Yap1 Activation Enables Bypass of Oncogenic Kras Addiction in Pancreatic Cancer
Open accessAbstract
Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible Kras(G12D)-driven mouse model of PDAC has established a critical role for sustained Kras(G12D) expression in tumor maintenance, providing a model to determine the potential for and the underlying mechanisms of Kras(G12D)-independent PDAC recurrence. Here, we show that some tumors undergo spontaneous relapse and are devoid of Kras(G12D) expression and downstream canonical MAPK signaling and instead acquire amplification and overexpression of the transcriptional coactivator Yap1. Functional studies established the role of Yap1 and the transcriptional factor Tead2 in driving Kras(G12D)-independent tumor maintenance. The Yap1/Tead2 complex acts cooperatively with E2F transcription factors to activate a cell cycle and DNA replication program. Our studies, along with corroborating evidence from human PDAC models, portend a novel mechanism of escape from oncogenic Kras addiction in PDAC.
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Activated Yap, through genetic amplification of YAP or WNT5a-mediated dysregulation of the Hippo pathway, enables bypass of Kras suppression in Kras-driven murine pancreatic cancer and lung cancer models.
“Previous studies have demonstrated that activated Yap, through genetic amplification of YAP- or WNT5a-mediated dysregulation of the Hippo pathway, enables bypass of Kras suppression in Kras-driven murine pancreatic cancer and lung cancer models (37–39).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [38]
The Abstract and Results section on enforced Yap1 expression report Yap1 amplification in recurrent murine pancreatic tumors and show that Yap1 can maintain those tumors after oncogenic Kras suppression. Our copy does not establish WNT5a-mediated Hippo dysregulation or bypass in a lung cancer model; its mention of lung metastases is not a lung cancer model. No page numbers are available in the indexed passages. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPrior studies using inducible suppression of KRAS via RNA interference or genetically engineered inducible KrasG12D alleles have suggested that amplification of YAP1 or induction of an epithelial-to-mesenchymal transition can confer a state of RAS independence and overcome KRASG12D suppression.
“Prior studies using inducible suppression of KRAS via RNA interference or genetically engineered inducible KrasG12D alleles (i.e., “iKras” model) have suggested that amplification of YAP1 or induction of an epithelial-to-mesenchymal transition (EMT) can confer a state of RAS independence and overcome KRASG12D suppression (35–38).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [36]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredYAP1 activation, through either gene amplification or activation of a non-canonical WNT pathway, is a major driver for bypassing KRAS dependency in PDAC.
“We had previously identified YAP1 activation, through either gene amplification or activation of a non-canonical WNT pathway, as a major driver for bypassing KRAS dependency in PDAC.9,11”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [9]
The Results section ('Yap1 is amplified in iKras− relapse tumors and required for tumor growth'; page unavailable) supports YAP1 amplification-driven bypass of Kras dependence in PDAC. The cited paper also shows that enforced Yap1 expression permits tumor maintenance after Kras extinction, but the passages do not support activation through a non-canonical WNT pathway as a mechanism. (LLM, conf=0.88)
Experimental — accuracy not yet measuredActivation of YAP1 oncogene drives resistance to genetic inactivation of KRAS* in a GEM model of PDAC, confirmed in KRAS*-driven CRC.
“Using a genetically engineered mouse (GEM) model of PDAC driven by inducible KRASG12D, we recently demonstrated that activation of the YAP1 oncogene drives resistance to genetic inactivation of KRAS∗, a finding further confirmed in KRAS∗-driven colorectal cancer (CRC).”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [9]
The Introduction and Results (page numbers unavailable) describe an inducible KrasG12D mouse model of PDAC in which Yap1 activation enables tumor growth after KrasG12D extinction. The copy does not establish the claimed confirmation in KRAS-driven colorectal cancer; its Discussion mentions KRAS-dependent human cancer cells without identifying them as CRC. (LLM, conf=0.88)
Experimental — accuracy not yet measuredYAP1 is one of the major drivers of bypassing oncogene addiction and promoting acquired resistance to targeted therapies in several cancer types.
“The YAP1 oncogene has been well established as one of the major drivers of bypassing oncogene addiction and promoting acquired resistance to targeted therapies in several cancer types, including pancreatic cancer, lung cancer, colorectal cancer, melanoma, and glioblastoma.9,10,38,39,40”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [9]
The Discussion (page unavailable) reports that Yap1 enables pancreatic tumors to escape dependence on oncogenic Kras and describes this as a potential mechanism of resistance to Kras inhibition. It presents a similar role in other malignancies as a possibility, not an established finding, and does not establish YAP1-driven acquired resistance to targeted therapies across the other cancer types listed. (LLM, conf=0.88)
Experimental — accuracy not yet measured
YAP/TAZ interact with oncogenic KRAS-mediated signaling and modulate the response to KRAS inhibition.
“Similarly, it has long been known that YAP/TAZ interact with oncogenic KRAS-mediated signaling and modulate the response to KRAS inhibition.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [103]
The Results section (‘Enforced Yap1 expression enables tumor maintenance upon KrasG12D extinction in PDAC’; page not provided) reports that Yap1 allowed tumors to resist regression after oncogenic Kras was switched off. The Discussion describes this as a mechanism of resistance to Kras inhibition. The cited evidence concerns Yap1, not TAZ, and tests Kras extinction rather than a KRAS-inhibiting drug. (LLM, conf=0.87)
Experimental — accuracy not yet measuredA mesenchymal-like differentiation state can act as a resistance mechanism to KRAS inhibitors.
“A mesenchymal-like differentiation state can act as a resistance mechanism to KRAS inhibitors [126,128,130].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [130]
In a PDAC mouse model, inactivation of KRAS G12D led to spontaneous tumor relapse.
“An early study of a PDAC mouse model showed that inactivation of KRAS G12D led to spontaneous tumor relapse [103].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [103]
YAP1 amplification and YAP1/TEAD2 signaling enabled relapsed tumors to bypass oncogenic KRAS addiction for tumor maintenance.
