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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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“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
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“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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
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“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]
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“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]
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“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]
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In the citing paper
“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 the citing paper
“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 the citing paper
“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]
In the citing paper
“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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“In human pancreatic ductal adenocarcinoma, YAP/TEAD2 complex with E2F in response to loss of oncogenic RAS signaling and induce cell proliferation and survival 80 .”
BackgroundTEAD Inhibition Overcomes YAP1/TAZ-Driven Primary and Acquired Resistance to KRASG12C Inhibitors
Edwards, A. C., Stalnecker, C. A., Jean Morales, A., Taylor, K. E., Klomp, J. E., Klomp, J. A., Waters, A. M., Sudhakar, N., Hallin, J., Tang, T. T., et al. (2023) · Cancer Research · doi:10.1158/0008-5472.can-23-2994 · Cited by 91
Synthetic Lethal Vulnerabilities in KRAS-Mutant Cancers
Aguirre, A. J., & Hahn, W. C. (2018) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a031518 · Cited by 90
“…KRAS mutations depend on sustained expression of the oncogene for cell proliferation and viability (Podsypanina et al. 2008; Singh et al. 2009; Collins et al. 2012; Ying et al. 2012; Kapoor et al. 2014; Shao et al. 2014; Hayes et al. 2016), making oncogenic KRAS a high-priority therapeutic target.”
BackgroundMethodAddressing intra-tumoral heterogeneity and therapy resistance
Rybinski, B., & Yun, K. (2016) · Oncotarget · doi:10.18632/oncotarget.11875 · Cited by 95
“For example, stiffness activates the Hippo/YAP/ TAZ pathway, which then provides HER2 amplified breast cancer cells with resistance to lapatinib [108].”
BackgroundRaj, N., & Bam, R. (2019) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00159 · Cited by 94
IGF2BP2 promotes the progression of colorectal cancer through a YAP‐dependent mechanism
Cui, J., Tian, J., Wang, W., He, T., Li, X., Gu, C., Wang, L., Wu, J., & Shang, A. (2021) · Cancer Science · doi:10.1111/cas.15083 · Cited by 90
Ideno, N., Yamaguchi, H., Ghosh, B., Gupta, S., Okumura, T., Steffen, D. J., Fisher, C. G., Wood, L. D., Singhi, A. D., Nakamura, M., et al. (2018) · Gastroenterology · doi:10.1053/j.gastro.2018.08.006 · Cited by 80
Dual inhibition of KRASG12D and pan-ERBB is synergistic in pancreatic ductal adenocarcinoma
Gulay, K. C. M., Zhang, X., Pantazopoulou, V., Patel, J., Esparza, E., Pran Babu, D. S., Ogawa, S., Weitz, J., Ng, I., Mose, E. S., et al. (2023) · Cancer Research · doi:10.1158/0008-5472.can-23-1313 · Cited by 89
“Interestingly, both YAP protein and pYAP were increased after treatment, which recapitulated a known resistance mechanism to targeting oncogenic KRAS signaling (25).”
Transcriptional control of subtype switching ensures adaptation and growth of pancreatic cancer
Adams, C. R., Htwe, H. H., Marsh, T., Wang, A. L., Montoya, M., Subbaraj, L., Tward, A. D., Bardeesy, N. M., & Perera, R. M. (2019) · eLife · doi:10.7554/elife.45313 · Cited by 88
“Sustained KRAS* pathway suppression in the iKRAS model was shown to induce significant tumor regression; however, this was often followed by rapid tumor re-growth (Kapoor et al., 2014; Shao et al., 2014).”
BackgroundMethodInfluentialThe MST/Hippo Pathway and Cell Death: A Non-Canonical Affair
Fallahi, E., O’Driscoll, N. A., & Matallanas, D. (2016) · Genes · doi:10.3390/genes7060028 · Cited by 88
“Several works have shown that YAP can mediate oncogenic KRAS in different human tumour types [117,118] and even bypass oncogenic KRAS oncogenic addiction in pancreatic cancer [119].”
