KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer

Waters, Andrew M.; Der, Channing J.

doi:10.1101/cshperspect.a031435

Cited by 882Pancreatic and Hepatic Oncology ResearchProtein Kinase Regulation and GTPase SignalingCancer Genomics and Diagnostics

KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer

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Waters, Andrew M., Der, Channing J.·2018·Cold Spring Harbor Perspectives in Medicine

DOI 10.1101/cshperspect.a031435PMC PMC5995645

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Abstract

mutation frequency, pancreatic ductal adenocarcinoma (PDAC) is considered the most RAS-addicted of all cancers. We review the role of KRAS as a driver and therapeutic target in PDAC.

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PDAC is arguably the most RAS-addicted cancer, with substantial experimental evidence that mutant KRAS is essential for its growth.
“This high prevalence is significant as it makes PDAC arguably the most RAS-addicted cancer, with substantial experimental evidence that mutant KRAS is essential for its growth [107].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [107]
KRAS isoform is mutated in 84% of all RAS-mutant cancers, with near 100% mutation frequency in PDAC.
“In particular, the KRAS isoform is mutated in 84% of all RAS-mutant cancers, with a near 100% mutation frequency in PDAC.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [107]
The majority of KRAS mutations in PDAC are at codon 12, with the highest prevalence of G12D (35%), followed by G12V (20-30%), G12R (10-20%), Q61 (~5%), G12C (1-2%), and other rare mutations.
“The majority of KRAS mutations are at codon 12, with the highest prevalence of G12D mutation (35%), followed by G12V (20–30%), G12R (10–20%), Q61 (~5%), G12C (1–2%), and other rare muations9–12.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [9]
In pancreatic cancer, KRAS mutation is often the initiating genetic event leading to pancreatic intraepithelial neoplasms; other mutations include p53 (64%), SMAD4 (21%), and CDKN2A (17%).
“In pancreatic cancer, KRAS mutation is often the initiating genetic event leading to pancreatic intraepithelial neoplasms. Carcinogenesis and metastasis are stimulated by acquiring other mutations such as p53 (64%), SMAD4 (21%), and CDKN2A (17%) [63].”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [63]
Several potent and selective inhibitors targeting kinases in the Ras signaling network, especially MAPK and PI3K/mTOR components, have been created.
“A number of highly selective and potent inhibitors have been developed against kinases in the Ras signaling network particularly those in the MAPK and PI3K/mTOR pathways (9, 12).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [12]

