The DOI matches its Crossref record; 58 of the 59 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Hallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Cluster analysis and display of genome-wide expression patterns
Eisen, M. B., Spellman, P. T., Brown, P. O., & Botstein, D. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.25.14863 · Cited by 16,184
Bioconductor: open software development for computational biology and bioinformatics
Gentleman, R. C., Carey, V. J., Bates, D. M., Bolstad, B., Dettling, M., Dudoit, S., Ellis, B., Gautier, L., Ge, Y., Gentry, J., et al. (2004) · Genome biology · doi:10.1186/gb-2004-5-10-r80 · Cited by 12,082
Self-citationSmyth, G. K. (2004) · Statistical Applications in Genetics and Molecular Biology · doi:10.2202/1544-6115.1027 · Cited by 11,829
Spencer, P. M., Cameron, J. L., & Lin, L. (2000) · Cited by 7,202
Core Signaling Pathways in Human Pancreatic Cancers Revealed by Global Genomic Analyses
Jones, S., Zhang, X., Parsons, D. W., Lin, J. C.-H., Leary, R. J., Angenendt, P., Mankoo, P., Carter, H., Kamiyama, H., Jimeno, A., et al. (2008) · Science · doi:10.1126/science.1164368 · Cited by 3,969
Zhao, B., Wei, X., Li, W., Udan, R. S., Yang, Q., Kim, J., Xie, J., Ikenoue, T., Yu, J., Li, L., et al. (2007) · Genes & Development · doi:10.1101/gad.1602907 · Cited by 3,092
Java Treeview—extensible visualization of microarray data
Saldanha, A. J. (2004) · Bioinformatics · doi:10.1093/bioinformatics/bth349 · Cited by 2,991
Vincent, A., Herman, J. M., Schulick, R., Hruban, R. H., & Goggins, M. (2011) · The Lancet · doi:10.1016/s0140-6736(10)62307-0 · Cited by 2,678
Flagged first, then by citations
1 of the 59 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Items 501–600 of 716
Hsa_circ_0014784-induced YAP1 promoted the progression of pancreatic cancer by sponging miR-214-3p
Liu, B., Gong, Y., Jiang, Q., Wu, S., Han, B., Chen, F., Lin, Q., Wang, P., & Yang, D. (2023) · Cell Cycle · doi:10.1080/15384101.2023.2222519 · Cited by 10
Utilizing Salmonella to treat solid malignancies
Ebelt, N. D., & Manuel, E. R. (2017) · Journal of Surgical Oncology · doi:10.1002/jso.24644 · Cited by 10
“Interestingly, this work has uncovered an alternate progression pathway, which bypasses the requirement for Kras, involving overexpression of the transcriptional coactivator Yap1 that activates cell cycle and DNA replication programs to sustain PDAC growth.(88,89) Early in vitro studies targeting Yap1, using shRNA len…”
BackgroundMohamed, A. D., Shah, N., Hettmer, S., Vargesson, N., & Wackerhage, H. (2018) · Scientific Reports · doi:10.1038/s41598-018-33852-7 · Cited by 10
The clinical relevance of the Hippo pathway in pancreatic ductal adenocarcinoma
Drexler, R., Küchler, M., Wagner, K. C., Reese, T., Feyerabend, B., Kleine, M., & Oldhafer, K. J. (2020) · Journal of Cancer Research and Clinical Oncology · doi:10.1007/s00432-020-03427-z · Cited by 11
Ryu, H. J., Kim, C., Jang, H., Kim, S. I., Shin, S. J., Chung, K. Y., Torres-Cabala, C. A., & Kim, S. K. (2024) · Laboratory Investigation · doi:10.1016/j.labinv.2024.102048 · Cited by 10
An updated patent review of TEAD modulators (2022–present)
Xu, D., Zhong, J., Zeng, Y., Zhang, X., Wang, C., Luo, C., & Xiong, H. (2025) · Expert Opinion on Therapeutic Patents · doi:10.1080/13543776.2025.2522747 · Cited by 9
“In KRAS-driven mouse cancer models, YAP activation compensates for KRAS inhibition, allowing tumor growth independent of KRAS activity [27,28].”
Hao, F. (2022) · Clinical & Translational Oncology · doi:10.1007/s12094-022-02826-7 · Cited by 10
“It was reported that YAP appeared to take over KRAS as a cancer driver in KRASdependent NSCLC and knockdown of YAP affected cancer cell growth in vivo [54].”
