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1. Gain-of-Function RHOA Mutations Promote Focal Adhesion Kinase Activation and Dependency in Diffuse Gastric Cancer

Author

Zhang, Haisheng, Schaefer, Antje, Wang, Yichen, Hodge, Richard G, Blake, Devon R, Diehl, J Nathaniel, Papageorge, Alex G, Stachler, Matthew D, Liao, Jennifer, Zhou, Jin, Wu, Zhong, Akarca, Fahire G, de Klerk, Leonie K, Derks, Sarah, Pierobon, Mariaelena, Hoadley, Katherine A, Wang, Timothy C, Church, George, Wong, Kwok-Kin, Petricoin, Emanuel F, Cox, Adrienne D, Lowy, Douglas R, Der, Channing J, and Bass, Adam J

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Digestive Diseases, Cancer, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, 3T3 Cells, Animals, Antigens, CD, COS Cells, Cadherins, Chlorocebus aethiops, Focal Adhesion Kinase 1, Gain of Function Mutation, Gastric Mucosa, HEK293 Cells, Humans, Mice, Protein Kinase Inhibitors, Quinolones, Signal Transduction, Stomach Neoplasms, Sulfones, Xenograft Model Antitumor Assays, rhoA GTP-Binding Protein, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Diffuse gastric cancer (DGC) is a lethal malignancy lacking effective systemic therapy. Among the most provocative recent results in DGC has been that of highly recurrent missense mutations in the GTPase RHOA. The function of these mutations has remained unresolved. We demonstrate that RHOAY42C, the most common RHOA mutation in DGC, is a gain-of-function oncogenic mutant, and that expression of RHOAY42C with inactivation of the canonical tumor suppressor Cdh1 induces metastatic DGC in a mouse model. Biochemically, RHOAY42C exhibits impaired GTP hydrolysis and enhances interaction with its effector ROCK. RHOA Y42C mutation and Cdh1 loss induce actin/cytoskeletal rearrangements and activity of focal adhesion kinase (FAK), which activates YAP-TAZ, PI3K-AKT, and β-catenin. RHOAY42C murine models were sensitive to FAK inhibition and to combined YAP and PI3K pathway blockade. These results, coupled with sensitivity to FAK inhibition in patient-derived DGC cell lines, nominate FAK as a novel target for these cancers. SIGNIFICANCE: The functional significance of recurrent RHOA mutations in DGC has remained unresolved. Through biochemical studies and mouse modeling of the hotspot RHOAY42C mutation, we establish that these mutations are activating, detail their effects upon cell signaling, and define how RHOA-mediated FAK activation imparts sensitivity to pharmacologic FAK inhibitors.See related commentary by Benton and Chernoff, p. 182.This article is highlighted in the In This Issue feature, p. 161.

Published
2020

2. Determining the ERK-regulated phosphoproteome driving KRAS-mutant cancer

Author

Klomp, Jennifer E., primary, Diehl, J. Nathaniel, additional, Klomp, Jeffrey A., additional, Edwards, A. Cole, additional, Yang, Runying, additional, Morales, Alexis J., additional, Taylor, Khalilah E., additional, Drizyte-Miller, Kristina, additional, Bryant, Kirsten L., additional, Schaefer, Antje, additional, Johnson, Jared L., additional, Huntsman, Emily M., additional, Yaron, Tomer M., additional, Pierobon, Mariaelena, additional, Baldelli, Elisa, additional, Prevatte, Alex W., additional, Barker, Natalie K., additional, Herring, Laura E., additional, Petricoin, Emanuel F., additional, Graves, Lee M., additional, Cantley, Lewis C., additional, Cox, Adrienne D., additional, Der, Channing J., additional, and Stalnecker, Clint A., additional

Published
2024
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4. Recurrent RhoGAP gene fusion CLDN18-ARHGAP26 promotes RHOA activation and focal adhesion kinase and YAP-TEAD signalling in diffuse gastric cancer

Author

Zhang, Feifei, primary, Sahu, Varun, additional, Peng, Ke, additional, Wang, Yichen, additional, Li, Tianxia, additional, Bala, Pratyusha, additional, Aitymbayev, Daulet, additional, Sahgal, Pranshu, additional, Schaefer, Antje, additional, Der, Channing J, additional, Ryeom, Sandra, additional, Yoon, Sam, additional, Sethi, Nilay, additional, Bass, Adam J, additional, and Zhang, Haisheng, additional

