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A Comprehensive Survey of Ras Mutations in Cancer
Open accessAbstract
All mammalian cells express 3 closely related Ras proteins, termed H-Ras, K-Ras, and N-Ras, that promote oncogenesis when they are mutationally activated at codon 12, 13, or 61. Although there is a high degree of similarity among the isoforms, K-Ras mutations are far more frequently observed in cancer, and each isoform displays preferential coupling to particular cancer types. We examined the mutational spectra of Ras isoforms curated from large-scale tumor profiling and found that each isoform exhibits surprisingly distinctive codon mutation and amino-acid substitution biases. These findings were unexpected given that these mutations occur in regions that share 100% amino-acid sequence identity among the 3 isoforms. Of importance, many of these mutational biases were not due to differences in exposure to mutagens, because the patterns were still evident when compared within specific cancer types. We discuss potential genetic and epigenetic mechanisms, as well as isoform-specific differences in protein structure and signaling, that may promote these distinct mutation patterns and differential coupling to specific cancers. Cancer Res; 72(10); 2457–67. ©2012 AACR.
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“Approximately 90% of PDAC cases harbor a Kirsten rat sarcoma (KRAS) mutation (Prior et al., 2012).”
From The antitumoral effect of statins in pancreatic ductal adenocarcinoma: a scoping review (2026) · cites this paper as Prior et al., 2012
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“This specific mutation, present in ~3% of CRC cases, 2 is associated with significantly reduced progression-free survival (PFS) and overall survival (OS) compared to KRAS wildtype tumors.[3][4][5]”
From Garsorasib, a KRAS G12C inhibitor, with or without cetuximab, an EGFR antibody, in colorectal cancer cohorts of a phase II trial in advanced solid tumors with KRAS G12C mutation (2025) · cites this paper as [2]
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“Unlike other clinically actionable genomic alterations found in NSCLCs (such as EGFR and ALK aberrations), KRAS mutations, particularly KRASG12C and KRASG12V, are strongly associated with smoking29–31.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [29]
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“However, RAS mutations and the resulting deregulated signaling events are responsible for one third of all human cancers4 (Figure 1).”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [4]
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“Overall, KRAS is mutated in many cancers (predominantly adenocarcinomas), whereas NRAS mutations are prominent in melanoma and myeloid cancer4,15,16 (Fig. 1).”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [4]
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“The basis of the specific G12X mutation frequencies has remained unclear, except for the G12C transversion mutation (c.34G>T) associated with smoking in lung cancer [6,7].”
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“Mutations at codons 12, 13 and 61 account for over 99% of all RAS mutants detected in cancer [8].”
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Zhang, J., Park, D., Shin, D. M., & Deng, X. (2015) · Acta Biochimica et Biophysica Sinica · doi:10.1093/abbs/gmv118 · Cited by 20
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“The KRAS gene is known to be characterized by single base missense mutations, found predominantly at codons G12, G13, or Q61 [63,64].”
BackgroundKRAS4A induces metastatic lung adenocarcinomas in vivo in the absence of the KRAS4B isoform
Salmón, M., Paniagua, G., Lechuga, C. G., Fernández-García, F., Zarzuela, E., Álvarez, R., Musteanu, M., Guerra, C. E., Caleiras, E. J., Muñoz, J., et al. (2021) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2023112118 · Cited by 19
“T KRAS locus has gained prominence due to its involvement in as many as one-fourth of all human tumors (1, 2).”
BackgroundExtracting phylogenetic dimensions of coevolution reveals hidden functional signals
Colavin, A., Atolia, E., Bitbol, A., & Huang, K. C. (2022) · Scientific Reports · doi:10.1038/s41598-021-04260-1 · Cited by 21
“The Ras superfamily of membrane-associated small G-proteins is highly conserved and controls a broad range of cellular processes 66 , has inactive and active states that are regulated by a GTPase-activated protein 67 , and has been implicated in cancer 68 .”
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“long been associated with CNS tumors and cause approximately 30% of all cancers (Prior et al., 2012; Schubbert et al., 2007); however, only recently have these genes been directly implicated in focal epilepsy.”
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Optimization of melting analysis with TaqMan probes for detection of KRAS, NRAS, and BRAF mutations
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Inhibition of Ras-mediated signaling pathways in CML stem cells
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“Ras activating mutations or amplifications are observed in nearly one third of all human cancers [14].”
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“Another highly conserved mutation is located in the aligned position 102 that corresponds to mutations in Q61 in NRAS prevalently and is one of the residues involved in the binding function of all the Ras family members to GTP [31].”
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“Although codons 12, 13, and 61 are in regions that are identical for all RAS isoforms, the distribution of oncogenic mutations differs between these isoforms [21].”
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BackgroundDevelopment of a Nucleotide Exchange Inhibitor That Impairs Ras Oncogenic Signaling
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“The large majority of gain-of-function missense mutations that constitutively activate the Ras oncoproteins map at codons 12 (89%), 13 (9%), and 61 (1%) [79], which are the key participants in the interplay between Ras, nucleotides, and modulators (see also below).”
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ERβ Regulates NSCLC Phenotypes by Controlling Oncogenic RAS Signaling
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Fang, Z., Marshall, C. B., Yin, J. C., Mazhab‐Jafari, M. T., Gasmi-Seabrook, G. M. C., Smith, M. J., Nishikawa, T., Xu, Y., Neel, B. G., & Ikura, M. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.714196 · Cited by 18
“The Q61L mutation displaces the bridging water and significantly decreases GTP hydrolysis (38, 39).”