BackgroundMurakami, S., White, S. M., McIntosh, A. T., Nguyen, C. D. K., & Yi, C. (2023) · Nature Communications · doi:10.1038/s41467-023-37147-y · Cited by 9
Cellular collusion: cracking the code of immunosuppression and chemo resistance in PDAC
Musiu, C., Lupo, F., Agostini, A., Lionetto, G., Bevere, M., Paiella, S., Carbone, C., Corbo, V., Ugel, S., & Sanctis, F. D. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1341079 · Cited by 9
Fresques, T., & LaBarge, M. A. (2020) · Aging and Cancer · doi:10.1002/aac2.12011 · Cited by 9
Groth, C., Vaid, P. M., Khatpe, A. S., Prashali, N., Ahiya, A., Andrējeva, D., Chakladar, M., Nagarkar, S., Paul, R., Kelkar, D. A., et al. (2020) · G3 Genes Genomes Genetics · doi:10.1534/g3.120.401545 · Cited by 8
“Indeed, YAP overexpression has been causally linked to formation of specific human tumors (Kapoor et al. 2014; Shao et al. 2014).”
BackgroundSyndecan-1 and KRAS Gene Expression Signature Associates With Patient Survival in Pancreatic Cancer
Wu, Y., Huang, H., Fervers, B., & Lu, L. (2020) · Pancreas · doi:10.1097/mpa.0000000000001654 · Cited by 9
Natesh, N. S., White, B. M., Bennett-Boehm, M. M. C., Uz, M., Kandy, R. R. K., Batra, S. K., Mallapragada, S. K., & Rachagani, S. (2021) · Pharmaceutics · doi:10.3390/pharmaceutics13121987 · Cited by 9
Dong, X., Zhang, Y., Sun, Y., Nan, Q., Li, M., Ma, L., Zhang, L., Luo, J., Qi, Y., & Miao, Y. (2023) · BMC Medical Genomics · doi:10.1186/s12920-023-01571-2 · Cited by 8
Wang, S., Diao, S., Kim, H., Zou, J. Y., Li, K., & Koromilas, A. E. (2025) · Communications Biology · doi:10.1038/s42003-025-08740-2 · Cited by 8
“YAP1 displays a pro-survival role in colorectal, lung, and pancreatic cancers with KRAS mutations 16 – 19 .”
Lu, Y., Mu, Y., Chen, J., Guan, X., Guo, L., & Wu, C. (2022) · Theranostics · doi:10.7150/thno.72365 · Cited by 8
Self-citationWei, D., Yuan, L., Xu, X., Wu, C., Huang, Y., Zhang, J., Zhang, J., Jing, T., Liu, Y., & Wang, B. (2024) · Cancer Letters · doi:10.1016/j.canlet.2024.217284 · Cited by 10
Self-citationmicroRNA-205 acts as a tumor suppressor and directly targets YAP1 in glioma
Ji, T., Zhang, X., & Li, W. (2017) · Molecular Medicine Reports · doi:10.3892/mmr.2017.6748 · Cited by 8
“1 (33).”
RetractedPropofol Inhibits Proliferation and Invasion of Stomach Cancer Cells by Regulating miR-205/YAP1 Axis
Xian, X., Wang, Y.-T., & Jiang, X. (2020) · Cancer Management and Research · doi:10.2147/cmar.s270344 · Cited by 8
Self-citationCombined Inhibition of FOSL-1 and YAP Using siRNA-Lipoplexes Reduces the Growth of Pancreatic Tumor
Diego-González, L., Fernández‐Carrera, A., Igea, A., Martínez-Pérez, A., Oliveira, M. E. C. D. R., Gomes, A. C., Guerra, C. E., Barbacid, M., González‐Fernández, Á., & Simón‐Vázquez, R. (2022) · Cancers · doi:10.3390/cancers14133102 · Cited by 8
“Besides, YAP activation can even circumvent the need of KRAS activation in PDAC after the induced extinction of KRAS signaling [15].”
BackgroundRecent insight into the role and therapeutic potential of YAP/TAZ in gastrointestinal cancers
Wang, Y., Chen, H., Yu, J. Q., Kang, W., & To, K. F. (2022) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2022.188787 · Cited by 8
Self-citationAndo, T., Okamoto, K., Shintani, T., Yanamoto, S., Miyauchi, M., Gutkind, J. S., & Kajiya, M. (2022) · Journal of Personalized Medicine · doi:10.3390/jpm12101544 · Cited by 8
“YAP/TEAD2 cooperates with transcription factor E2F and promotes cell cycle gene expression during relapse of KRAS-independent pancreatic ductal adenocarcinoma [103].”