Published
2024
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5. RHOA L57V drives the development of diffuse gastric cancer through IGF1R-PAK1-YAP1 signaling

Author

Schaefer, Antje, primary, Hodge, Richard G., additional, Zhang, Haisheng, additional, Hobbs, G. Aaron, additional, Dilly, Julien, additional, Huynh, Minh V., additional, Goodwin, Craig M., additional, Zhang, Feifei, additional, Diehl, J. Nathaniel, additional, Pierobon, Mariaelena, additional, Baldelli, Elisa, additional, Javaid, Sehrish, additional, Guthrie, Karson, additional, Rashid, Naim U., additional, Petricoin, Emanuel F., additional, Cox, Adrienne D., additional, Hahn, William C., additional, Aguirre, Andrew J., additional, Bass, Adam J., additional, and Der, Channing J., additional

Published
2023
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6. RHOAL57V drives the development of diffuse gastric cancer through IGF1R-PAK1-YAP1 signaling.

Author

Schaefer, Antje, Hodge, Richard G., Zhang, Haisheng, Hobbs, G. Aaron, Dilly, Julien, Huynh, Minh V., Goodwin, Craig M., Zhang, Feifei, Diehl, J. Nathaniel, Pierobon, Mariaelena, Baldelli, Elisa, Javaid, Sehrish, Guthrie, Karson, Rashid, Naim U., Petricoin, Emanuel F., Cox, Adrienne D., Hahn, William C., Aguirre, Andrew J., Bass, Adam J., and Der, Channing J.

Subjects
STOMACH cancer, CELL receptors, GUANOSINE triphosphatase, CELL adhesion, CYTOSKELETON, RAS oncogenes, CADHERINS
Abstract

Cancer-associated mutations in the guanosine triphosphatase (GTPase) RHOA are found at different locations from the mutational hotspots in the structurally and biochemically related RAS. Tyr42-to-Cys (Y42C) and Leu57-to-Val (L57V) substitutions are the two most prevalent RHOA mutations in diffuse gastric cancer (DGC). RHOAY42C exhibits a gain-of-function phenotype and is an oncogenic driver in DGC. Here, we determined how RHOAL57V promotes DGC growth. In mouse gastric organoids with deletion of Cdh1, which encodes the cell adhesion protein E-cadherin, the expression of RHOAL57V, but not of wild-type RHOA, induced an abnormal morphology similar to that of patient-derived DGC organoids. RHOAL57V also exhibited a gain-of-function phenotype and promoted F-actin stress fiber formation and cell migration. RHOAL57V retained interaction with effectors but exhibited impaired RHOA-intrinsic and GAP-catalyzed GTP hydrolysis, which favored formation of the active GTP-bound state. Introduction of missense mutations at KRAS residues analogous to Tyr42 and Leu57 in RHOA did not activate KRAS oncogenic potential, indicating distinct functional effects in otherwise highly related GTPases. Both RHOA mutants stimulated the transcriptional co-activator YAP1 through actin dynamics to promote DGC progression; however, RHOAL57V additionally did so by activating the kinases IGF1R and PAK1, distinct from the FAK-mediated mechanism induced by RHOAY42C. Our results reveal that RHOAL57V and RHOAY42C drive the development of DGC through distinct biochemical and signaling mechanisms. Editor's summary: Mutations in the GTPase RHOA are common in a type of aggressive, hereditary gastric cancer caused by loss of CDH1, which encodes a cell adhesion receptor. Schaefer et al. found that the two most common RHOA mutations drive the development and progression of this cancer in distinct ways (see also the Focus by Benton and Chernoff). Both the Y42C and L57V mutations conferred a similar gain-of-function phenotype that promoted the interaction of RHOA with the actin cytoskeleton and activation of the transcriptional coactivator YAP1 to promote malignant transformation, growth, and cell motility in Cdh1-deficient mouse-derived gastric organoids. However, distinct from Y42C, L57V engaged the kinases PAK1 and IGF1R, and inhibition of either kinase suppressed the growth of organoids. These results reveal potential drug targets in the treatment of gastric cancer. —Leslie K. Ferrarelli [ABSTRACT FROM AUTHOR]