“YAP1 amplification and YAP1/TEAD2 signaling enabled relapsed tumors to bypass oncogenic KRAS addiction for tumor maintenance [103].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [103]
In an inducible KrasG12D-driven PDAC model, spontaneous tumor relapse occurred in the majority of animals following genetic extinction of KrasG12D.
“Similarly, our previous work using an inducible KrasG12D-driven PDAC model demonstrated spontaneous tumor relapse in the majority of animals following genetic extinction of KrasG12D.9”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [9]
In pancreatic cancer, KRAS dependency can be bypassed by elevated expression of transcription factor YAP1, which promotes EMT and confers cell-intrinsic resistance to KRAS loss.
“In the context of pancreatic cancer, KRAS dependency can be by-passed by the elevated expression of the transcription factor YAP1, which promotes EMT and confers cell-intrinsic resistance to KRAS loss (84, 85).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [85]
In preclinical models with tumor suppressor loss, withdrawal of mutant Ras signaling leads to tumors that can recur in a Ras-independent manner.
“withdrawal of mutant Ras signaling in preclinical models that include loss of tumor suppressor function leads to tumors that can re-occur in a Ras-independent fashion67.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [67]
Some KRAS-mutant cancer cells, including lung and pancreatic cancer cells, can survive in the absence of the KRAS oncogene.
“some KRAS-mutant cancer cells, including lung (20) and pancreatic cancer cells (21, 22), can survive in the absence of the KRAS oncogene.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [21]
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BackgroundThe Hippo Pathway: Biology and Pathophysiology
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“It has been observed that YAP amplification rescued Kras-mutant pancreatic cancer cells when Kras was inhibited (48).”
BackgroundPancreatic cancer: Advances and challenges
Halbrook, C. J., Lyssiotis, C. A., Pasca di Magliano, M., & Maitra, A. (2023) · Cell · doi:10.1016/j.cell.2023.02.014 · Cited by 1,321 · see citing works
Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth
Zanconato, F., Forcato, M., Battilana, G., Azzolin, L., Quaranta, E., Bodega, B., Rosato, A., Bicciato, S., Cordenonsi, M., & Piccolo, S. (2015) · Nature Cell Biology · doi:10.1038/ncb3216 · Cited by 1,219 · see citing works
Targeting KRAS mutant cancers with a covalent G12C-specific inhibitor
Janes, M. R., Zhang, J., Li, L.-S., Hansen, R., Peters, U., Guo, X., Chen, Y., Babbar, A., Firdaus, S. J., Darjania, L., et al. (2018) · Cell · doi:10.1016/j.cell.2018.01.006 · Cited by 1,172 · see citing works
“…have observed heterogeneous dependence for sustained KRAS expression (<50% addicted) across KRASmutant cancer cell lines (Hayes et al., 2016; Kapoor et al., 2014; Lamba et al., 2014; Patricelli et al., 2016; Shao et al., 2014; Singh et al., 2009; Sunaga et al., 2011; Vartanian et al.,…”
BackgroundSelf-citationYAP/TAZ upstream signals and downstream responses
Totaro, A., Panciera, T., & Piccolo, S. (2018) · Nature Cell Biology · doi:10.1038/s41556-018-0142-z · Cited by 1,086 · see citing works
The emerging roles of YAP and TAZ in cancer
Moroishi, T., Hansen, C. G., & Guan, K. (2015) · Nature reviews. Cancer · doi:10.1038/nrc3876 · Cited by 1,155 · see citing works
Drugging the ‘undruggable’ cancer targets
Dang, C. V., Reddy, E. P., Shokat, K. M., & Soucek, L. (2017) · Nature Reviews Cancer · doi:10.1038/nrc.2017.36 · Cited by 927 · see citing works
“Studies by Ronald DePinho’s group 47 showed that some tumours induced by Kras G12D undergo spontaneous relapse following Kras G12D ablation owing to amplification and overexpression of the Yes-associated protein 1 ( Yap1 ) transcriptional coactivator, which drives Kras G12D -independent tumour…”
Hippo–YAP/TAZ signalling in organ regeneration and regenerative medicine
Moya, I. M., & Halder, G. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0086-y · Cited by 981 · see citing works
Targeting the Hippo pathway in cancer, fibrosis, wound healing and regenerative medicine
Dey, A., Varelas, X., & Guan, K.-L. (2020) · Nature Reviews Drug Discovery · doi:10.1038/s41573-020-0070-z · Cited by 860 · see citing works
KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer
Waters, A. M., & Der, C. J. (2018) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a031435 · Cited by 875 · see citing works
The Hippo Signaling Pathway in Development and Disease
Zheng, Y., & Pan, D. (2019) · Developmental Cell · doi:10.1016/j.devcel.2019.06.003 · Cited by 867 · see citing works
“profiling and chromatin immunoprecipitation analysis confirmed that genes related to cell proliferation and cell death are enriched among all Hippo target genes in both Drosophila and mammals (Kapoor et al., 2014; Oh et al., 2013; Zanconato et al., 2015).”
BackgroundRole of oncogenic KRAS in the diagnosis, prognosis and treatment of pancreatic cancer
Buscail, L., Bournet, B., & Cordelier, P. (2020) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-019-0245-4 · Cited by 721 · see citing works
KRAS and YAP1 Converge to Regulate EMT and Tumor Survival
Shao, D. D., Xue, W., Krall, E. B., Bhutkar, A., Piccioni, F., Wang, X., Schinzel, A. C., Sood, S., Rosenbluh, J., Kim, J. W., et al. (2014) · Cell · doi:10.1016/j.cell.2014.06.004 · Cited by 744 · see citing works
The Hippo effector YAP promotes resistance to RAF- and MEK-targeted cancer therapies
Lin, L., Sabnis, A. J., Chan, E., Olivas, V., Cade, L., Pazarentzos, E., Asthana, S., Neel, D., Yan, J. J., Lu, X., et al. (2015) · Nature Genetics · doi:10.1038/ng.3218 · Cited by 551 · see citing works
Targeting YAP-Dependent MDSC Infiltration Impairs Tumor Progression
Wang, G., Lü, X., Dey, P., Deng, P., Wu, C.-C., Jiang, S., Fang, Z., Zhao, K., Konaparthi, R., Hua, S., et al. (2015) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-0224 · Cited by 556 · see citing works
“Chromatin Immunoprecipitation ChIP was performed as described (26) using YAP1 antibody from Novus.”