BackgroundTNFα-YAP/p65-HK2 axis mediates breast cancer cell migration
Gao, Y., Yang, Y., Yuan, F., Huang, J., Xu, W., Mao, B., Yuan, Z., & Bi, W. (2017) · Oncogenesis · doi:10.1038/oncsis.2017.83 · Cited by 88
The Hippo Signaling Pathway in Cancer: A Cell Cycle Perspective
Xiao, Y., & Dong, J. (2021) · Cancers · doi:10.3390/cancers13246214 · Cited by 84
Rapid idiosyncratic mechanisms of clinical resistance to KRAS G12C inhibition
Tsai, Y., Woodcock, M. G., Azam, S. H., Thorne, L. B., Kanchi, K., Parker, J. S., Vincent, B. G., & Pecot, C. V. (2022) · DOAJ (DOAJ: Directory of Open Access Journals) · Cited by 87
Mokhtari, R. B., Ashayeri, N., Baghaie, L., Sambi, M., Satari, K., Baluch, N., Bosykh, D. A., Szewczuk, M. R., & Chakraborty, S. (2023) · Cancers · doi:10.3390/cancers15133468 · Cited by 92
dNTP metabolism links mechanical cues and YAP/TAZ to cell growth and oncogene‐induced senescence
Santinon, G., Brian, I., Pocaterra, A., Romani, P., Franzolin, E., Rampazzo, C., Bicciato, S., & Dupont, S. (2018) · The EMBO Journal · doi:10.15252/embj.201797780 · Cited by 93
“In more advanced tumours, YAP/ TAZ cooperate with Ras, such that they can even substitute for Ras addiction in well-formed tumours; in this case, YAP/TAZ and Ras converge on regulation of proliferation-associated genes (Kapoor et al , 2014; Shao et al , 2014; Zhang et al , 2014).”
Emerging role of Hippo pathway in gastric and other gastrointestinal cancers
Kang, W. (2016) · World Journal of Gastroenterology · doi:10.3748/wjg.v22.i3.1279 · Cited by 86
Too many targets, not enough patients: rethinking neuroblastoma clinical trials
Fletcher, J. I., Ziegler, D. S., Trahair, T. N., Marshall, G. M., Haber, M., & Norris, M. D. (2018) · Nature reviews. Cancer · doi:10.1038/s41568-018-0003-x · Cited by 86
GLUT and HK: Two primary and essential key players in tumor glycolysis
Yadav, D., Yadav, A., Bhattacharya, S., Dagar, A., Kumar, V., & Rani, R. (2024) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2024.03.001 · Cited by 87
KRAS, YAP, and obesity in pancreatic cancer: A signaling network with multiple loops
Eibl, G., & Rozengurt, E. (2017) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2017.10.007 · Cited by 88
Targeting the Hippo Signaling Pathway for Tissue Regeneration and Cancer Therapy
Juan, W. C., & Hong, W. (2016) · Genes · doi:10.3390/genes7090055 · Cited by 88
“Mechanistically, YAP cooperates with E2F transcription factors to activate a cell cycle and DNA replication program to promote tumor maintenance that does not depend on KRAS expression [113].”
BackgroundRegulation of localization and function of the transcriptional co-activator YAP by angiomotin
Moleirinho, S., Hoxha, S., Mandati, V., Curtale, G., Troutman, S. A., Ehmer, U., & Kissil, J. L. (2017) · eLife · doi:10.7554/elife.23966 · Cited by 86
“Importantly, recent studies revealed YAP plays a key role in developing resistance to RAF- and MEK-targeted therapies in lung and colon cancer cells (Lin et al., 2015) and cancer relapse in KRAS-driven colon and pancreatic can- cers (Kapoor et al., 2014; Shao et al., 2014).”