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Hayes, 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
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NMR-based functional profiling of RASopathies and oncogenic RAS mutations
Smith, M. J., Neel, B. G., & Ikura, M. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1218173110 · Cited by 257 · see citing works
Divergent Roles for RalA and RalB in Malignant Growth of Human Pancreatic Carcinoma Cells
Lim, K.-H., O'Hayer, K., Adam, S. J., Kendall, S. D., Campbell, P. M., Der, C. J., & Counter, C. M. (2006) · Current Biology · doi:10.1016/j.cub.2006.10.023 · Cited by 250 · see citing works
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Precursor Lesions for Sporadic Pancreatic Cancer: PanIN, IPMN, and MCN
Distler, M., Aust, D. E., Weitz, J., Pilarsky, C. P., & Grützmann, R. (2014) · BioMed Research International · doi:10.1155/2014/474905 · Cited by 219 · see citing works
Activation Mechanism of Oncogenic Deletion Mutations in BRAF, EGFR, and HER2
Foster, S. A., Whalen, D. M., Özen, A., Wongchenko, M. J., Yin, J., Yen, I., Schaefer, G., Mayfield, J. D., Chmielecki, J., Stephens, P. J., et al. (2016) · Cancer Cell · doi:10.1016/j.ccell.2016.02.010 · Cited by 215 · see citing works
Amplification of the Driving Oncogene, KRAS or BRAF , Underpins Acquired Resistance to MEK1/2 Inhibitors in Colorectal Cancer Cells
Little, A. S., Balmanno, K., Sale, M. J., Newman, S., Dry, J. R., Hampson, M., Edwards, P. A., Smith, P. D., & Cook, S. J. (2011) · Science Signaling · doi:10.1126/scisignal.2001752 · Cited by 211 · see citing works
Genetically Engineered Mouse Models of Pancreatic Cancer: The KPC Model ( LSL‐Kras G12D/+ ;LSL‐Trp53 R172H/+ ;Pdx‐1‐Cre ), Its Variants, and Their Application in Immuno‐oncology Drug Discovery
Lee, J. W., Komar, C. A., Bengsch, F., Graham, K. L., & Beatty, G. L. (2016) · Current Protocols in Pharmacology · doi:10.1002/cpph.2 · Cited by 209 · see citing works
KRAS G12D Mutation Subtype Is A Prognostic Factor for Advanced Pancreatic Adenocarcinoma
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Inactivation of Smad4 Accelerates KrasG12D-Mediated Pancreatic Neoplasia
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Reduction in the requirement of oncogenic Ras signaling to activation of PI3K/AKT pathway during tumor maintenance
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Requirement for Interaction of PI3-Kinase p110α with RAS in Lung Tumor Maintenance
Castellano, E., Sheridan, C., Thin, M. Z., Nye, E. L., Spencer‐Dene, B., Diefenbacher, M. E., Moore, C., Kumar, M. S., Murillo, M. M., Gronroos, E. C., et al. (2013) · Cancer Cell · doi:10.1016/j.ccr.2013.09.012 · Cited by 184 · see citing works
RalGDS is required for tumor formation in a model of skin carcinogenesis
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Metastatic pancreatic cancer is dependent on oncogenic Kras in mice
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Oncogenic BRAF Deletions That Function as Homodimers and Are Sensitive to Inhibition by RAF Dimer Inhibitor LY3009120
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Rare Codons Regulate KRas Oncogenesis
Lampson, B. L., Pershing, N. L., Prinz, J. A., Lacsina, J. R., Marzluff, W. F., Nicchitta, C. V., MacAlpine, D. M., & Counter, C. M. (2012) · Current Biology · doi:10.1016/j.cub.2012.11.031 · Cited by 150 · see citing works
C-Raf Is Required for the Initiation of Lung Cancer by K-RasG12D
Karreth, F. A., Frese, K. K., DeNicola, G. M., Baccarini, M., & Tuveson, D. A. (2011) · Cancer Discovery · doi:10.1158/2159-8290.cd-10-0044 · Cited by 149 · see citing works
Genetic Basis of Pancreas Cancer Development and Progression: Insights from Whole-Exome and Whole-Genome Sequencing
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Wild-Type H- and N-Ras Promote Mutant K-Ras-Driven Tumorigenesis by Modulating the DNA Damage Response
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Early Requirement of Rac1 in a Mouse Model of Pancreatic Cancer
Heid, I., Lubeseder–Martellato, C., Sipos, B., Mazur, P. K., Lesina, M., Schmid, R. M., & Siveke, J. T. (2011) · Gastroenterology · doi:10.1053/j.gastro.2011.04.043 · Cited by 139 · see citing works
GEMMs as preclinical models for testing pancreatic cancer therapies
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p21-Activated Kinase 1 Is Required for Efficient Tumor Formation and Progression in a Ras-Mediated Skin Cancer Model