BackgroundScientific Misconduct: Falsification, Fabrication, and Misappropriation of Credit
Vaux, D. L. (2016) · Springer eBooks · doi:10.1007/978-981-287-098-8_26 · Cited by 8
Resistance Mechanisms to Cyclin-Dependent Kinase Inhibitors
Wiedemeyer, W. R. (2018) · Resistance to Targeted Anti-Cancer Therapeutics · doi:10.1007/978-3-319-67932-7_8 · Cited by 7
A Pump-Free Strategy for the Controllable Generation of Alginate Microgels as Cellular Microcarriers
Qin, X., Gan, Z., Liu, H., Tao, T., He, J., Li, X., Shang, D., Li, X., Xie, F., & Qin, J. (2024) · ACS Biomaterials Science & Engineering · doi:10.1021/acsbiomaterials.4c00375 · Cited by 9
YAP, TAZ, and Hippo-Dysregulating Fusion Proteins in Cancer
Driskill, J. H., Dermawan, J. K. T. K., Antonescu, C. R., & Pan, D. (2024) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-061223-094639 · Cited by 8
Nuclear localization of YAP in pancreatic cancer: More players besides Hippo pathway
Xie, Y., Qin, C. Y., Zhang, X., Li, Z., Zhao, B., Li, T., Zhao, Y., Yan, Y., Shi, H., Huang, L., et al. (2025) · Cancer Letters · doi:10.1016/j.canlet.2025.217864 · Cited by 7
Oncogenic YAP sensitizes cells to CHK1 inhibition via CDK4/6 driven G1 acceleration
Gertzmann, D., Presek, C., Mattes, A. L., Sänger, M., Zoller, M., Schülein‐Völk, C., Ade, C. P., Eilers, M., & Gaubatz, S. (2025) · EMBO Reports · doi:10.1038/s44319-025-00514-5 · Cited by 8
“Furthermore, YAP-induced acceleration of fork speed may also be related to E2F activation (Ehmer and Sage, 2016; Kapoor et al, 2014), as E2F-dependent transcription has been shown to regulate overall replication capacity and the rate of DNA synthesis (Pennycook et al, 2020).”
If Virchow and Ehrlich Had Dreamt Together: What the Future Holds for KRAS-Mutant Lung Cancer
Köhler, J., & Janne, P. A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22063025 · Cited by 7
“Among others, these include YAP pathway activation [115] and increased KRAS(G12C) expression via EGFR or aurora kinase signaling [116].”
BackgroundNIPPER, M. J., Xu, Y., Liu, J., Yin, X., Liu, Z., Ye, Z., Zhang, J., Chen, Y., & Wang, P. (2024) · Cells · doi:10.3390/cells13020186 · Cited by 8
“Furthermore, YAP1 activation is an important mechanism in driving pancreatic tumor growth in KRAS-independent PDAC recurrence [14].”
BackgroundSelf-citationInteraction of noncoding RNAs with hippo signaling pathway in cancer cells and cancer stem cells
Abedimanesh, S., Safaralizadeh, R., Jahanafrooz, Z., Najafi, S., Amini, M. A., Nazarloo, S. S., Mahdavi, S. Z. B., Baradaran, B., Jebelli, A., & Mokhtarzadeh, A. A. (2024) · Non-coding RNA Research · doi:10.1016/j.ncrna.2024.06.006 · Cited by 7
“Increased YAP/TAZ activity has been reported in uveal melanomas [41], colo-rectal cancer [42,43], pancreatic ductal adenocarcinoma [44], and lung cancer [45].”
BackgroundRASpecting the oncogene: New pathways to therapeutic advances
Stout, M. C., & Campbell, P. M. (2018) · Biochemical Pharmacology · doi:10.1016/j.bcp.2018.10.022 · Cited by 7
Li, S., Wang, W., Zi, J., Sun, M.-T., Mei, W., Yang, N., Zhang, R., Yu, M., & Xiong, W. (2020) · Translational Cancer Research · doi:10.21037/tcr.2020.04.16 · Cited by 7
“edu/gsea), as previously described (19,20).”