Cortés, E., Lachowski, D., Robinson, B. K., Sarper, M., Teppo, J., Thorpe, S. D., Lieberthal, T. J., Iwamoto, K., Lee, D. A., Okada, M., et al. (2018) · EMBO Reports · doi:10.15252/embr.201846557 · Cited by 84
“YAP activity has been shown to promote PDAC independently of KRas mutations [54], and hence, this proposed feedback cycle may be integral to this phenomenon.”
eIF5A-PEAK1 Signaling Regulates YAP1/TAZ Protein Expression and Pancreatic Cancer Cell Growth
Strnádel, J., Choi, S., Fujimura, K., Wang, H., Zhang, W., Wyse, M. M., Wright, T., Gross, E. T. E., Peinado, C. D., Park, H. W., et al. (2017) · Cancer Research · doi:10.1158/0008-5472.can-16-2594 · Cited by 84
“First, KRASinduced upregulation of this pathway may serve to bypass normal anchorage-dependent cell growth control mechanisms and promote significant morphological and hyperplastic responses (10, 18, 20, 23, 24, 28).”
Self-citationA Classical Epithelial State Drives Acute Resistance to KRAS Inhibition in Pancreatic Cancer
Singhal, A., Styers, H. C., Rub, J., Li, Z., Torborg, S. R., Kim, J. Y., Grbovic-Huezo, O., Feng, H., Tarcan, Z. C., Sahin Ozkan, H., et al. (2024) · Cancer Discovery · doi:10.1158/2159-8290.cd-24-0740 · Cited by 84
Murakami, S., Nemazanyy, I., White, S. M., Chen, H., Nguyen, C. D. K., Graham, G. T., Saur, D., Pende, M., & Yi, C. (2019) · Developmental Cell · doi:10.1016/j.devcel.2019.07.022 · Cited by 83
“, 2019b) and previous studies establishing Yap as a main resistance mechanism towards Kras inhibition (Kapoor et al., 2014; Shao et al., 2014), our study further ratifies Yap as a true achilles’ heel and compelling target for Kras mutant pancreatic tumors.”
BackgroundDetermining the ERK-regulated phosphoproteome driving KRAS-mutant cancer
Klomp, J. E., Diehl, J. N., Klomp, J. A., Edwards, A. C., Yang, R., Morales, A. J., Taylor, K. E., Drizyte-Miller, K., Bryant, K. L., Schaefer, A., et al. (2024) · Science · doi:10.1126/science.adk0850 · Cited by 83
“RHOpromotionofactinstressfiberscan activateYAP1( 44 ), a well-validated driver of KRAS independence ( 45 , 46 ).”
BackgroundKnudsen, E. S., Kumarasamy, V. M., Chung, S., Ruiz, A., Vail, P. J., Tzetzo, S. L., Wu, J., Nambiar, R., Sivinski, J., Chauhan, S. S., et al. (2020) · Gut · doi:10.1136/gutjnl-2020-321000 · Cited by 83
“8 Thus, targeting multiple pathways to control oncogenic signalling is likely important for limiting adaptation that emerge after inhibiting critical genetic nodes in PDAC.”
Role of Integrins in Resistance to Therapies Targeting Growth Factor Receptors in Cancer
Silva, E. C. D., Dontenwill, M., Choulier, L., & Lehmann, M. (2019) · Cancers · doi:10.3390/cancers11050692 · Cited by 81
“Studies from two different laboratories conjointly established that YAP and TAZ activation drive mutant KRAS-independent tumor growth and progression [171,172].”
BackgroundDent, P., Booth, L. A., Roberts, J. L., Liu, J., Poklepovic, A. S., Lalani, A. S., Tuveson, D. A., Martinez, J., & Hancock, J. F. (2019) · Oncogene · doi:10.1038/s41388-019-0849-8 · Cited by 80
The Crosstalk between Src and Hippo/YAP Signaling Pathways in Non-Small Cell Lung Cancer (NSCLC)
Hsu, P., Yang, C., Jablons, D. M., & You, L. (2020) · Cancers · doi:10.3390/cancers12061361 · Cited by 85
“Two studies [67,68] found that some K-ras-mutated NSCLC cells relapse after K-ras exhaustion without the re-expression of the K-ras transgene.”
