primary, Sánchez, Violeta, primary, Kurupi, Richard, primary, Moore, Preston D., primary, Pinto, Joseph A., primary, Doimi, Franco D., primary, Gómez, Henry, primary, Horiuchi, Dai, primary, Goga, Andrei, primary, Lehmann, Brian D., primary, Bauer, Joshua A., primary, Pietenpol, Jennifer A., primary, Ross, Jeffrey S., primary, Palmer, Gary A., primary, Yelensky, Roman, primary, Cronin, Maureen, primary, Miller, Vincent A., primary, Stephens, Phillip J., primary, and Arteaga, Carlos L., primary

Published
2023
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22. Supplementary Figure S3 from PARP Inhibition Enhances Radiotherapy of SMAD4-Deficient Human Head and Neck Squamous Cell Carcinomas in Experimental Models

Author

Hernandez, Ariel L., primary, Young, Christian D., primary, Bian, Li, primary, Weigel, Kelsey, primary, Nolan, Kyle, primary, Frederick, Barbara, primary, Han, Gangwen, primary, He, Guanting, primary, Devon Trahan, G., primary, Rudolph, Michael C., primary, Jones, Kenneth L., primary, Oweida, Ayman J., primary, Karam, Sana D., primary, Raben, David, primary, and Wang, Xiao-Jing, primary

Published
2023
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23. Supplementary Figures from Smad7 Promotes Healing of Radiotherapy-Induced Oral Mucositis without Compromising Oral Cancer Therapy in a Xenograft Mouse Model

Author

Luo, Jingjing, primary, Bian, Li, primary, Blevins, Melanie A., primary, Wang, Dongyan, primary, Liang, Chao, primary, Du, Danfeng, primary, Wu, Fanglong, primary, Holwerda, Barry, primary, Zhao, Rui, primary, Raben, David, primary, Zhou, Hongmei, primary, Young, Christian D., primary, and Wang, Xiao-Jing, primary

Published
2023
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24. Data from Smad7 Promotes Healing of Radiotherapy-Induced Oral Mucositis without Compromising Oral Cancer Therapy in a Xenograft Mouse Model

Author

Luo, Jingjing, primary, Bian, Li, primary, Blevins, Melanie A., primary, Wang, Dongyan, primary, Liang, Chao, primary, Du, Danfeng, primary, Wu, Fanglong, primary, Holwerda, Barry, primary, Zhao, Rui, primary, Raben, David, primary, Zhou, Hongmei, primary, Young, Christian D., primary, and Wang, Xiao-Jing, primary

Published
2023
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25. Supplementary Table S1 from PARP Inhibition Enhances Radiotherapy of SMAD4-Deficient Human Head and Neck Squamous Cell Carcinomas in Experimental Models

Author

Hernandez, Ariel L., primary, Young, Christian D., primary, Bian, Li, primary, Weigel, Kelsey, primary, Nolan, Kyle, primary, Frederick, Barbara, primary, Han, Gangwen, primary, He, Guanting, primary, Devon Trahan, G., primary, Rudolph, Michael C., primary, Jones, Kenneth L., primary, Oweida, Ayman J., primary, Karam, Sana D., primary, Raben, David, primary, and Wang, Xiao-Jing, primary

Published
2023
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26. Data from Conditional Loss of ErbB3 Delays Mammary Gland Hyperplasia Induced by Mutant PIK3CA without Affecting Mammary Tumor Latency, Gene Expression, or Signaling

Author

Young, Christian D., primary, Pfefferle, Adam D., primary, Owens, Philip, primary, Kuba, María G., primary, Rexer, Brent N., primary, Balko, Justin M., primary, Sánchez, Violeta, primary, Cheng, Hailing, primary, Perou, Charles M., primary, Zhao, Jean J., primary, Cook, Rebecca S., primary, and Arteaga, Carlos L., primary

Published
2023
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27. Supplementary Information from Conditional Loss of ErbB3 Delays Mammary Gland Hyperplasia Induced by Mutant PIK3CA without Affecting Mammary Tumor Latency, Gene Expression, or Signaling

Author

Young, Christian D., primary, Pfefferle, Adam D., primary, Owens, Philip, primary, Kuba, María G., primary, Rexer, Brent N., primary, Balko, Justin M., primary, Sánchez, Violeta, primary, Cheng, Hailing, primary, Perou, Charles M., primary, Zhao, Jean J., primary, Cook, Rebecca S., primary, and Arteaga, Carlos L., primary

Published
2023
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29. An ERBB1-3 Neutralizing Antibody Mixture With High Activity Against Drug-Resistant HER2+ Breast Cancers With ERBB Ligand Overexpression

Author

Schwarz, Luis J., Hutchinson, Katherine E., Rexer, Brent N., Estrada, Mónica Valeria, Gonzalez Ericsson, Paula I., Sanders, Melinda E., Dugger, Teresa C., Formisano, Luigi, Guerrero-Zotano, Angel, Red-Brewer, Monica, Young, Christian D., Lantto, Johan, Pedersen, Mikkel W., Kragh, Michael, Horak, Ivan D., and Arteaga, Carlos L.