Jia, L., Zhang, Y., Pu, F., Yang, C., Yang, S., Yu, J., Xu, Z., Yang, H., Zhou, Y., & Zhu, S. (2022) · Aging · doi:10.18632/aging.203921 · Cited by 7
“YES-associated protein 1 (YAP1), a critical downstream effector of the Hippo-YAP pathway, has been found to promote PDAC development and progression, even in the absence of oncogenic gene Kras [45].”
BackgroundFerguson, R., Aughton, K., Evans, A., Shaw, V. E., Armstrong, J. A., Ware, A., Bennett, L. G., Costello, E., & Greenhalf, W. (2023) · Current Issues in Molecular Biology · doi:10.3390/cimb45030164 · Cited by 7
Shepard, A., Hoxha, S., Troutman, S. A., Harbaugh, D., Kareta, M. S., & Kissil, J. L. (2021) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2021.100962 · Cited by 7
“In these tumors, YAP/TEAD2 are shown to cooperate with E2F to activate transcriptional programs driving the cell cycle and DNA replication (14).”
BackgroundAdaptive NetworkProfiler for Identifying Cancer Characteristic-Specific Gene Regulatory Networks
Park, H., Shimamura, T., Imoto, S., & Miyano, S. (2017) · Journal of Computational Biology · doi:10.1089/cmb.2017.0120 · Cited by 7
“Furthermore, the activation of the YAP1 in pancreatic cancer is also demonstrated (Kapoor et al., 2014).”
Mahadevan, K. K., Maldonado, A. S., Li, B., Bickert, A. A., Perdyan, A., Kumbhar, S. V., Piya, S., Sockwell, A. M., Morse, S. J., Arian, K. A., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.02.28.640711 · Cited by 7
Self-citationDifferential Response and Resistance to KRAS-Targeted Therapy
Liu, Z., Lenz, H., Yu, J., & Zhang, L. (2025) · Molecular Carcinogenesis · doi:10.1002/mc.23908 · Cited by 7
“An early study of a PDAC mouse model showed that inactivation of KRAS G12D led to spontaneous tumor relapse [106].”
Theardy, M. S., Takeda, M., Sorokin, A., Chen, S., Yang, Z., Wang, X., Kanikarla, P., Coker, O., Nguyen, P., Wei, Y., et al. (2025) · Cell Reports Medicine · doi:10.1016/j.xcrm.2025.102253 · Cited by 6
“9–11 However, the molecular mechanisms underlying the re-activation of the RTK-RAS signaling pathway, as well as the contribution of YAP1 activation to the development of resistance to KRAS* inhibitors, remain to be elucidated.”
InfluentialSelf-citationHu, P., Dou, R., Qi, Z., Liu, G., & Su, Y. (2024) · The Journal of Gene Medicine · doi:10.1002/jgm.70006 · Cited by 6
VCPIP1 facilitates pancreatic adenocarcinoma progression via Hippo/YAP signaling
Liu, Z., Zhang, C., Gai, Y., Su, P., Wang, B., Liu, P., Wang, L., Lin, Y., Zhu, J., & Tan, X. (2025) · Cell Death and Disease · doi:10.1038/s41419-025-07746-2 · Cited by 7
The progress of miR-205 regulating apoptosis in cancer
Chai, D., Du, H., & Shi, Y. (2025) · Frontiers in Oncology · doi:10.3389/fonc.2025.1532659 · Cited by 6
“YAP1 is usually considered as a carcinogen in tumors, which can promote the development of many cancers, including gastric cancer (70).”
Ouyang, H., Wu, S., Li, W., Grey, M. J., Wu, W., & Hansen, S. H. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.113486 · Cited by 6
Cao, F., Jiang, Y., Chang, L., Du, H., Chang, D., Pan, C., Huang, X., Yu, D., Zhang, M., Fan, Y., et al. (2023) · Cell Death and Disease · doi:10.1038/s41419-023-05951-5 · Cited by 6
“The increasing studies, showing these genes as drivers for PDAC development and metastasis, have shown the need of developing therapeutic drugs to target these genes for cancer therapy [25 – 27].”