Published
2023
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7. Supplementary Video S1 from Gain-of-Function RHOA Mutations Promote Focal Adhesion Kinase Activation and Dependency in Diffuse Gastric Cancer

Author

Zhang, Haisheng, primary, Schaefer, Antje, primary, Wang, Yichen, primary, Hodge, Richard G., primary, Blake, Devon R., primary, Diehl, J. Nathaniel, primary, Papageorge, Alex G., primary, Stachler, Matthew D., primary, Liao, Jennifer, primary, Zhou, Jin, primary, Wu, Zhong, primary, Akarca, Fahire G., primary, de Klerk, Leonie K., primary, Derks, Sarah, primary, Pierobon, Mariaelena, primary, Hoadley, Katherine A., primary, Wang, Timothy C., primary, Church, George, primary, Wong, Kwok-Kin, primary, Petricoin, Emanuel F., primary, Cox, Adrienne D., primary, Lowy, Douglas R., primary, Der, Channing J., primary, and Bass, Adam J., primary

Published
2023
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8. Supplementary Table S4 from Gain-of-Function RHOA Mutations Promote Focal Adhesion Kinase Activation and Dependency in Diffuse Gastric Cancer

Author

Zhang, Haisheng, primary, Schaefer, Antje, primary, Wang, Yichen, primary, Hodge, Richard G., primary, Blake, Devon R., primary, Diehl, J. Nathaniel, primary, Papageorge, Alex G., primary, Stachler, Matthew D., primary, Liao, Jennifer, primary, Zhou, Jin, primary, Wu, Zhong, primary, Akarca, Fahire G., primary, de Klerk, Leonie K., primary, Derks, Sarah, primary, Pierobon, Mariaelena, primary, Hoadley, Katherine A., primary, Wang, Timothy C., primary, Church, George, primary, Wong, Kwok-Kin, primary, Petricoin, Emanuel F., primary, Cox, Adrienne D., primary, Lowy, Douglas R., primary, Der, Channing J., primary, and Bass, Adam J., primary

Published
2023
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9. Data from Gain-of-Function RHOA Mutations Promote Focal Adhesion Kinase Activation and Dependency in Diffuse Gastric Cancer

Author

Zhang, Haisheng, primary, Schaefer, Antje, primary, Wang, Yichen, primary, Hodge, Richard G., primary, Blake, Devon R., primary, Diehl, J. Nathaniel, primary, Papageorge, Alex G., primary, Stachler, Matthew D., primary, Liao, Jennifer, primary, Zhou, Jin, primary, Wu, Zhong, primary, Akarca, Fahire G., primary, de Klerk, Leonie K., primary, Derks, Sarah, primary, Pierobon, Mariaelena, primary, Hoadley, Katherine A., primary, Wang, Timothy C., primary, Church, George, primary, Wong, Kwok-Kin, primary, Petricoin, Emanuel F., primary, Cox, Adrienne D., primary, Lowy, Douglas R., primary, Der, Channing J., primary, and Bass, Adam J., primary

Published
2023
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10. Supplementary Figures from Gain-of-Function RHOA Mutations Promote Focal Adhesion Kinase Activation and Dependency in Diffuse Gastric Cancer

Author

Zhang, Haisheng, primary, Schaefer, Antje, primary, Wang, Yichen, primary, Hodge, Richard G., primary, Blake, Devon R., primary, Diehl, J. Nathaniel, primary, Papageorge, Alex G., primary, Stachler, Matthew D., primary, Liao, Jennifer, primary, Zhou, Jin, primary, Wu, Zhong, primary, Akarca, Fahire G., primary, de Klerk, Leonie K., primary, Derks, Sarah, primary, Pierobon, Mariaelena, primary, Hoadley, Katherine A., primary, Wang, Timothy C., primary, Church, George, primary, Wong, Kwok-Kin, primary, Petricoin, Emanuel F., primary, Cox, Adrienne D., primary, Lowy, Douglas R., primary, Der, Channing J., primary, and Bass, Adam J., primary

Published
2023
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11. Supplementary Table from Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth of HRAS Mutant Head and Neck Squamous Cell Carcinoma