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A phase IB trial of the oral MEK inhibitor trametinib (GSK1120212) in combination with everolimus in patients with advanced solid tumors
Tolcher, A. W., Bendell, J. C., Papadopoulos, K. P., Burris, H. A., Patnaik, A., Jones, S. F., Rasco, D. W., Cox, D. S., Durante, M., Bellew, K. M., et al. (2014) · Annals of Oncology · doi:10.1093/annonc/mdu482 · Cited by 132 · see citing works
Targeting RAS-mutant cancers: is ERK the key?
Ryan, M. B., Der, C., Wang-Gillam, A., & Cox, A. (2015) · Trends in Cancer · doi:10.1016/j.trecan.2015.10.001 · Cited by 125 · see citing works
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Targeting Inhibitors of the Tumor Suppressor PP2A for the Treatment of Pancreatic Cancer
Farrell, A. S., Allen-Petersen, B., Daniel, C. J., Wang, X., Wang, Z., Rodriguez, S., Impey, S., Oddo, J., Vitek, M. P., Lopez, C., et al. (2014) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-13-0542 · Cited by 114 · see citing works
Ral small GTPase signaling and oncogenesis: More than just 15minutes of fame
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Disruption of p16 and Activation of Kras in Pancreas Increase Ductal Adenocarcinoma Formation and Metastasis in vivo
Qiu, W., Sahin, F., Iacobuzio-Donahue, C. A., Garcia-Carracedo, D., Wang, W. M., Kuo, C.-Y., Chen, D., Arking, D. E., Lowy, A. M., Hruban, R. H., et al. (2011) · Oncotarget · doi:10.18632/oncotarget.357 · Cited by 99 · see citing works
Dual PI3K/mTOR Inhibitors Induce Rapid Overactivation of the MEK/ERK Pathway in Human Pancreatic Cancer Cells through Suppression of mTORC2
Soares, H. P., Ming, M., Mellon, M., Young, S. H., Han, L., Sinnet-Smith, J., & Rozengurt, E. (2015) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-14-0669 · Cited by 97 · see citing works
The importance of Raf dimerization in cell signaling
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Discovery of 1-(3,3-Dimethylbutyl)-3-(2-fluoro-4-methyl-5-(7-methyl-2-(methylamino)pyrido[2,3-d]pyrimidin-6-yl)phenyl)urea (LY3009120) as a Pan-RAF Inhibitor with Minimal Paradoxical Activation and Activity against BRAF or RAS Mutant Tumor Cells
Henry, J. R., Kaufman, M. D., Peng, S.-B., Ahn, Y. M., Caldwell, T. M., Vogeti, L., Telikepalli, H., Lu, W.-P., Hood, M. M., Rutkoski, T. J., et al. (2015) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.5b00067 · Cited by 86 · see citing works
Genetic Deletion of RALA and RALB Small GTPases Reveals Redundant Functions in Development and Tumorigenesis
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Dormant Cancer Cells Contribute to Residual Disease in a Model of Reversible Pancreatic Cancer
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Rare codons capacitate Kras-driven de novo tumorigenesis
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The RalB Small GTPase Mediates Formation of Invadopodia through a GTPase-Activating Protein-Independent Function of the RalBP1/RLIP76 Effector
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Aberrant Overexpression of the Rgl2 Ral Small GTPase-specific Guanine Nucleotide Exchange Factor Promotes Pancreatic Cancer Growth through Ral-dependent and Ral-independent Mechanisms
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Identification of PLX 4032‐resistance mechanisms and implications for novel RAF inhibitors
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Inhibition of mutant BRAF splice variant signaling by next‐generation, selective RAF inhibitors
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Evaluating TBK1 as a Therapeutic Target in Cancers with Activated IRF3
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Molecular Pathways: Targeting RAC–p21-Activated Serine–Threonine Kinase Signaling in RAS-Driven Cancers
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A Correction to the Research Article Titled: “Amplification of the Driving Oncogene, KRAS or BRAF , Underpins Acquired Resistance to MEK1/2 Inhibitors in Colorectal Cancer Cells” by A. S. Little, K. Balmanno, M. J. Sale, S. Newman, J. R. Dry, M. Hampson, P. A. W. Edwards, P. D. Smith, S. J. Cook
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A phase I/Ib study of trametinib (GSK1120212) alone and in combination with gemcitabine in Japanese patients with advanced solid tumors
Kasuga, A., Nakagawa, K., Fumio, N., Shimizu, T., Naruge, D., Nishina, S., Kitamura, H., Kurata, T., Takasu, A., Fujisaka, Y., et al. (2015) · Investigational New Drugs · doi:10.1007/s10637-015-0270-2 · Cited by 19 · see citing works