Acinar Ductal Metaplasia: Yap Fills a Gap
Means, A. L., & Logsdon, C. D. (2016) · Gastroenterology · doi:10.1053/j.gastro.2016.07.022 · Cited by 6
Nuclear localization of TEF3-1 promotes cell cycle progression and angiogenesis in cancer
Teng, K., Deng, C., Xu, J., Men, Q., Lei, T., Di, D., Liu, T., Li, W., & Liu, X. (2016) · Oncotarget · doi:10.18632/oncotarget.7342 · Cited by 7
“In pancreatic cancer, YAP1 also portends a novel mechanism for an oncogenic gene [5].”
Cheng, Y., Huang, H., Han, Y., & Zhu, Y. (2020) · Translational Cancer Research · doi:10.21037/tcr-20-3155 · Cited by 6
“Recent studies have evaluated the aberrantly high expression of YAP that facilitates the development of pancreatic ductal adenocarcinoma, serous ovarian carcinoma, pulmonary small cell carcinoma, urinary bladder carcinoma (6-9).”
BackgroundConvergent Science Physical Oncology
Nieva, J. J., Bethel, K. J., Baas, C., & Kühn, P. (2015) · Convergent Science Physical Oncology · doi:10.1088/2057-1739/1/1/010201 · Cited by 6
Anticipating resistance to KRAS inhibition: a novel role for USP21 in macropinocytosis regulationPreprint
Crawford, H. C. (2021) · Genes & Development · doi:10.1101/gad.348971.121 · Cited by 6
Scribble Deficiency Promotes Pancreatic Ductal Adenocarcinoma Development and Metastasis
Bermejo‐Rodríguez, C., Henríquez, J. A., Caligiuri, G., Teles, S. P., Park, Y., Evans, A., Barrera, L. N., Neeße, A., Grützmann, R., Aust, D. E., et al. (2024) · Cancer Research · doi:10.1158/0008-5472.can-23-3419 · Cited by 5
The Hippo signaling pathway modulates pancreatic tissue homeostasis
Wang, X., Du, J., Li, H., Cao, Z., Cheng, Z., & Wang, Z. (2025) · Cell Death Discovery · doi:10.1038/s41420-025-02636-0 · Cited by 6
Genomic evolution of pancreatic cancer at single-cell resolution
Zhang, H., Sashittal, P., Karnoub, E.-R. R., Jakatdar, A., Umeda, S., Hong, J., Noronha, A. M., Cardenas, A., Erakky, A., McIntyre, C. A., et al. (2026) · Nature Genetics · doi:10.1038/s41588-025-02468-9 · Cited by 5
“This is consistent with mouse models suggesting the loss of oncogenic Kras signaling after PDAC formation is tolerable 27,28 .”
McAndrews, K. M., Mahadevan, K. K., Li, B., Comptdaer, A. M., Sockwell, A. M., Morse, S. J., Kelly, P. J., Patel, S. I., Kirtley, M. L., Diaz, B. A. M., et al. (2026) · The EMBO Journal · doi:10.1038/s44318-026-00854-5 · Cited by 10
“…et al, 2022; Kemp et al, 2023; Mahadevan et al, 2023b), similar to what has been reported with genetic KRAS * suppression and inhibition of the KRAS * and receptor tyrosine kinase (RTK) signaling pathways with small molecule inhibitors (Holohan et al, 2013; Kapoor et al, 2014; Viale et al, 2014).”
Self-citationIn Silico Identification of Dysregulated miRNAs Targeting KRAS Gene in Pancreatic Cancer
Garibaldi-Ríos, A. F., Figuera, L. E., Zúñiga‐González, G. M., Gómez‐Meda, B. C., García-Verdín, P. M., Carrillo-Dávila, I. A., Gutiérrez-Hurtado, I. A., Torres-Mendoza, B. M., & Gallegos‐Arreola, M. P. (2024) · Diseases · doi:10.3390/diseases12070152 · Cited by 5
“The above findings highlight the potential of miRNAs as biomarkers and possible therapeutic targets in the treatment of PC; however, experimental validation is needed to confirm these results.”
ResultSynthetic lethality through Gsk3β inhibition in glioma stem cells via the WNT-WWC1-YAP axis
Ren, F., Yi, Y., Lu, T., Liu, X., Cui, G., Huang, S. M., Parada, L. F., & Chen, J. (2025) · Oncogene · doi:10.1038/s41388-025-03418-9 · Cited by 7
Hippo Pathway Key to Ploidy Checkpoint
Zhao, B., & Guan, K. (2014) · Cell · doi:10.1016/j.cell.2014.07.041 · Cited by 6
“It was recently found that the gain of YAP activity is an important mechanism during relapse of K-Ras-dependent cancers after Ras inhibition (Kapoor et al., 2014; Shao et al., 2014).”