Author

Javaid, Sehrish, primary, Schaefer, Antje, primary, Goodwin, Craig M., primary, Nguyen, Victoria V., primary, Massey, Frances L., primary, Pierobon, Mariaelena, primary, Gambrell-Sanders, Da'Jhnae, primary, Waters, Andrew M., primary, Lambert, Kathryn N., primary, Diehl, J. Nathaniel, primary, Hobbs, G. Aaron, primary, Wood, Kris C., primary, Petricoin, Emanuel F., primary, Der, Channing J., primary, and Cox, Adrienne D., primary

Published
2023
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12. Data from Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth of HRAS Mutant Head and Neck Squamous Cell Carcinoma

Author

Javaid, Sehrish, primary, Schaefer, Antje, primary, Goodwin, Craig M., primary, Nguyen, Victoria V., primary, Massey, Frances L., primary, Pierobon, Mariaelena, primary, Gambrell-Sanders, Da'Jhnae, primary, Waters, Andrew M., primary, Lambert, Kathryn N., primary, Diehl, J. Nathaniel, primary, Hobbs, G. Aaron, primary, Wood, Kris C., primary, Petricoin, Emanuel F., primary, Der, Channing J., primary, and Cox, Adrienne D., primary

Published
2023
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13. Supplementary Methods from Gain-of-Function RHOA Mutations Promote Focal Adhesion Kinase Activation and Dependency in Diffuse Gastric Cancer

Author

Zhang, Haisheng, primary, Schaefer, Antje, primary, Wang, Yichen, primary, Hodge, Richard G., primary, Blake, Devon R., primary, Diehl, J. Nathaniel, primary, Papageorge, Alex G., primary, Stachler, Matthew D., primary, Liao, Jennifer, primary, Zhou, Jin, primary, Wu, Zhong, primary, Akarca, Fahire G., primary, de Klerk, Leonie K., primary, Derks, Sarah, primary, Pierobon, Mariaelena, primary, Hoadley, Katherine A., primary, Wang, Timothy C., primary, Church, George, primary, Wong, Kwok-Kin, primary, Petricoin, Emanuel F., primary, Cox, Adrienne D., primary, Lowy, Douglas R., primary, Der, Channing J., primary, and Bass, Adam J., primary

Published
2023
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14. Supplementary Data from Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth of HRAS Mutant Head and Neck Squamous Cell Carcinoma

Author

Javaid, Sehrish, primary, Schaefer, Antje, primary, Goodwin, Craig M., primary, Nguyen, Victoria V., primary, Massey, Frances L., primary, Pierobon, Mariaelena, primary, Gambrell-Sanders, Da'Jhnae, primary, Waters, Andrew M., primary, Lambert, Kathryn N., primary, Diehl, J. Nathaniel, primary, Hobbs, G. Aaron, primary, Wood, Kris C., primary, Petricoin, Emanuel F., primary, Der, Channing J., primary, and Cox, Adrienne D., primary

Published
2023
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15. Supplementary Figure from Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth of HRAS Mutant Head and Neck Squamous Cell Carcinoma

Author

Javaid, Sehrish, primary, Schaefer, Antje, primary, Goodwin, Craig M., primary, Nguyen, Victoria V., primary, Massey, Frances L., primary, Pierobon, Mariaelena, primary, Gambrell-Sanders, Da'Jhnae, primary, Waters, Andrew M., primary, Lambert, Kathryn N., primary, Diehl, J. Nathaniel, primary, Hobbs, G. Aaron, primary, Wood, Kris C., primary, Petricoin, Emanuel F., primary, Der, Channing J., primary, and Cox, Adrienne D., primary

Published
2023
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16. Supplementary Data from Aberrant Expression and Subcellular Localization of ECT2 Drives Colorectal Cancer Progression and Growth

Author

Cook, Danielle R., primary, Kang, Melissa, primary, Martin, Timothy D., primary, Galanko, Joseph A., primary, Loeza, Gabriela H., primary, Trembath, Dimitri G., primary, Justilien, Verline, primary, Pickering, Karen A., primary, Vincent, David F., primary, Jarosch, Armin, primary, Jurmeister, Philipp, primary, Waters, Andrew M., primary, Hibshman, Priya S., primary, Campbell, Andrew D., primary, Ford, Catriona A., primary, Keku, Temitope O., primary, Yeh, Jen Jen, primary, Lee, Michael S., primary, Cox, Adrienne D., primary, Fields, Alan P., primary, Sandler, Robert S., primary, Sansom, Owen J., primary, Sers, Christine, primary, Schaefer, Antje, primary, and Der, Channing J., primary