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Pancreatic 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
Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer
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Autophagy-dependent ferroptosis drives tumor-associated macrophage polarization via release and uptake of oncogenic KRAS protein
Dai, E., Han, L., Liu, J., Xie, Y., Kroemer, G., Klionsky, D. J., Zeh, H. J., Kang, R., Wang, J., & Tang, D. (2020) · Autophagy · doi:10.1080/15548627.2020.1714209 · Cited by 613 · see citing works
G-quadruplexes: a promising target for cancer therapy
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Sotorasib in KRAS p.G12C–Mutated Advanced Pancreatic Cancer
Strickler, J. H., Satake, H., George, T. J., Yaeger, R., Hollebecque, A., Garrido-Laguna, I., Schuler, M., Burns, T. F., Coveler, A. L., Falchook, G. S., et al. (2023) · New England Journal of Medicine · doi:10.1056/nejmoa2208470 · Cited by 527 · see citing works
Ferroptotic damage promotes pancreatic tumorigenesis through a TMEM173/STING-dependent DNA sensor pathway
Dai, E., Han, L., Liu, J., Xie, Y., Zeh, H. J., Kang, R., Bai, L., & Tang, D. (2020) · Nature Communications · doi:10.1038/s41467-020-20154-8 · Cited by 428 · see citing works
Therapeutic developments in pancreatic cancer
Hu, Z., & O'Reilly, E. M. (2023) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-023-00840-w · Cited by 425 · see citing works
From state-of-the-art treatments to novel therapies for advanced-stage pancreatic cancer
Nevala-Plagemann, C., Hidalgo, M. M., & Garrido‐Laguna, I. (2019) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-019-0281-6 · Cited by 391 · see citing works
Efficacy of a small-molecule inhibitor of KrasG12D in immunocompetent models of pancreatic cancer
Kemp, S. B., Cheng, N., Markosyan, N., Sor, R., Kim, I.-K., Hallin, J., Shoush, J., Quinones, L., Brown, N. V., Bassett, J. B., et al. (2023) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-1066 · Cited by 370 · see citing works
KRAS mutation in pancreatic cancer
Luo, J. (2021) · Seminars in Oncology · doi:10.1053/j.seminoncol.2021.02.003 · Cited by 360 · see citing works
Achieving clinical success with BET inhibitors as anti-cancer agents
Shorstova, T., Foulkes, W. D., & Witcher, M. (2021) · British Journal of Cancer · doi:10.1038/s41416-021-01321-0 · Cited by 358 · see citing works
Translational and therapeutic evaluation of RAS-GTP inhibition by RMC-6236 in RAS-driven cancers
Jiang, J., Jiang, L., Maldonato, B. J., Wang, Y., Holderfield, M., Aronchik, I., Winters, I. P., Salman, Z., Blaj, C., Menard, M., et al. (2024) · Cancer Discovery · doi:10.1158/2159-8290.cd-24-0027 · Cited by 343 · see citing works
Molecular epidemiology and diagnostics of KRAS mutations in human cancer
Timar, J., & Kashofer, K. (2020) · Cancer and Metastasis Reviews · doi:10.1007/s10555-020-09915-5 · Cited by 334 · see citing works
The Current Treatment Paradigm for Pancreatic Ductal Adenocarcinoma and Barriers to Therapeutic Efficacy
Principe, D. R., Underwood, P. W., Korc, M., Trevino, J. G., Munshi, H. G., & Rana, A. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.688377 · Cited by 253 · see citing works
Translational advances in pancreatic ductal adenocarcinoma therapy
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ssGSEA score-based Ras dependency indexes derived from gene expression data reveal potential Ras addiction mechanisms with possible clinical implications
Yi, M., Nissley, D. V., McCormick, F. P., & Stephens, R. M. (2020) · Scientific Reports · doi:10.1038/s41598-020-66986-8 · Cited by 237 · see citing works
Atypical KRASG12R Mutant Is Impaired in PI3K Signaling and Macropinocytosis in Pancreatic Cancer
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Targeting Pin1 renders pancreatic cancer eradicable by synergizing with immunochemotherapy
Koikawa, K., Kibe, S., Suizu, F., Sekino, N., Kim, N., Manz, T. D., Pinch, B. J., Akshinthala, D., Verma, A., Gaglia, G., et al. (2021) · Cell · doi:10.1016/j.cell.2021.07.020 · Cited by 235 · see citing works
The KRAS-G12C inhibitor: activity and resistance
Liu, J., Kang, R., & Tang, D. (2021) · Cancer Gene Therapy · doi:10.1038/s41417-021-00383-9 · Cited by 222 · see citing works
The pancreatic cancer genome revisited
Hayashi, A., Hong, J., & Iacobuzio-Donahue, C. A. (2021) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-021-00463-z · Cited by 211 · see citing works
Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer
Wasko, U. N., Jiang, J., Dalton, T. C., Curiel-Garcia, A., Edwards, A. C., Wang, Y., Lee, B., Orlen, M., Tian, S., Stalnecker, C. A., et al. (2024) · Nature · doi:10.1038/s41586-024-07379-z · Cited by 209 · see citing works
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The path to the clinic: a comprehensive review on direct KRASG12C inhibitors
Kwan, A. K., Piazza, G. A., Keeton, A. B., & Leite, C. A. (2022) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-021-02225-w · Cited by 192 · see citing works