Self-citationGenetics and biology of pancreatic ductal adenocarcinoma
Ying, H., Dey, P., Yao, W., Kimmelman, A. C., Draetta, G. F., Maitra, A., & DePinho, R. A. (2016) · Genes & Development · doi:10.1101/gad.275776.115 · Cited by 527 · see citing works
“…importantly, while multiple mechanisms leading to resistance to KRAS inactivation have been identified in various experimental models, these KRAS-bypass pancreatic tumors exhibit expression signatures reminiscent of a subset of human PDACs; namely, the quasimesenchymal subtype (Kapoor et al. 2014).”
InfluentialSelf-citationComprehensive Molecular Characterization of the Hippo Signaling Pathway in Cancer
Wang, Y., Xu, X., Maglic, D., Dill, M. T., Mojumdar, K., Ng, P. K.-S., Jeong, K. J., Tsang, Y. H., Moreno, D., Bhavana, V. H., et al. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.10.001 · Cited by 500 · see citing works
“Other identified associated somatic driver events included EGFR, KRAS, and PDGFR copy number changes, consistent with the reported functional coupling of these pathways with Hippo pathway signaling (Chaib et al., 2017; Kapoor et al., 2014; Lin et al., 2015; Shao et al., 2014).”
BackgroundSelf-citationKurppa, K. J., Liu, Y., To, C., Zhang, T., Fan, M., Vajdi, A., Knelson, E. H., Xie, Y., Lim, K., Cejas, P., et al. (2020) · Cancer Cell · doi:10.1016/j.ccell.2019.12.006 · Cited by 475 · see citing works
“Intriguingly, the ability of YAP to compensate for the loss of dominant oncogene in MAPK-dependent cancers has been previously shown in the context of mutant KRAS-driven NSCLC and pancreatic ductal adenocarcinoma (Kapoor et al., 2014; Shao et al., 2014).”
BackgroundSelf-citationYAP/TAZ Signaling and Resistance to Cancer Therapy
Nguyen, C. D. K., & Yi, C. (2019) · Trends in Cancer · doi:10.1016/j.trecan.2019.02.010 · Cited by 437 · see citing works
“Studies assessing tumor relapse following extinction of oncogenic Kras in a genetically engineered mouse model of advanced Pancreatic Ductal Adenocarcinoma (PDAC), and detected amplification of the Yap gene locus in three out of eight relapsed tumors analyzed [36].”
BackgroundSenescence-Induced Vascular Remodeling Creates Therapeutic Vulnerabilities in Pancreas Cancer
Ruscetti, M., Morris, J. P., Mezzadra, R., Russell, J., Leibold, J., Romesser, P. B., Simon, J., Kulick, A., Ho, Y.-J., Fennell, M., et al. (2020) · Cell · doi:10.1016/j.cell.2020.03.008 · Cited by 424 · see citing works
“KRAS mutations occur in over 90% of human PDAC, and mouse models implicate oncogenic KRAS in initiating and maintaining tumorigenesis as well as the stromal changes that accompany disease progression (Collins et al., 2012a, 2012b; Kapoor et al., 2014).”
Hippo Pathway in Cancer: Aberrant Regulation and Therapeutic Opportunities
Calses, P. C., Crawford, J. J., Lill, J. R., & Dey, A. (2019) · Trends in cancer · doi:10.1016/j.trecan.2019.04.001 · Cited by 423 · see citing works
YAP and TAZ: a signalling hub of the tumour microenvironment
Zanconato, F., Cordenonsi, M., & Piccolo, S. (2019) · Nature reviews. Cancer · doi:10.1038/s41568-019-0168-y · Cited by 379 · see citing works
YAP/TAZ functions and their regulation at a glance
Pocaterra, A., Romani, P., & Dupont, S. (2020) · Journal of Cell Science · doi:10.1242/jcs.230425 · Cited by 368 · see citing works
“…or GNA13 induces YAP/TAZ through the activation of RHO, whereas activation of G-protein subunit alpha S (GNAS) inhibits YAP/TAZ through activation of members of the protein kinase A (PKA) family (Feng et al., 2014; Iglesias-Bartolome et al., 2015; Kim et al., 2013; Yu et al., 2012; 2013; 2014).”
BackgroundWang, S., Zheng, Y., Yang, F., Zhu, L., Zhu, X.-Q., Wang, Z.-F., Wu, X.-L., Zhou, C.-H., Yan, J.-Y., Hu, B.-Y., et al. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00659-4 · Cited by 369 · see citing works
“However, YAP is required for the induction of ADM progression to PanIN, and PanIN progression to pancreatic cancer.87,88 Accumulating studies have demonstrated that YAP is a critical player in pancreatic cancer progression in KRAS mutant mice.88 Active YAP promotes pancreatic tumor tumorigenesis, development, metastas…”
BackgroundSelf-citationKRAS mutation in pancreatic cancer
Luo, J. (2021) · Seminars in Oncology · doi:10.1053/j.seminoncol.2021.02.003 · Cited by 360 · see citing works
“In the context of pancreatic cancer, KRAS dependency can be by-passed by the elevated expression of the transcription factor YAP1, which promotes EMT and confers cell-intrinsic resistance to KRAS loss (84, 85).”