BackgroundRole of Yes-associated Protein-1 in Gastrointestinal Cancers and Hepatocellular Carcinoma
Qian, X., Zhang, W., Yang, H., Zhang, L., Kang, N., & Lai, J. (2021) · Exploratory Research and Hypothesis in Medicine · doi:10.14218/erhm.2021.00017 · Cited by 5
Koromilas, A. E. (2022) · BioEssays · doi:10.1002/bies.202200026 · Cited by 5
Shi, H., Zou, Y., Wang, X., Wang, G., Gao, Y., Yi, F., Xu, J., Yin, Y., Li, D., & Li, M. (2023) · Discover Oncology · doi:10.1007/s12672-023-00699-y · Cited by 5
The RAS and YAP1 dance, who is leading?
Corbo, V., Ponz‐Sarvisé, M., & Tuveson, D. A. (2014) · The EMBO Journal · doi:10.15252/embj.201490014 · Cited by 5
“In agreement with the aforementioned studies, Hong and colleagues confirm that YAP1 is required for efficient RAS-induced cellular transformation and tumor formations in vivo (Nguyen et al , 2014; Shao et al , 2014).”
Scientific Misconduct: Falsification, Fabrication, and Misappropriation of Credit
Vaux, D. L. (2015) · Springer eBooks · doi:10.1007/978-981-287-079-7_26-1 · Cited by 5
Enlund, S., Sinha, I., Amor, A. R., Fard, S. S., Tamm, E. P., Jiang, Q., Lundin, V., Nilsson, A., & Holm, F. (2022) · eJHaem · doi:10.1002/jha2.634 · Cited by 4
“Importantly, DFFB interplay with SOX2 [20], YAP1 [22] and MYCN [32] provide a theoretical foundation of its role in survival and proliferation.”
BackgroundInfluentialThe Hippo Signaling Pathway: A Candidate New Drug Target for Malignant Tumors
Nishio, M., Goto, H., SUZUKI, M. T., Fujimoto, A., Mimori, K., & Suzuki, A. (2015) · Springer eBooks · doi:10.1007/978-4-431-55651-0_7 · Cited by 5
“In an inducible KrasG12D-driven mouse PDAC model, the mutants can develop malignancies in which KrasG12D and downstream MAPK activation are lost, but DNA amplifi cation and/or mRNA overexpression of YAP1 are acquired [ 52 , 53 ].”
BackgroundChen, P., Zhou, C., Li, B., & Yang, C. (2020) · PubMed Central · Cited by 5
Hagenbeek, T. J., Zbieg, J. R., Smith, R., Paul, S., Gerosa, L., Torrini, C., Guarnaccia, A. D., Ong, C. C., Lacap, J. A., Ning, M., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-74722-5 · Cited by 4
“Additionally, nuclear YAP/TAZ activity has been identi fi ed as a resistance mechanism to targeted therapies toward KRAS, EGFR, ALK, RAF, MEK, AR, and CDK4/6 20 – 29 .”
He, J., Li, G., Wu, Y., Zhang, T., Yao, M., Zang, M., Zou, J., Song, J., Li, L., Chen, Q., et al. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1391399 · Cited by 4
“Loss of the Hippo pathway may have a signi fi cant impact on tumors carrying RAS/RAF mutations (Kapoor et al., 2014; Lin et al., 2015).”
BackgroundWang, S., Shao, D., Gao, X., Zhao, P., Kong, F., Deng, J., Yang, L., Shang, W., Sun, Y., & Fu, Z. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1480701 · Cited by 6
“The expression of abnormal TEAD has been observed to impact important oncogenes, including MYC (4, 5), KRAS (6), BRAF (7), LKB1 (8), and NF2 (9, 10).”