KRAS Suppression-Induced Degradation of MYC Is Antagonized by a MEK5-ERK5 Compensatory Mechanism
Vaseva, A. V., Blake, D. R., Gilbert, T. S. K., Ng, S., Hostetter, G. H., Azam, S. H., Ozkan‐Dagliyan, I., Gautam, P., Bryant, K. L., Pearce, K. H., et al. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.10.001 · Cited by 181 · see citing works
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Comprehensive pan-cancer genomic landscape of KRAS altered cancers and real-world outcomes in solid tumors
Lee, J. K., Sivakumar, S., Schrock, A. B., Madison, R., Fabrizio, D., Gjoerup, O., Ross, J. S., Frampton, G. M., Napalkov, P., Montesion, M., et al. (2022) · npj Precision Oncology · doi:10.1038/s41698-022-00334-z · Cited by 187 · see citing works
Autophagy as a therapeutic target in pancreatic cancer
Piffoux, M., Eriau, E., & Cassier, P. A. (2020) · British Journal of Cancer · doi:10.1038/s41416-020-01039-5 · Cited by 182 · see citing works
Combination Therapies with CDK4/6 Inhibitors to Treat KRAS- Mutant Pancreatic Cancer
Goodwin, C. M., Waters, A. M., Klomp, J. E., Javaid, S., Bryant, K. L., Stalnecker, C. A., Drizyte-Miller, K., Papke, B., Yang, R., Amparo, A. M., et al. (2023) · Cancer Research · doi:10.1158/0008-5472.can-22-0391 · Cited by 168 · see citing works
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Drugging KRAS: Current perspectives and state-of-art review
Parikh, K., Banna, G., Liu, S. V., Friedlaender, A., Desai, A., Subbiah, V., & Addeo, A. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01375-4 · Cited by 164 · see citing works
KRAS(G12D) can be targeted by potent inhibitors via formation of salt bridge
Mao, Z., Xiao, H., Shen, P., Yang, Y., Xue, J., Yang, Y., Shang, Y., Zhang, L., Li, X., Zhang, Y., et al. (2022) · Cell Discovery · doi:10.1038/s41421-021-00368-w · Cited by 158 · see citing works
The plasticity of pancreatic cancer metabolism in tumor progression and therapeutic resistance
Biancur, D. E., & Kimmelman, A. C. (2018) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2018.04.011 · Cited by 151 · 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
Oncogene-like addiction to aneuploidy in human cancers
Girish, V., Lakhani, A. A., Thompson, S. L., Scaduto, C. M., Brown, L. M., Hagenson, R. A., Sausville, E. L., Mendelson, B. E., Kandikuppa, P. K., Lukow, D. A., et al. (2023) · Science · doi:10.1126/science.adg4521 · Cited by 146 · see citing works
Novel Insights on the Use of L-Asparaginase as an Efficient and Safe Anti-Cancer Therapy
Trimpont, M. V., Peeters, E., Visser, Y. D., Schalk, A. M., Mondelaers, V., Moerloose, B. D., Lavie, A., Lammens, T., Goossens, S., & Vlierberghe, P. V. (2022) · Cancers · doi:10.3390/cancers14040902 · Cited by 143 · see citing works
Fusobacterium nucleatum induces proliferation and migration in pancreatic cancer cells through host autocrine and paracrine signaling
Udayasuryan, B., Ahmad, R. N., Nguyen, T. T. D., Umaña, A., Roberts, L. M., Sobol, P., Jones, S. D., Munson, J. M., Slade, D. J., & Verbridge, S. S. (2022) · Science Signaling · doi:10.1126/scisignal.abn4948 · Cited by 144 · see citing works
Discovery, Preclinical Characterization, and Early Clinical Activity of JDQ443, a Structurally Novel, Potent, and Selective Covalent Oral Inhibitor of KRASG12C
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Authors: Waters, A. M., & Der, C. J.
Affiliations: University of North Carolina at Chapel Hill (US)
ORCID: Waters, Andrew M.
Der, Channing J.
Venue: Cold Spring Harbor Perspectives in Medicine
Publisher: Cold Spring Harbor Laboratory
Published: 2017-12-11
Volume: 8
Issue: 9
Pages: a031435
ISSN: 2157-1422 (ISSN-L)
DOI: 10.1101/cshperspect.a031435
PMC: PMC5995645
OpenAlex: W2771729549
Cited by: 875
References: 109
Citations by year: 2026: 73 · 2025: 112 · 2024: 121 · 2023: 118 · 2022: 153 · 2021: 157 · 2020: 98 · 2019: 35 · 2018: 8
Type: posted content
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Cold Spring Harbor Perspectives in Medicine (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
Funders: U.S. Department of Defense
American Association for Cancer Research
Pancreatic Cancer Action Network
Lustgarten Foundation
National Science Council
National Institutes of Health (5r01ca042978-30)
National Cancer Institute (CA042978, CA203657, P01CA203657, R01CA175747, T32CA009156, P50CA196510, R01-CA042978, CA199235, U01CA199235, CA196510, P30CA016086)
Topics: Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Keywords: KRAS, pancreatic ductal adenocarcinoma, pancreatic cancer, driver mutations, therapeutic target, KRAS inhibitors
MeSH terms: Adenocarcinoma, Animals, Humans, Mutation, Signal Transduction, Proto-Oncogene Proteins p21(ras), Carcinoma, Pancreatic Ductal, Protein Kinase Inhibitors, Molecular Targeted Therapy

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KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer

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