Pettazzoni, P., Viale, A., Shah, P. K., Carugo, A., Ying, H., Wang, H., Genovese, G., Seth, S., Minelli, R., Green, T., et al. (2015) · Cancer Research · doi:10.1158/0008-5472.can-14-1854 · Cited by 83
“An improved and comprehensive understanding of these and additional mechanisms that allow survival of tumors cells despite suppression of mutant KRASmediated signaling (16,47) will define possibly definitive therapeutic strategies.”
BackgroundSelf-citationOncogenic KRAS blockade therapy: renewed enthusiasm and persistent challenges
Tang, D., Kroemer, G., & Kang, R. (2021) · Molecular Cancer · doi:10.1186/s12943-021-01422-7 · Cited by 80
Takeda, M., Yoshida, S., Inoue, T., Sekido, Y., Hata, T., Hamabe, A., Ogino, T., Miyoshi, N., Uemura, M., Yamamoto, H., et al. (2025) · Cancers · doi:10.3390/cancers17030428 · Cited by 82
“Our group has previously re-ported that in a mouse model with inducible KRAS expression, specifically in the pancreas (via doxycycline administration), some tumors recur even with prolonged KRAS inhibition [65].”
Yuan, Y., Li, D., Li, H., Wang, L., TIAN, G., & DONG, Y. (2015) · Molecular Medicine Reports · doi:10.3892/mmr.2015.4550 · Cited by 79
“Yes-associated protein (YAP) overexpression has been reported for several human tumor entities, including prostate, ovarian, colon, liver, lung and pancreatic cancer (8-10).”
BackgroundKulkarni, M., Tan, T. Z., Sulaiman, N. B. S., Lamar, J. M., Bansal, P., Cui, J., Qiao, Y., & Ito, Y. (2018) · Oncotarget · doi:10.18632/oncotarget.24419 · Cited by 78
“Oncogenic co-operation of YAP with E2F or FOS/AP-1 drives KRAS independent recurrence of KRAS-induced pancreatic and lung tumors [34, 35].”
BackgroundHippo Signaling in the Liver – A Long and Ever-Expanding Story
Manmadhan, S., & Ehmer, U. (2019) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00033 · Cited by 80
“Several studies showed that YAP/TEAD co-operate with E2F transcription factors downstream of retinoblastoma signaling to promote proliferation in cancer, including in liver cancer (Ehmer et al., 2014; Kapoor et al., 2014; Ehmer and Sage, 2015; Fitamant et al., 2015; Hiemer et al., 2015; Shi et al., 2016).”
BackgroundYang, Y., Zhang, H., Huang, S., & Chu, Q. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12020709 · Cited by 77
“Studies have reported that the PI3K pathway can be activated by signalings other than KRAS [103], and that amplification and the overexpression of the transcriptional coactivator Yap1 can also drive KRAS-independent PDAC tumor maintenance [104].”
BackgroundGPER is a mechanoregulator of pancreatic stellate cells and the tumor microenvironment
Cortés, E., Sarper, M., Robinson, B. K., Lachowski, D., Chronopoulos, A., Thorpe, S. D., Lee, D. A., & Hernández, A. E. D. R. (2018) · EMBO Reports · doi:10.15252/embr.201846556 · Cited by 81
“Importantly, YAP activation has been recently shown to trigger Kras-independent PDAC maintenance [46], and in Kras-dependent PDAC, YAP is critically required for progression to invasive PDAC in mice [47].”