BackgroundKRAS Inhibition Activates an Actionable CD24 “Do Not Eat Me” Signal in Pancreatic Cancer
Wei, Y., Liu, M., Yen, E.-Y., Yao, J., Xun, Z., Nguyen, P. T.-M., Wang, X., Yang, Z., Yousef, A. M. G., Pan, D. N., et al. (2025) · Cancer Research · doi:10.1158/0008-5472.can-25-2024 · Cited by 5
Self-citationTransient proliferation by reversible YAP and mitogen control of the cyclin D1/p27 ratio
Ferrick, K. R., Upadhya, S. W., Fan, Y., Ratnayeke, N., Teruel, M. N., & Meyer, T. (2026) · Communications Biology · doi:10.1038/s42003-026-09590-2 · Cited by 6
“We show that transient proliferation responses are initiated by YAP activation increasing receptor tyrosine kinases like EGFR and mitogen signaling to increase the cyclin D1/p27 ratio above a critical threshold.”
Effect of F11R Gene Knockdown on Malignant Biological Behaviors of Pancreatic Cancer Cells
Zhang, H., Zhang, R., Yao, J., Hu, X., Pu, Y., He, S., Yu, J., Zhu, H., Mu, B., & Zhao, C. (2022) · Journal of Oncology · doi:10.1155/2022/3379027 · Cited by 5
Hippo signaling in cancer: regulatory mechanisms and therapeutic strategies
Huang, Z., Tan, Y., Zhang, W., Tang, X., Nice, E. C., & Huang, C. (2023) · Australian Journal of Chemistry · doi:10.1071/ch22241 · Cited by 4
All Roads Lead to Rome: YAP/TAZ Activity Influences Efficacy of KRASG12C Inhibitors
Johnson, C. W., & Haigis, K. M. (2023) · Cancer Research · doi:10.1158/0008-5472.can-23-3547 · Cited by 4
Long, X., Steurer, B., Wong, C. W., Kozlova, E., Naumov, V., Pun, F. W., Aliper, A., Ren, F., & Zhavoronkov, A. A. (2024) · Future Medicine AI · doi:10.2217/fmai-2023-0019 · Cited by 4
Breast cancer drug resistance: Decoding the roles of Hippo pathway crosstalk
Dehghanian, F., Ghahnavieh, L. E., Nilchi, A. N., Khalilian, S., & Joonbakhsh, R. (2024) · Gene · doi:10.1016/j.gene.2024.148424 · Cited by 4
YAP activation is robust to dilution
Jones, I., Arias-García, M., Vargas, P. P., Beykou, M., Dent, L., Chaudhuri, T. P., Roumeliotis, T. I., Choudhary, J. S., Sero, J., & Bakal, C. (2024) · Molecular Omics · doi:10.1039/d4mo00100a · Cited by 4
Liu, H., Lin, Z., Guo, Y., Zhou, Y., & Li, W. (2024) · Pharmaceuticals · doi:10.3390/ph17101352 · Cited by 4
“YAP1 is a context-specific driver for PDAC [33], and its activation allows pancreatic cancer cells to bypass oncogenic KRAS dependency [34].”
BackgroundDrivers of Pancreatic Cancer: Beyond the Big 4
Porcza, L. M., Ballesteros-Cillero, R., Lam, L. T., Maiello, C., & Leslie, N. R. (2025) · Cancers · doi:10.3390/cancers17142354 · Cited by 5
“The clinical significance of this is supported by data showing that Hippo pathway activation is able to bypass the dependence of PDAC on KRAS mutations and also drive resistance to KRAS G12C inhibitor therapy [127,128].”