BackgroundSymbiotic Macrophage-Glioma Cell Interactions Reveal Synthetic Lethality in PTEN-Null Glioma
Chen, P., Zhao, D., Li, J., Liang, X., Li, J., Chang, A. H., Henry, V. K., Lan, Z., Spring, D. J., Rao, G., et al. (2019) · Cancer Cell · doi:10.1016/j.ccell.2019.05.003 · Cited by 338 · see citing works
“YAP1 is a key regulator of LOX transcription in GBM, and the Hippo-YAP1 pathway is known to play an important role in cancer progression (Johnson and Halder, 2014; Kapoor et al., 2014).”
BackgroundSelf-citationMcCormick, F. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-2662 · Cited by 320 · see citing works
“Overexpression of YAP1 (YESassociated protein 1) rescued KRAS cells in which KRAS had been knocked down (34), in established tumors in which KRAS had been ablated (35), or in tumor cells that escape fromMEKor BRAF inhibition (36).”
BackgroundMutational dynamics between primary and relapse neuroblastomas
Schramm, A. R., Köster, J., Assenov, Y., Althoff, K., Peifer, M., Mahlow, E., Odersky, A., Beißer, D., Ernst, C., Henssen, A. G., et al. (2015) · Nature Genetics · doi:10.1038/ng.3349 · Cited by 303 · see citing works
Establishment of mouse expanded potential stem cells
Yang, J. P., Ryan, D. J., Wang, W., Tsang, J. C.-H., Lan, G., Masaki, H., Gao, X., Antunes, L., Yu, Y., Zhu, Z., et al. (2017) · Nature · doi:10.1038/nature24052 · Cited by 300 · see citing works
Towards targeting of shared mechanisms of cancer metastasis and therapy resistance
Weiß, F., Lauffenburger, D. A., & Friedl, P. (2022) · Nature reviews. Cancer · doi:10.1038/s41568-021-00427-0 · Cited by 294 · see citing works
Shih, D. J. H., Nayyar, N., Bihun, I. V., Dagogo‐Jack, I., Gill, C. M., Aquilanti, E., Bertalan, M. S., Kaplan, A. B., D’Andrea, M. R., Chukwueke, U. N., et al. (2020) · Nature Genetics · doi:10.1038/s41588-020-0592-7 · Cited by 291 · see citing works
YAP Drives Growth by Controlling Transcriptional Pause Release from Dynamic Enhancers
Galli, G. G., Carrara, M., Yuan, W.-C., Valdes-Quezada, C., Gurung, B., Pepe-Mooney, B., Zhang, T., Geeven, G., Gray, N. S., de Laat, W., et al. (2015) · Molecular Cell · doi:10.1016/j.molcel.2015.09.001 · Cited by 290 · see citing works
“The remarkable effects of Hippo/YAP on organ growth and its potential to crosstalk with multiple oncogenic signaling cascades (Barry et al., 2013; Kapoor et al., 2014) make this pathway a very attractive target for cancer therapeutics.”
Analysis of the role of the Hippo pathway in cancer
Han, Y. (2019) · Journal of Translational Medicine · doi:10.1186/s12967-019-1869-4 · Cited by 290 · see citing works
Molecular alterations and targeted therapy in pancreatic ductal adenocarcinoma
Qian, Y., Gong, Y., Fan, Z., Luo, G., Huang, Q., Deng, S., Cheng, H., Jin, K., Ni, Q., Yu, X., et al. (2020) · Journal of Hematology & Oncology · doi:10.1186/s13045-020-00958-3 · Cited by 312 · see citing works
Transcriptional Co-repressor Function of the Hippo Pathway Transducers YAP and TAZ
Kim, M., Kim, T., Johnson, R. L., & Lim, D. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.03.015 · Cited by 287 · see citing works
“YAP is crucial for cancer development induced by an Lkb1 deficiency, b-catenin activation, or oncogenic Ras mutation (Kapoor et al., 2014; Mohseni et al., 2014; Rosenbluh et al., 2012; Shao et al., 2014).”
BackgroundSelf-citationYAP/TAZ Signaling as a Molecular Link between Fibrosis and Cancer
Noguchi, S. F., Saito, A., & Nagase, T. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19113674 · Cited by 280 · see citing works
“Moreover, YAP can rescue cell death induced by the suppression of KRAS in cancer cells [100,101].”
BackgroundOncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
Santana-Codina, N., Roeth, A. A., Zhang, Y., Yang, A., Mashadova, O., Asara, J. M., Wang, X., Bronson, R. T., Lyssiotis, C. A., Ying, H., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-07472-8 · Cited by 252 · see citing works
Self-citationMechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer
Dilly, J., Hoffman, M. T., Abbassi, L., Li, Z., Paradiso, F., Parent, B. D., Hennessey, C. J., Jordan, A. C., Morgado, M., Dasgupta, S., et al. (2024) · Cancer Discovery · doi:10.1158/2159-8290.cd-24-0177 · Cited by 276 · see citing works
Self-citationPlatelets reduce anoikis and promote metastasis by activating YAP1 signaling
Haemmerle, M., Taylor, M., Gutschner, T., Pradeep, S., Cho, M. S., Sheng, J., Lyons, Y., Nagaraja, A. S., Dood, R. L., Wen, Y., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-00411-z · Cited by 272 · see citing works
Emerging role of tumor cell plasticity in modifying therapeutic response
Qin, S., Jiang, J., Lü, Y., Nice, E. C., Huang, C., Zhang, J., & He, W. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00313-5 · Cited by 274 · see citing works
Self-citationTumors and Mitochondrial Respiration: A Neglected Connection
Viale, A., Corti, D., & Draetta, G. F. (2015) · Cancer Research · doi:10.1158/0008-5472.can-15-0491 · Cited by 265 · see citing works
“These surviving cells were extremely enriched in tumor-initiating cells (16) and eventually were responsible for tumor relapse (19).”
Self-citationNoland, C. L., Gierke, S., Schnier, P. D., Murray, J. M., Sandoval, W. N., Sagolla, M. S., Dey, A., Hannoush, R. N., Fairbrother, W. J., & Cunningham, C. N. (2015) · Structure · doi:10.1016/j.str.2015.11.005 · Cited by 268 · see citing works
“, 2006), and recent data have revealed that YAP is essential for the progression of pancreatic ductal adenocarcinoma in Kras-mutant mice (Kapoor et al., 2014).”