Published
2023
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17. Supplementary Figures from Aberrant Expression and Subcellular Localization of ECT2 Drives Colorectal Cancer Progression and Growth

Author

Cook, Danielle R., primary, Kang, Melissa, primary, Martin, Timothy D., primary, Galanko, Joseph A., primary, Loeza, Gabriela H., primary, Trembath, Dimitri G., primary, Justilien, Verline, primary, Pickering, Karen A., primary, Vincent, David F., primary, Jarosch, Armin, primary, Jurmeister, Philipp, primary, Waters, Andrew M., primary, Hibshman, Priya S., primary, Campbell, Andrew D., primary, Ford, Catriona A., primary, Keku, Temitope O., primary, Yeh, Jen Jen, primary, Lee, Michael S., primary, Cox, Adrienne D., primary, Fields, Alan P., primary, Sandler, Robert S., primary, Sansom, Owen J., primary, Sers, Christine, primary, Schaefer, Antje, primary, and Der, Channing J., primary

Published
2023
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18. Data from Aberrant Expression and Subcellular Localization of ECT2 Drives Colorectal Cancer Progression and Growth

Author

Cook, Danielle R., primary, Kang, Melissa, primary, Martin, Timothy D., primary, Galanko, Joseph A., primary, Loeza, Gabriela H., primary, Trembath, Dimitri G., primary, Justilien, Verline, primary, Pickering, Karen A., primary, Vincent, David F., primary, Jarosch, Armin, primary, Jurmeister, Philipp, primary, Waters, Andrew M., primary, Hibshman, Priya S., primary, Campbell, Andrew D., primary, Ford, Catriona A., primary, Keku, Temitope O., primary, Yeh, Jen Jen, primary, Lee, Michael S., primary, Cox, Adrienne D., primary, Fields, Alan P., primary, Sandler, Robert S., primary, Sansom, Owen J., primary, Sers, Christine, primary, Schaefer, Antje, primary, and Der, Channing J., primary

Published
2023
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19. Functional and biological heterogeneity of KRAS Q61 mutations

Author

Huynh, Minh V., primary, Hobbs, G. Aaron, additional, Schaefer, Antje, additional, Pierobon, Mariaelena, additional, Carey, Leiah M., additional, Diehl, J. Nathaniel, additional, DeLiberty, Jonathan M., additional, Thurman, Ryan D., additional, Cooke, Adelaide R., additional, Goodwin, Craig M., additional, Cook, Joshua H., additional, Lin, Lin, additional, Waters, Andrew M., additional, Rashid, Naim U., additional, Petricoin, Emanuel F., additional, Campbell, Sharon L., additional, Haigis, Kevin M., additional, Simeone, Diane M., additional, Lyssiotis, Costas A., additional, Cox, Adrienne D., additional, and Der, Channing J., additional

Published
2022
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21. Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth of HRAS Mutant Head and Neck Squamous Cell Carcinoma

Author

Javaid, Sehrish, primary, Schaefer, Antje, additional, Goodwin, Craig M., additional, Nguyen, Victoria V., additional, Massey, Frances L., additional, Pierobon, Mariaelena, additional, Gambrell-Sanders, Da'Jhnae, additional, Waters, Andrew M., additional, Lambert, Kathryn N., additional, Diehl, J. Nathaniel, additional, Hobbs, G. Aaron, additional, Wood, Kris C., additional, Petricoin, Emanuel F., additional, Der, Channing J., additional, and Cox, Adrienne D., additional

Published
2022
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22. Aberrant Expression and Subcellular Localization of ECT2 Drives Colorectal Cancer Progression and Growth