TMT‐based proteomics analysis of the effects of Qianjinweijing Tang on lung cancer
Huo, B., Song, Y., Tan, B., Li, J., Zhang, J., Zhang, F., & Chang, L. (2021) · Biomedical Chromatography · doi:10.1002/bmc.5116 · Cited by 4
Self-citationPei, P., Gregori, A., Bergonzini, C., Ali, M., Mantini, G., Schmidt, T., Finamore, F., Rodrigues, S. M. F., Frampton, A. E., McDonnell, L. A., et al. (2023) · International Journal of Radiation Oncology*Biology*Physics · doi:10.1016/j.ijrobp.2023.10.035 · Cited by 4
Inactivation of the Hippo Tumor Suppressor Pathway Promotes MelanomaPreprint
Vittoria, M. A., Kingston, N. M., Xia, E., Hong, R., Huang, L., McDonald, S., Tilston-Lünel, A., Darp, R., Campbell, J. D., Lang, D., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.05.04.442615 · Cited by 4
Targeting the Hippo pathway in cancers via ubiquitination dependent TEAD degradationPreprint
Pham, T. H., Pahuja, K. B., Hagenbeek, T. J., Zbieg, J., Noland, C. L., Pham, V. C., Yao, X., Rose, C. M., Browder, K. C., Lee, H.-J., et al. (2024) · eLife · doi:10.7554/elife.92450.2 · Cited by 5
McAndrews, K. M., Mahadevan, K. K., Li, B., Sockwell, A. M., Morse, S. J., Kelly, P. J., Patel, S. I., Kirtley, M. L., Diaz, B. A. M., Lyu, H., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.01.29.635543 · Cited by 4
Self-citationZhang, Y., Ren, Y., Dong, G., Jiao, Q., Guo, N., Gao, P., Li, Y., Wang, Y., & Zhao, W. (2024) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-24-0060 · Cited by 3
Self-citationMolecular Biomarkers for the Diagnosis and Prognostication of Pancreatic Ductal Adenocarcinoma
Sun, J. X., Awad, M. A., Hwang, J., & Villano, A. M. (2025) · Journal of Personalized Medicine · doi:10.3390/jpm15060236 · Cited by 6
Pancreatic Cancer and Diabetes: Insights, Hypotheses, and Next Steps
Hill, J. L. E., Hill, T. G., Parslow, D., & Hill, D. J. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262110245 · Cited by 4
The Multi-Faceted Landscape of TEAD Inhibition: a 2017–2025 Patent and Literature Review
Chen, V. Y., Wan, J., Ding, X., Ren, F., & Zhavoronkov, A. A. (2026) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2026.109609 · Cited by 3
Mahadevan, K. K., Maldonado, A. S., Li, B., Bickert, A. A., Perdyan, A., Kumbhar, S. V., Piya, S., Sockwell, A. M., Morse, S. J., Arian, K. A., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-75960-3 · Cited by 12
Self-citationA review and perspective paper: Ras oncogene gets modest, from kingpin to mere henchman
Camonis, J., Aushev, V. N., Zueva, E., & Zalcman, G. (2024) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-024-05449-z · Cited by 3
Intratumor heterogeneity in KRAS signaling shapes treatment resistance
Petrenko, O., Kirillov, V., D’Amico, S., & Reich, N. C. (2024) · iScience · doi:10.1016/j.isci.2024.111662 · Cited by 3
Ras and the Hippo Pathway in Cancer
O’Neill, E. E. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-803505-4.00002-3 · Cited by 2
Mechanisms of Hippo pathway in the pancreatic cancer
Xie, R., & Chen, R. (2020) · Journal of Pancreatology · doi:10.1097/jp9.0000000000000041 · Cited by 4
A “Janus” face of the RASSF4 signal in cell fate
Liu, A., Zhou, K., Martínez, M., López-Torres, B., Martínez, M., Martínez‐Larrañaga, M., Wang, X., Anadón, A., & Arés, I. (2021) · Journal of Cellular Physiology · doi:10.1002/jcp.30592 · Cited by 3
Guan, H., & Deng, L. (2022) · Anti-Cancer Drugs · doi:10.1097/cad.0000000000001269 · Cited by 3
KRAS Addiction Promotes Cancer Cell Adaptation in Harsh Microenvironment Through Macropinocytosis
Seguin, L. (2022) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-3-030-94004-1_10 · Cited by 3
Iraqi, M., Bolel, P., Sarkar, R., Bhattacharya, B., Ahmad, M. A., Edri, A., Roisman, L. C., Elkabets, M., Shalata, W., Peled, N., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232214054 · Cited by 3
Cellular responses after (neratinib plus pemetrexed) exposure in NSCLC cells
Booth, L. A., Poklepovic, A. S., Hancock, J. F., & Dent, P. (2023) · Anti-Cancer Drugs · doi:10.1097/cad.0000000000001442 · Cited by 3
Lukose, G., Assaad, M. A., Driskill, J. H., Levine, M. F., Gundem, G., Semaan, A., Wilkes, D. C., Spigland, N., Medina-Martinez, J. S., Sboner, A., et al. (2024) · Pathology - Research and Practice · doi:10.1016/j.prp.2024.155726 · Cited by 3
Yi, M., Zhu, R., & Stephens, R. M. (2018) · PLoS ONE · doi:10.1371/journal.pone.0207590 · Cited by 3
Therapeutic Targeting of RAS Mutant Cancers
Stites, E. C., Paskvan, K. V., & Kato, S. (2022) · Cambridge University Press eBooks · doi:10.1017/9781009064828 · Cited by 2
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