BackgroundHayes, T. K., Neel, N. F., Hu, C., Gautam, P., Chénard, M., Long, B. J., Aziz, M., Kassner, M., Bryant, K. L., Pierobon, M., et al. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.11.011 · Cited by 266 · see citing works
“Together, our data suggest ERK and PI3K inhibitors as a potential clinically relevant combination therapy in KRAS-mutant PDAC.”
BackgroundInfluentialActin remodeling confers BRAF inhibitor resistance to melanoma cells through YAP/TAZ activation
Kim, M. H., Kim, J., Hong, H., Lee, J. J.-K., Lee, J., Jung, E., & Kim, J. (2015) · The EMBO Journal · doi:10.15252/embj.201592081 · Cited by 259 · see citing works
“In line with our results, a recently published study also demonstrated that E2F1 and YAP cooperate to enable bypass of oncogenic KRAS addiction (Kapoor et al , 2014).”
InfluentialGenomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer
Dey, P., Baddour, J., Muller, F., Wu, C. C., Wang, H., Liao, W.-T., Lan, Z., Chen, A., Gutschner, T., Kang, Y., et al. (2017) · Nature · doi:10.1038/nature21052 · Cited by 264 · see citing works
Self-citationYAP/TAZ: Drivers of Tumor Growth, Metastasis, and Resistance to Therapy
Thompson, B. J. (2020) · BioEssays · doi:10.1002/bies.201900162 · Cited by 262 · see citing works
Regulation of TEAD Transcription Factors in Cancer Biology
Huh, H., Kim, D., Jeong, H.-S., & Park, H. (2019) · Cells · doi:10.3390/cells8060600 · Cited by 259 · see citing works
“TEAD2 was shown to act cooperatively with the E2F transcription factor to promote a cell-cycle gene expression program, which enabled the bypass of oncogenic KRAS addiction in PDAC and evoked KRAS-independent tumor relapse [171].”
BackgroundEpithelial memory of inflammation limits tissue damage while promoting pancreatic tumorigenesis
Poggetto, E. D., Ho, I., Balestrieri, C., Yen, E.-Y., Zhang, S.-J., Citron, F., Shah, R., Corti, D., Diaferia, G., Li, C.-Y., et al. (2021) · Science · doi:10.1126/science.abj0486 · Cited by 222 · see citing works
Self-citationTranslational advances in pancreatic ductal adenocarcinoma therapy
Hosein, A. N., Dougan, S. K., Aguirre, A. J., & Maitra, A. (2022) · Nature Cancer · doi:10.1038/s43018-022-00349-2 · Cited by 249 · see citing works
YAP/TAZ as master regulators in cancer: modulation, function and therapeutic approaches
Piccolo, S., Panciera, T., Contessotto, P., & Cordenonsi, M. (2022) · Nature Cancer · doi:10.1038/s43018-022-00473-z · Cited by 250 · see citing works
Molecular Pathogenesis of Pancreatic Cancer
Grant, T. J., Hua, K., & Singh, A. (2016) · Progress in Molecular Biology and Translational Science · doi:10.1016/bs.pmbts.2016.09.008 · Cited by 237 · see citing works
Metabolic networks in mutant KRAS-driven tumours: tissue specificities and the microenvironment
Kerk, S. A., Papagiannakopoulos, T. Y., Shah, Y. M., & Lyssiotis, C. A. (2021) · Nature reviews. Cancer · doi:10.1038/s41568-021-00375-9 · Cited by 238 · see citing works
The Hippo Pathway in Liver Homeostasis and Pathophysiology
Driskill, J. H., & Pan, D. (2020) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-030420-105050 · Cited by 232 · see citing works
“Many studies have identified target genes of YAP/TAZ to be those that control cell proliferation, cell migration, epithelial-mesenchymal transition, extracellular matrix organization, and cytoskeletal organization (30, 39, 40).”
BackgroundYAP Is Essential for Treg-Mediated Suppression of Antitumor Immunity
Ni, X., Tao, J., Barbi, J. J., Chen, Q., Park, B. V., Li, Z., Zhang, N., Lebid, A., Ramaswamy, A., Wei, P., et al. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-17-1124 · Cited by 235 · see citing works
Disease implications of the Hippo/YAP pathway
Plouffe, S. W., Hong, A. W., & Guan, K. (2015) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2015.01.003 · Cited by 229 · see citing works
“A similar study found that in an inducible KRAS-driven PDAC mouse model where removal of KRAS resulted in complete tumor regression, some mice later developed spontaneous tumors due to YAP amplification and increased YAP-TEAD2 transcriptional activity [91].”
ResultSyndecan 1 is a critical mediator of macropinocytosis in pancreatic cancer
Yao, W., Rose, J. L., Wang, W., Seth, S., Jiang, H., Taguchi, A., Liu, J., Yan, L., Kapoor, A., Hou, P., et al. (2019) · Nature · doi:10.1038/s41586-019-1062-1 · Cited by 214 · see citing works
Self-citationPanciera, T., Citron, A., Biagio, D. D., Battilana, G., Gandin, A., Giulitti, S., Forcato, M., Bicciato, S., Panzetta, V., Fusco, S., et al. (2020) · Nature Materials · doi:10.1038/s41563-020-0615-x · Cited by 223 · see citing works
“Our findings offer mechanistic support to previous observations connecting YAP activity to Ras-induced tumorigenesis 23,27–29 .”