Published
2017
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33. Epidermal growth factor receptor signaling in precancerous keratinocytes promotes neighboring head and neck cancer squamous cell carcinoma cancer stem cell‐like properties and phosphoinositide 3‐kinase inhibitor insensitivity

Author

Nguyen, Khoa A., primary, Keith, Madison J., additional, Keysar, Stephen B., additional, Hall, Spencer C., additional, Bimali, Anamol, additional, Jimeno, Antonio, additional, Wang, Xiao‐Jing, additional, and Young, Christian D., additional

Published
2022
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37. Deletion of p53 and Hyper-Activation of PIK3CA in Keratin-15+ Stem Cells Lead to the Development of Spontaneous Squamous Cell Carcinoma

Author

Chen, Samantha M. Y., primary, Li, Bian, additional, Nicklawsky, Andrew G., additional, Krinsky, Alexandra L., additional, Brunetti, Tonya, additional, Woolaver, Rachel A., additional, Wang, Xiaoguang, additional, Chen, Zhangguo, additional, Young, Christian D., additional, Gao, Dexiang, additional, Wang, Xiao-Jing, additional, and Wang, Jing H., additional

Published
2020
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40. Correction: Association of FGFR1 with ERα Maintains Ligand-Independent ER Transcription and Mediates Resistance to Estrogen Deprivation in ER+ Breast Cancer

Author

Formisano, Luigi, primary, Stauffer, Kimberly M., additional, Young, Christian D., additional, Bhola, Neil E., additional, Guerrero-Zotano, Angel L., additional, Jansen, Valerie M., additional, Estrada, Mónica M., additional, Hutchinson, Katherine E., additional, Giltnane, Jennifer M., additional, Schwarz, Luis J., additional, Lu, Yao, additional, Balko, Justin M., additional, Deas, Olivier, additional, Cairo, Stefano, additional, Judde, Jean-Gabriel, additional, Mayer, Ingrid A., additional, Sanders, Melinda, additional, Dugger, Teresa C., additional, Bianco, Roberto, additional, Stricker, Thomas, additional, and Arteaga, Carlos L., additional

Published
2019
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41. Smad7 Promotes Healing of Radiotherapy-Induced Oral Mucositis without Compromising Oral Cancer Therapy in a Xenograft Mouse Model

Author

Luo, Jingjing, primary, Bian, Li, additional, Blevins, Melanie A., additional, Wang, Dongyan, additional, Liang, Chao, additional, Du, Danfeng, additional, Wu, Fanglong, additional, Holwerda, Barry, additional, Zhao, Rui, additional, Raben, David, additional, Zhou, Hongmei, additional, Young, Christian D., additional, and Wang, Xiao-Jing, additional

Published
2019
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45. Association of FGFR1 with ERα Maintains Ligand-Independent ER Transcription and Mediates Resistance to Estrogen Deprivation in ER+ Breast Cancer

Author

Formisano, Luigi, primary, Stauffer, Kimberly M., additional, Young, Christian D., additional, Bhola, Neil E., additional, Guerrero-Zotano, Angel L., additional, Jansen, Valerie M., additional, Estrada, Mónica M., additional, Hutchinson, Katherine E., additional, Giltnane, Jennifer M., additional, Schwarz, Luis J., additional, Lu, Yao, additional, Balko, Justin M., additional, Deas, Olivier, additional, Cairo, Stefano, additional, Judde, Jean-Gabriel, additional, Mayer, Ingrid A., additional, Sanders, Melinda, additional, Dugger, Teresa C., additional, Bianco, Roberto, additional, Stricker, Thomas, additional, and Arteaga, Carlos L., additional

Published
2017
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46. Genomic profiling of ER+breast cancers after short-term estrogen suppression reveals alterations associated with endocrine resistance

Author

Giltnane, Jennifer M., primary, Hutchinson, Katherine E., additional, Stricker, Thomas P., additional, Formisano, Luigi, additional, Young, Christian D., additional, Estrada, Monica V., additional, Nixon, Mellissa J., additional, Du, Liping, additional, Sanchez, Violeta, additional, Ericsson, Paula Gonzalez, additional, Kuba, Maria G., additional, Sanders, Melinda E., additional, Mu, Xinmeng J., additional, Van Allen, Eliezer M., additional, Wagle, Nikhil, additional, Mayer, Ingrid A., additional, Abramson, Vandana, additional, Gόmez, Henry, additional, Rizzo, Monica, additional, Toy, Weiyi, additional, Chandarlapaty, Sarat, additional, Mayer, Erica L., additional, Christiansen, Jason, additional, Murphy, Danielle, additional, Fitzgerald, Kerry, additional, Wang, Kai, additional, Ross, Jeffrey S., additional, Miller, Vincent A., additional, Stephens, Phillip J., additional, Yelensky, Roman, additional, Garraway, Levi, additional, Shyr, Yu, additional, Meszoely, Ingrid, additional, Balko, Justin M., additional, and Arteaga, Carlos L., additional

Published
2017
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