Author

Cook, Danielle R., primary, Kang, Melissa, additional, Martin, Timothy D., additional, Galanko, Joseph A., additional, Loeza, Gabriela H., additional, Trembath, Dimitri G., additional, Justilien, Verline, additional, Pickering, Karen A., additional, Vincent, David F., additional, Jarosch, Armin, additional, Jurmeister, Philipp, additional, Waters, Andrew M., additional, Hibshman, Priya S., additional, Campbell, Andrew D., additional, Ford, Catriona A., additional, Keku, Temitope O., additional, Yeh, Jen Jen, additional, Lee, Michael S., additional, Cox, Adrienne D., additional, Fields, Alan P., additional, Sandler, Robert S., additional, Sansom, Owen J., additional, Sers, Christine, additional, Schaefer, Antje, additional, and Der, Channing J., additional

Published
2022
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24. Functional and biological heterogeneity of KRASQ61 mutations.

Author

Huynh, Minh V., Hobbs, G. Aaron, Schaefer, Antje, Pierobon, Mariaelena, Carey, Leiah M., Diehl, J. Nathaniel, DeLiberty, Jonathan M., Thurman, Ryan D., Cooke, Adelaide R., Goodwin, Craig M., Cook, Joshua H., Lin, Lin, Waters, Andrew M., Rashid, Naim U., Petricoin III, Emanuel F., Campbell, Sharon L., Haigis, Kevin M., Simeone, Diane M., Lyssiotis, Costas A., and Cox, Adrienne D.

Subjects
RAS proteins, GUANOSINE triphosphatase, PANCREATIC duct, RAS oncogenes, MISSENSE mutation
Abstract

Missense mutations at the three hotspots in the guanosine triphosphatase (GTPase) RAS—Gly12, Gly13, and Gln61 (commonly known as G12, G13, and Q61, respectively)—occur differentially among the three RAS isoforms. Q61 mutations in KRAS are infrequent and differ markedly in occurrence. Q61H is the predominant mutant (at 57%), followed by Q61R/L/K (collectively 40%), and Q61P and Q61E are the rarest (2 and 1%, respectively). Probability analysis suggested that mutational susceptibility to different DNA base changes cannot account for this distribution. Therefore, we investigated whether these frequencies might be explained by differences in the biochemical, structural, and biological properties of KRASQ61 mutants. Expression of KRASQ61 mutants in NIH 3T3 fibroblasts and RIE-1 epithelial cells caused various alterations in morphology, growth transformation, effector signaling, and metabolism. The relatively rare KRASQ61E mutant stimulated actin stress fiber formation, a phenotype distinct from that of KRASQ61H/R/L/P, which disrupted actin cytoskeletal organization. The crystal structure of KRASQ61E was unexpectedly similar to that of wild-type KRAS, a potential basis for its weak oncogenicity. KRASQ61H/L/R-mutant pancreatic ductal adenocarcinoma (PDAC) cell lines exhibited KRAS-dependent growth and, as observed with KRASG12-mutant PDAC, were susceptible to concurrent inhibition of ERK-MAPK signaling and of autophagy. Our results uncover phenotypic heterogeneity among KRASQ61 mutants and support the potential utility of therapeutic strategies that target KRASQ61 mutant–specific signaling and cellular output. A portrait of rare RAS mutants: Mutations in the RAS family of proteins promote various cancers, of which mutations at Gln61 (also referred to as Q61) are relatively and unexpectedly rare in KRAS. Huynh et al. compared the structural, biochemical, and biological effects of Gln61 mutations in KRAS (see also Sealover and Kortum). The Q61E mutant had weaker metabolic activity and induced greater cell adhesion and less motility than the other mutants, thus potentially explaining the relative rarity of this mutant. Nonetheless, other aspects made Gln61 mutant KRAS pancreatic cancer cells susceptible to the same inhibitors that are currently in trials to treat tumors dependent on the more common KRAS mutants. The findings may both broaden and differentiate treatment strategies for these rarer mutant KRAS–driven tumors. [ABSTRACT FROM AUTHOR]

Published
2022
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25. Targeting p130Cas- and microtubule-dependent MYC regulation sensitizes pancreatic cancer to ERK MAPK inhibition