Dey, P., Li, J., Zhang, J., Chaurasiya, S., Strom, A., Wang, H., Liao, W.-T., Cavallaro, F., Denz, P., Bernard, V., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0297 · Cited by 213 · see citing works
“On the basis of these findings, we speculated that infiltrating Th2 cells Cytokines Mediated Tumor Progression in PDAC RESEARCH ARTICLE APRIL 2020 CANCER DISCOVERY | 617 Murine T cells are predominantly CD4+ type Analysis of T-cell infiltration (iMC) GATA3+CD4+ T cells infiltrate murine PanIN Pdx1-Cre;LSL-KrasG12D scR…”
BackgroundInfluentialSelf-citationGruber, R., Panayiotou, R., Nye, E. L., Spencer‐Dene, B., Stamp, G., & Behrens, A. (2016) · Gastroenterology · doi:10.1053/j.gastro.2016.05.006 · Cited by 214 · see citing works
“The reliance of established PDAC tumors on KRas expression can be alleviated by up-regulation of the transcriptional regulator YAP1.(19) YAP1 has also been implicated in progression from PanIN to PDAC,(20) but its contribution at the reprogramming stage is unclear.”
BackgroundInfluentialYAP/TAZ as therapeutic targets in cancer
Zanconato, F., Battilana, G., Cordenonsi, M., & Piccolo, S. (2016) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2016.05.002 · Cited by 216 · see citing works
“Yet, some tumors spontaneously relapse in the absence of any KRASG12D overexpression through amplification of the YAP1 locus, as such providing genetic evidence that YAPoverexpressing cellular clones are positively selected upon KRAS-inactivation [26].”
BackgroundTEAD and YAP regulate the enhancer network of human embryonic pancreatic progenitors
Cebola, I., Rodríguez-Seguí, S., Cho, C. H., Bessa, J., Rovira, M., Luengo, M., Chhatriwala, M., Berry, A. A., Ponsa-Cobas, J., Maestro, M., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3160 · Cited by 212 · see citing works
Yes-Associated Protein Mediates Immune Reprogramming in Pancreatic Ductal Adenocarcinoma
Murakami, S., Shahbazian, D., Surana, R., Zhang, W.-Y., Chen, H., Graham, G., White, S. M., Weiner, L., & Yi, C.-L. (2016) · Oncogene · doi:10.1038/onc.2016.288 · Cited by 197 · see citing works
“Subsequent studies showed that YAP could also substitute oncogenic KRAS in promoting the growth of PDAC tumors as well as lung adenocarcinomas (Kapoor et al 2014, Shao et al 2014), and confer resistance to MAPK pathway inhibitors in KRAS or BRAF mutant tumor cells (Hugo et al 2015, Kim et al 2015,…”
BackgroundHagenbeek, T. J., Zbieg, J. R., Hafner, M., Mroue, R., Lacap, J. A., Sodir, N. M., Noland, C. L., Afghani, S., Kishore, A., Bhat, K. P., et al. (2023) · Nature Cancer · doi:10.1038/s43018-023-00577-0 · Cited by 215 · see citing works
Pobbati, A. V., Han, X. Y., Hung, A. W., Seetoh, W.-G., Huda, N., Chen, G.-Y., Kang, C., Chia, C. S. B., Luo, X., Hong, W., et al. (2015) · Structure · doi:10.1016/j.str.2015.09.009 · Cited by 212 · see citing works
“Hyperactivation of TEAD-YAP contributes to various human cancers, such as prostate cancer (Knight et al., 2008) and pancreatic cancer (Hucl et al., 2007; Kapoor et al., 2014).”
McAndrews, K. M., Xiao, F., Chronopoulos, A., LeBleu, V. S., Kugeratski, F. G., & Kalluri, R. (2021) · Life Science Alliance · doi:10.26508/lsa.202000875 · Cited by 216 · see citing works
“…suggest that while inducible extinction of Kras in genetically engineered mouse models results in complete regression of pancreatic tumors in the short term, a subset of those tumors recur in the long term by escaping Kras oncogenic addiction through a YAP1-mediated transcriptional program (23).”
BackgroundTankyrase Inhibitors Target YAP by Stabilizing Angiomotin Family Proteins
Wang, W., Li, N., Li, X., Tran, M. K., Han, X., & Chen, J. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.09.014 · Cited by 208 · see citing works
“Notably, recent studies demonstrated that YAP overexpression promoted resistance to KRAS-, RAF-, and MEK-targeted cancer therapies (Kapoor et al., 2014; Lin et al., 2015; Shao et al., 2014), highlighting the need to target YAP for cancer treatment.”
Hsu, P., Jablons, D. M., Yang, C., & You, L. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20153821 · Cited by 207 · see citing works
“Two studies [95,96] reported that YAP appears to take over K-ras as a cancer driver in K-ras mutant NSCLC and found that some K-ras mutant NSCLC cells relapsed after K-ras extinction without re-expression of the K-ras transgene.”
BackgroundXPO1-dependent nuclear export is a druggable vulnerability in KRAS-mutant lung cancer
Kim, J., McMillan, E., Kim, H. S., Venkateswaran, N., Makkar, G., Rodriguez-Canales, J., Villalobos, P., Neggers, J. E., Mendiratta, S., Wei, S., et al. (2016) · Nature · doi:10.1038/nature19771 · Cited by 202 · see citing works
Song, S., Xie, M., Scott, A. W., Jin, J., Ma, L., Dong, X., Skinner, H. D., Johnson, R. L., Ding, S., & Ajani, J. A. (2017) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-17-0560 · Cited by 200 · see citing works
“YAP1 also crosstalks with and activates many oncogenic signaling pathways, such as KRAS (16, 17), RhoA (18, 19), and Wnt/b-catenin (20, 21), to mediate tumor growth and therapy resistance (15, 20, 22, 23).”