JNK signaling is converted from anti- to pro-tumor pathway by Ras-mediated switch of Warts activity
Enomoto, M., Kizawa, D., Ohsawa, S., & Igaki, T. (2015) · Developmental Biology · doi:10.1016/j.ydbio.2015.05.001 · Cited by 74
Santana-Codina, N., Chandhoke, A. S., Yu, Q., Małachowska, B., Kuljanin, M., Gikandi, A., Stańczak, M., Gableske, S., Jedrychowski, M. P., Scott, D. A., et al. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.03.021 · Cited by 77
YAP/TAZ Activation Drives Uveal Melanoma Initiation and Progression
Li, H., Li, Q., Dang, K., Ma, S., Cotton, J. L., Yang, S., Zhu, L. J., DENG, A. C., Ip, Y. T., Johnson, R. L., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.03.021 · Cited by 77
“Ras activation is associated with YAP regulation in different tumor contexts (Kapoor et al., 2014; Shao et al., 2014; Garcia-Rendueles et al., 2015).”
Self-citationWang, H., Lu, B., Cabrera, J. C., Zhang, Y., Yang, Z., McAllister, G., Lindeman, A., Reece-Hoyes, J. S., Tallarico, J. A., Russ, C., et al. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.722967 · Cited by 79
“YAP hyper-activation can also overcome KRAS dependence in mouse tumor models (48, 49).”
BackgroundSelf-citationAlternate RASSF1 Transcripts Control SRC Activity, E-Cadherin Contacts, and YAP-Mediated Invasion
Vlahov, N., Scrace, S., Soto, M. S., Grawenda, A. M., Bradley, L., Paňková, D., Papaspyropoulos, A., Yee, K. S. Y., Buffa, F. M., Goding, C. R., et al. (2015) · Current Biology · doi:10.1016/j.cub.2015.09.072 · Cited by 79
“Moreover, RASSF1A activation of the hippo pathway both restricts YAP1 binding to TEAD [6] and is a direct substrate of RAS signaling in the pancreas [7], supporting the potential crosstalk in pancreatic tumor development [8, 9].”
BackgroundClinical Trials and Progress in Metastatic Colon Cancer
Mody, K., & Bekaii‐Saab, T. (2018) · Surgical Oncology Clinics of North America · doi:10.1016/j.soc.2017.11.008 · Cited by 76
Hgf/Met activation mediates resistance to BRAF inhibition in murine anaplastic thyroid cancers
Knauf, J. A., Luckett, K. A., Chen, K.-Y., Voza, F. A., Socci, N. D., Ghossein, R. A., & Fagin, J. A. (2018) · Journal of Clinical Investigation · doi:10.1172/jci120966 · Cited by 77
Mahadevan, K. K., LeBleu, V. S., Ramirez, E. V., Chen, Y., Li, B., Sockwell, A. M., Gagea, M., Sugimoto, H., Sthanam, L. K., Tampe, D., et al. (2023) · Developmental Cell · doi:10.1016/j.devcel.2023.07.025 · Cited by 76
Self-citationClonality and Evolutionary History of Rhabdomyosarcoma
Chen, L., Shern, J. F., Wei, J. S., Yohe, M. E., Song, Y., Hurd, L., Liao, H., Catchpoole, D. R., Skapek, S. X., Barr, F. G., et al. (2015) · PLoS Genetics · doi:10.1371/journal.pgen.1005075 · Cited by 77
Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS
Kitajima, S., Asahina, H., Chen, T., Guo, S., Quiceno, L. G., Cavanaugh, J. D., Merlino, A. A., Tange, S., Terai, H., Kim, J. W., et al. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.08.009 · Cited by 75
“In the other study, tumors that arose after suppression of mutant KRAS expression in a PDAC GEMM were found to have YAP1 amplification (Kapoor et al., 2014).”
Self-citationYAP1 oncogene is a context-specific driver for pancreatic ductal adenocarcinoma
Tu, B., Yao, J., Ferri-Borgogno, S., Zhao, J., Chen, S., Wang, Q., Yan, L., Zhou, X., Zhu, C., Bang, S., et al. (2019) · JCI Insight · doi:10.1172/jci.insight.130811 · Cited by 75
Self-citation
Metadata
- 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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