Author

Waters, Andrew M., primary, Khatib, Tala O., additional, Papke, Bjoern, additional, Goodwin, Craig M., additional, Hobbs, G. Aaron, additional, Diehl, J. Nathaniel, additional, Yang, Runying, additional, Edwards, A. Cole, additional, Walsh, Katherine H., additional, Sulahian, Rita, additional, McFarland, James M., additional, Kapner, Kevin S., additional, Gilbert, Thomas S.K., additional, Stalnecker, Clint A., additional, Javaid, Sehrish, additional, Barkovskaya, Anna, additional, Grover, Kajal R., additional, Hibshman, Priya S., additional, Blake, Devon R., additional, Schaefer, Antje, additional, Nowak, Katherine M., additional, Klomp, Jennifer E., additional, Hayes, Tikvah K., additional, Kassner, Michelle, additional, Tang, Nanyun, additional, Tanaseichuk, Olga, additional, Chen, Kaisheng, additional, Zhou, Yingyao, additional, Kalkat, Manpreet, additional, Herring, Laura E., additional, Graves, Lee M., additional, Penn, Linda Z., additional, Yin, Hongwei H., additional, Aguirre, Andrew J., additional, Hahn, William C., additional, Cox, Adrienne D., additional, and Der, Channing J., additional

Published
2021
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28. Low-Dose Vertical Inhibition of the RAF-MEK-ERK Cascade Causes Apoptotic Death of KRAS Mutant Cancers

Author

Ozkan-Dagliyan, Irem, primary, Diehl, J. Nathaniel, additional, George, Samuel D., additional, Schaefer, Antje, additional, Papke, Bjoern, additional, Klotz-Noack, Kathleen, additional, Waters, Andrew M., additional, Goodwin, Craig M., additional, Gautam, Prson, additional, Pierobon, Mariaelena, additional, Peng, Sen, additional, Gilbert, Thomas S.K., additional, Lin, Kevin H., additional, Dagliyan, Onur, additional, Wennerberg, Krister, additional, Petricoin, Emanuel F., additional, Tran, Nhan L., additional, Bhagwat, Shripad V., additional, Tiu, Ramon V., additional, Peng, Sheng-Bin, additional, Herring, Laura E., additional, Graves, Lee M., additional, Sers, Christine, additional, Wood, Kris C., additional, Cox, Adrienne D., additional, and Der, Channing J., additional

Published
2020
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30. Targeting P130Cas- and Microtubule-Dependent MYC Regulation Sensitizes Pancreatic Cancer to ERK MAPK Inhibition

Author

Waters, Andrew M., primary, Khatib, Tala O., additional, Papke, Bjoern, additional, Goodwin, Craig, additional, Hobbs, G. Aaron, additional, Diehl, J. Nathaniel, additional, Walsh, Katherine H., additional, Sulahian, Rita, additional, McFarland, James, additional, Kapner, Kevin K., additional, Gilbert, Thomas S. K., additional, Stalnecker, Clint A., additional, Javaid, Sehrish, additional, Barkovskaya, Anna, additional, Grover, Kajal R., additional, Blake, Devon R., additional, Schaefer, Antje, additional, Nowak, Katherine M., additional, Klomp, Jennifer E., additional, Hayes, Tikvah K., additional, Kassner, Michelle, additional, Tang, Nanyun, additional, Tanaseichuk, Olga, additional, Chen, Kaisheng, additional, Zhou, Yingyao, additional, Herring, Laura E., additional, Graves, Lee M., additional, Yin, Hongwei, additional, Aguirre, Andrew J., additional, Hahn, William C., additional, Cox, Adrienne D., additional, and Der, Channing J., additional

Published
2020
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31. Inflammation-sensitive myosin-x functionally supports leukocyte extravasation by Cdc42-mediated ICAM-1-rich endothelial filopodia formation

Author

Kroon, Jeffrey, Schaefer, Antje, Van Rijssel, Jos, Hoogenboezem, Mark, Van Alphen, Floris, Hordijk, Peter, Stroes, Erik S.G., Strömblad, Staffan, Van Rheenen, Jacco, Van Buul, Jaap D., Kroon, Jeffrey, Schaefer, Antje, Van Rijssel, Jos, Hoogenboezem, Mark, Van Alphen, Floris, Hordijk, Peter, Stroes, Erik S.G., Strömblad, Staffan, Van Rheenen, Jacco, and Van Buul, Jaap D.