BackgroundSelf-citationOTUB2 Promotes Cancer Metastasis via Hippo-Independent Activation of YAP and TAZ
Zhang, Z., Du, J., Wang, S., Shao, L., Jin, K., Li, F., Wei, B., Ding, W., Fu, P., van Dam, H., et al. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.10.030 · Cited by 195 · see citing works
Oncogenic <i>Kras</i> drives invasion and maintains metastases in colorectal cancer
Boutin, A. T., Liao, W.-T., Wang, M., Hwang, S. S., Karpinets, T. V., Cheung, H., Chu, G. C., Jiang, S., Hu, J., Chang, K., et al. (2017) · Genes & Development · doi:10.1101/gad.293449.116 · Cited by 195 · see citing works
“…of pathways downstream from activated KRAS (Pylayeva-Gupta et al. 2011), the existence of alternative KRAS-independent proliferation/ survival signaling pathways such as YAP (Kapoor et al. 2014), and/or the intratumoral genomic heterogeneity of the KRAS mut allele across the cancer cell population.”
Self-citationKRAS drives immune evasion in a genetic model of pancreatic cancer
Ischenko, I., D’Amico, S., Rao, M., Li, J., Hayman, M. J., Powers, S., Petrenko, O., & Reich, N. C. (2021) · Nature Communications · doi:10.1038/s41467-021-21736-w · Cited by 185 · see citing works
Muthalagu, N., Monteverde, T., Raffo-Iraolagoitia, X., Wiesheu, R., Whyte, D., Hedley, A., Laing, S., Kruspig, B., Upstill-Goddard, R., Shaw, R., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0620 · Cited by 182 · see citing works
“Interestingly, cell lines that lacked increased KRASG12D allelic dosage contained amplifications of alternative oncogenes that encode proteins that may serve as potentially rate-limiting RAS effectors, including MYC, YAP1, and NF-κB (9, 14).”
BackgroundSurvival of pancreatic cancer cells lacking KRAS function
Muzumdar, M. D., Chen, P.-Y., Dorans, K. J., Chung, K. M., Bhutkar, A., Hong, E., Noll, E. M., Sprick, M. R., Trumpp, A., & Jacks, T. (2017) · Nature Communications · doi:10.1038/s41467-017-00942-5 · Cited by 177 · see citing works
KRAS-related proteins in pancreatic cancer
Mann, K. M., Ying, H., Juan, J. M., Jenkins, N. A., & Copeland, N. G. (2016) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2016.09.003 · Cited by 186 · see citing works
“Please cite this article as: Mann, K.M., et al., KRAS-related proteins in pan 10.1016/j.pharmthera.2016.09.003 The survival of these incipient tumor cells may explain the spontaneous tumor recurrence following KRAS extinction in the iKrasmodel (Kapoor et al., 2014).”
BackgroundInfluentialSelf-citationA time for YAP1: Tumorigenesis, immunosuppression and targeted therapy
Shibata, M., Ham, K., & Hoque, M. O. (2018) · International Journal of Cancer · doi:10.1002/ijc.31561 · Cited by 188 · see citing works
“In pancreatic cancer, YAP1 activation enables the bypass of oncogenic KRAS addiction.(62) These insights reinforce that YAP1 plays its oncogenic roles by an independent pathway from KRAS.”
BackgroundA p53 Super-tumor Suppressor Reveals a Tumor Suppressive p53-Ptpn14-Yap Axis in Pancreatic Cancer
Mello, S. S., Valente, L. J., Raj, N., Seoane, J. A., Flowers, B. M., McClendon, J., Bieging-Rolett, K. T., Lee, J., Ivanochko, D., Kozak, M. M., et al. (2017) · Cancer Cell · doi:10.1016/j.ccell.2017.09.007 · Cited by 179 · see citing works
“Recent studies continue to illuminate the contribution of new proteins to PDACdevelopment, such as the Yap transcriptional coactivator, which is essential for progression of preneoplastic lesions to PDAC in mouse models and can even substitute for Kras activation (Kapoor et al., 2014; Zhang et al., 2014).”
InfluentialEmerging evidence on the role of the Hippo/YAP pathway in liver physiology and cancer
Yimlamai, D., Fowl, B. H., & Camargo, F. D. (2015) · Journal of Hepatology · doi:10.1016/j.jhep.2015.07.008 · Cited by 174 · see citing works
“Some phenotypes include intestinal cell fate changes through Klf4 [69], enable pancreatic adenocarcinoma relapse utilizing E2F and TEAD2 [70], specifying the mouse trophectoderm in conjunction with RBP-J [71] as well as facilitating epithelial to mesenchymal transition in lung cancer through co-binding with KRAS/FOS […”
Pearson, J. D., Huang, K., Pacal, M., McCurdy, S. R., Lü, S., Aubry, A., Yu, T., Wadosky, K. M., Zhang, L., Wang, T., et al. (2021) · Cancer Cell · doi:10.1016/j.ccell.2021.06.016 · Cited by 172 · see citing works
“Thus, YAP suppresses YAPoff cancers through TEAD binding and gene activation, identical to the oncogenic mechanism in YAPon cancers (He et al., 2019; Kapoor et al., 2014; Ota and Sasaki, 2008).”
BackgroundSRC tyrosine kinase activates the YAP/TAZ axis and thereby drives tumor growth and metastasis
Lamar, J. M., Xiao, Y., Norton, E., Jiang, Z.-G., Gerhard, G. M., Kooner, S., Warren, J. S. A., & Hynes, R. O. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.004364 · Cited by 169 · see citing works
The Hippo pathway in normal development and cancer
Maugeri‐Saccà, M., & Maria, R. D. (2018) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2017.12.011 · Cited by 165 · see citing works
RAS Synthetic Lethal Screens Revisited: Still Seeking the Elusive Prize?
Downward, J. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-2180 · Cited by 162 · see citing works
“Recently, it has been shown that upregulation of YAP1 function can relieve KRAS oncogene addiction, and it is likely that KRAS deletion from HCT116 or DLD1 colon cancer cells will have subjected them to such a selective event (40, 41).”
BackgroundMarchetti, C., Zyner, K. G., Ohnmacht, S. A., Robson, M. P., Haider, S. M., Morton, J. P., Marsico, G., Vo, T. D., Laughlin, S., Ahmed, A. A., et al. (2018) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.7b01781 · Cited by 166 · see citing works
Control of stem cell renewal and fate by YAP and TAZ
Driskill, J. H., & Pan, D. (2023) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-023-00644-5 · Cited by 165 · see citing works
“YAP drives the recurrence of KRAS -mutant pancreatic cancer after KRAS knockdown 151 , and YAP is required in KRAS -mutant lung cancers that have grown resistant to MEK and TBK/JAK inhibitors 152 .”