Published
2018

32. Inflammation-sensitive myosin-x functionally supports leukocyte extravasation by Cdc42-mediated ICAM-1-rich endothelial filopodia formation

Author

CMM Sectie Molecular Cancer Research, Cancer, Kroon, Jeffrey, Schaefer, Antje, Van Rijssel, Jos, Hoogenboezem, Mark, Van Alphen, Floris, Hordijk, Peter, Stroes, Erik S.G., Strömblad, Staffan, Van Rheenen, Jacco, Van Buul, Jaap D., CMM Sectie Molecular Cancer Research, Cancer, Kroon, Jeffrey, Schaefer, Antje, Van Rijssel, Jos, Hoogenboezem, Mark, Van Alphen, Floris, Hordijk, Peter, Stroes, Erik S.G., Strömblad, Staffan, Van Rheenen, Jacco, and Van Buul, Jaap D.

Published
2018

33. Inflammation-Sensitive Myosin-X Functionally Supports Leukocyte Extravasation by Cdc42-Mediated ICAM-1–Rich Endothelial Filopodia Formation

Author

Kroon, Jeffrey, primary, Schaefer, Antje, additional, van Rijssel, Jos, additional, Hoogenboezem, Mark, additional, van Alphen, Floris, additional, Hordijk, Peter, additional, Stroes, Erik S. G., additional, Strömblad, Staffan, additional, van Rheenen, Jacco, additional, and van Buul, Jaap D., additional

Published
2018
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37. RHOAL57Vdrives the development of diffuse gastric cancer through IGF1R-PAK1-YAP1 signaling

Author

Schaefer, Antje, Hodge, Richard G., Zhang, Haisheng, Hobbs, G. Aaron, Dilly, Julien, Huynh, Minh V., Goodwin, Craig M., Zhang, Feifei, Diehl, J. Nathaniel, Pierobon, Mariaelena, Baldelli, Elisa, Javaid, Sehrish, Guthrie, Karson, Rashid, Naim U., Petricoin, Emanuel F., Cox, Adrienne D., Hahn, William C., Aguirre, Andrew J., Bass, Adam J., and Der, Channing J.

Published
2023
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39. A local VE-cadherin and Trio-based signaling complex stabilizes endothelial junctions through Rac1

Author

Timmerman, Ilse, primary, Heemskerk, Niels, additional, Kroon, Jeffrey, additional, Schaefer, Antje, additional, van Rijssel, Jos, additional, Hoogenboezem, Mark, additional, van Unen, Jakobus, additional, Goedhart, Joachim, additional, Gadella, Theodorus W. J., additional, Yin, Taofei, additional, Wu, Yi, additional, Huveneers, Stephan, additional, and van Buul, Jaap D., additional

Published
2015
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41. A local VE-cadherin/Trio-based signaling complex stabilizes endothelial junctions through Rac1

Author

Timmerman, Ilse, primary, Heemskerk, Niels, additional, Kroon, Jeffrey, additional, Schaefer, Antje, additional, van Rijssel, Jos, additional, Hoogenboezem, Mark, additional, van Unen, Jakobus, additional, Goedhart, Joachim, additional, Gadella, Theodorus W. J., additional, Yin, Taofei, additional, Wu, Yi, additional, Huveneers, Stephan, additional, and van Buul, Jaap D., additional

Published
2015
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42. Actin-binding proteins differentially regulate endothelial cell stiffness, ICAM-1 function and neutrophil transmigration

Author

Schaefer, Antje, primary, te Riet, Joost, additional, Ritz, Katja, additional, Hoogenboezem, Mark, additional, Anthony, Eloise C., additional, Mul, Frederik P. J., additional, de Vries, Carlie J., additional, Daemen, Mat J., additional, Figdor, Carl G., additional, van Buul, Jaap D., additional, and Hordijk, Peter L., additional

Published
2014
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45. The Human Minor Histocompatibility Antigen1 Is a RhoGAP

Author

de Kreuk, Bart-Jan, primary, Schaefer, Antje, additional, Anthony, Eloise C., additional, Tol, Simon, additional, Fernandez-Borja, Mar, additional, Geerts, Dirk, additional, Pool, Jos, additional, Hambach, Lothar, additional, Goulmy, Els, additional, and Hordijk, Peter L., additional

Published
2013
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