BackgroundKitai, H., Ebi, H., Tomida, S., Floros, K. V., Kotani, H., Adachi, Y., Oizumi, S., Nishimura, M., Faber, A. C., & Yano, S. (2016) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-1377 · Cited by 162 · see citing works
miR-375 is involved in Hippo pathway by targeting YAP1/TEAD4-CTGF axis in gastric carcinogenesis
Kang, W., Huang, T., Zhou, Y., Zhang, J., Lung, R. W. M., TONG, J. H. M., Chan, A. W. H., Zhang, B., Wong, C. C., Wu, F., et al. (2018) · Cell Death and Disease · doi:10.1038/s41419-017-0134-0 · Cited by 159 · see citing works
Self-citationChapeau, E. A., Sansregret, L., Galli, G. G., Chêne, P., Wartmann, M., Mourikis, T. P., Jaaks, P., Baltschukat, S., Barbosa, I. A. M., Bauer, D., et al. (2024) · Nature Cancer · doi:10.1038/s43018-024-00754-9 · Cited by 163 · see citing works
“TEAD2 paralog activation by YAP has been shown to compensate for loss of KRAS G12D activity in PDAC tumor models 5 , suggesting a benefit to co-inhibiting KRAS G12D and TEAD2.”
Tumor Microenvironment Remodeling Enables Bypass of Oncogenic KRAS Dependency in Pancreatic Cancer
Hou, P., Kapoor, A., Zhang, Q., Li, J., Wu, C.-J., Li, J., Lan, Z., Tang, M., Ma, X., Ackroyd, J. J., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0597 · Cited by 154 · see citing works
“The iKPC cells were transfected with luciferase-mCherry reporter as described previously (17).”
BackgroundMethodInfluentialSelf-citationControl of Proliferation and Cancer Growth by the Hippo Signaling Pathway
Ehmer, U., & Sage, J. (2015) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-15-0305 · Cited by 156 · see citing works
“Although this method did not specifically inhibit the YAP/TEAD interaction, transcriptional programs that are likely dependent on TEAD were significantly altered in thismodel, including E2F target genes (23, 128), as well as targets of HNF4a and FOXA2 (153).”
BackgroundInfluentialChen, Y.-A., Lu, C.-Y., Cheng, T., Pan, S., Chen, H., & Chang, N. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.00060 · Cited by 155 · see citing works
Chen, C., Yuan, W., Zhou, Q., Shao, B., Guo, Y., Wang, W., Yang, S., Guo, Y., Zhao, L., Dang, Q., et al. (2021) · Theranostics · doi:10.7150/thno.51342 · Cited by 151 · see citing works
YAP1 and its fusion proteins in cancer initiation, progression and therapeutic resistance
Szulzewsky, F., Holland, E. C., & Vasioukhin, V. I. (2021) · Developmental Biology · doi:10.1016/j.ydbio.2020.12.018 · Cited by 154 · see citing works
The Hippo Pathway: Immunity and Cancer
Taha, Z., van Rensburg, H. J. J., & Yang, X. (2018) · Cancers · doi:10.3390/cancers10040094 · Cited by 150 · see citing works
A Small Molecule with Big Impact: MRTX1133 Targets the KRASG12D Mutation in Pancreatic Cancer
Wei, D., Wang, L., Zuo, X., Maitra, A., & Bresalier, R. S. (2023) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-23-2098 · Cited by 163 · see citing works
- Authors
- Kapoor, A., Yao, W., Ying, H., Hua, S., Liewen, A., Wang, Q., Zhong, Y., Wu, C.-J., Sadanandam, A., Hu, B., Chang, Q., Chu, G. C., Al-Khalil, R., Jiang, S., Xia, H., Fletcher-Sananikone, E., Lim, C., Horwitz, G. I., Viale, A., Pettazzoni, P., Sanchez, N., Wang, H., Protopopov, A., Zhang, J., Heffernan, T., Johnson, R. L., Chin, L., Wang, Y. A., Draetta, G., & DePinho, R. A.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Institute of Cancer Research (GB)
- Brigham and Women's Hospital (US)
- Corresponding author
- Ying, Haoqiang
- DePinho, Ronald A.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 158
- Issue
- 1
- Pages
- 185-197
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4109295
- OpenAlex
- W2157912474
- Cited by
- 716
- References
- 59
- Citations by year
- 2026: 29 · 2025: 45 · 2024: 65 · 2023: 67 · 2022: 56 · 2021: 74 · 2020: 63 · 2019: 70 · 2018: 59 · 2017: 60 · 2016: 49 · 2015: 62 · 2014: 16
- FWCI
- 31.06
- Type
- journal article
- Language
- en
- Update notices
- erratum (2019-11-14)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute for Health and Care Research
- National Cancer Institute (CA-16672, U01CA084313, P30CA016672, P01CA117969)
- National Institute of Diabetes and Digestive and Kidney Diseases (R56DK094865, R01DK102611)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- YAP, TEAD2, KRAS G12D, pancreatic ductal adenocarcinoma, tumor recurrence, MAPK signaling, E2F transcription factors, cell cycle, DNA replication, transcriptional coactivator
- MeSH terms
- YAP-Signaling Proteins, TEA Domain Transcription Factors, Adenocarcinoma, Animals, Cell Cycle, Disease Models, Animal, DNA Replication, DNA-Binding Proteins, Humans, Pancreatic Neoplasms, Phosphoproteins, Proto-Oncogene Proteins, Transcription Factors, Proto-Oncogene Proteins p21(ras), ras Proteins, Cell Cycle Proteins, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, Adaptor Proteins, Signal Transducing, E2F Transcription Factors, Mice
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