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“Compared with other malignancies, there is a higher prevalence of NRAS mutations over HRAS and KRAS (8%, 3%, and 3%, respectively) in thyroid carcinoma [9].”
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“1A), we examined their tyrosine phosphorylation in an isogenic system using parental SW48 human colorectal cells (KRAS wild-type) and variants of these cells engineered to harbor two common KRAS mutations – G12D or G13D (6).”
MethodSingh, K., Pruski, M. A., Polireddy, K., Jones, N. C., Chen, Q., Yao, J., Dar, W. A., McAllister, F. M., Ju, C., Eltzschig, H. K., et al. (2019) · Oncogene · doi:10.1038/s41388-019-1031-z · Cited by 18
The Hypervariable Region of K-Ras4B Governs Molecular Recognition and Function
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Oncogenic K-Ras4B Dimerization Enhances Downstream Mitogen-activated Protein Kinase Signaling
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“recruits Raf-1 (C-Raf) to the plasma membrane and activates its kinase activity more efficiently than other Ras isoforms [21,22].”
BackgroundTebar, F., Chavero, A., Agell, N., Lu, A., Rentero, C., Enrich, C., & Grewal, T. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21103680 · Cited by 21
“NRas mutations are prominant in skin (<25%) and hematological (<15%) cancers [82] and HRas mutations often exist in head and neck cancers.”
BackgroundGregório, C., Soares‐Lima, S. C., Alemar, B., Recamonde‐Mendoza, M., Camuzi, D., de Souza-Santos, P. T., Rivero, R. C., Machado, S. M. D. S., Osvaldt, A. B., Ashton‐Prolla, P., et al. (2020) · Cancers · doi:10.3390/cancers12071735 · Cited by 19
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Acetylsalicylic Acid Governs the Effect of Sorafenib in RAS -Mutant Cancers
Hammerlindl, H., Menon, D. R., Hammerlindl, S., Emran, A. A., Torrano, J., Sproesser, K., Thakkar, D., Xiao, M., Atkinson, V. G., Gabrielli, B. G., et al. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-2118 · Cited by 18
“WhileKRAS and HRAS only play a minor role for melanoma, KRAS in particular is frequently mutated in other cancers, including lung, colon, and pancreatic carcinomas (3).”
BackgroundVarQ: A Tool for the Structural and Functional Analysis of Human Protein Variants
Radusky, L., Modenutti, C. P., Delgado, J., Bustamante, J. P., Vishnopolska, S. A., Kiel, C., Serrano, L. G., Marti, M. A., & Turjanski, A. G. (2018) · Frontiers in Genetics · doi:10.3389/fgene.2018.00620 · Cited by 18
“…HRAS structures, one bound to GNP (i.e., PDB id 3DDC), other to GTP (i.e., PDB id 4K81) and another one with no ligand (i.e., PDB id 6AXG), and reported mutations in the binding pocket have been proposed to modify signaling cascades, which are involved in different diseases (Prior et al., 2012).”
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Advances in Vaccine-Based Therapies for Pancreatic Cancer
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“KRAS driver mutations are present in approximately 90% of PDAC tumors [39], and as a result, a universal vaccine targeting mutant KRAS is highly desirable for PDAC.”
Marasco, M., Kumar, D., Borrego, S. G., Seale, T. S., Maddalena, G., Mezzadra, R., Belanger, K., Cole, S., Perez, B., Luan, W., et al. (2025) · Cancer Discovery · doi:10.1158/2159-8290.cd-24-0614 · Cited by 17
Targeting the KRAS Oncogene for Patients with Metastatic Colorectal Cancer
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“Mutations in KRAS occur in approximately 40% of CRC cases, with the most frequent alterations found in codons 12, 13, and 61 [3,5,6].”
Update on Phytochemical and Biological Studies on Rocaglate Derivatives from Aglaia Species
Agarwal, G., Chang, L., Soejarto, D. D., & Kinghorn, A. D. (2021) · Planta Medica · doi:10.1055/a-1401-9562 · Cited by 17
“RAS proteins are imperative for triggering multiple signaling pathways required for cell proliferation and survival [91].”
BackgroundWild-Type KRAS Allele Effects on Druggable Targets in KRAS Mutant Lung Adenocarcinomas
Baldelli, E., Gazzah, E. E., Moran, J. C., Hodge, K. A., Manojlovic, Z., Bassiouni, R., Carpten, J. D., Ludovini, V., Baglivo, S., Crinò, L., et al. (2021) · Genes · doi:10.3390/genes12091402 · Cited by 17
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Multiple medicinal chemistry strategies of targeting KRAS: State-of-the art and future directions
Shang, Y., Fu, S., Hao, Q., Ying, H., Wang, J., & Shen, T. (2024) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2023.107092 · Cited by 17
Membrane lipids drive formation of KRAS4b-RAF1 RBDCRD nanoclusters on the membrane
Shrestha, R., Carpenter, T. S., Van, Q. N., Agamasu, C., Tonelli, M., Aydin, F., Chen, D., Gülten, G., Glosli, J. N., López, C. A., et al. (2024) · Communications Biology · doi:10.1038/s42003-024-05916-0 · Cited by 17
“61, lockRAS in a GTP “ on ” state, constitutively activating the pathway, and leading to enhanced proliferation and dysregulated cell growth 3 .”
BackgroundRamalingam, P. S., Premkumar, T., Sundararajan, V., Hussain, M. S., & Arumugam, S. (2024) · Discover Oncology · doi:10.1007/s12672-024-01455-6 · Cited by 18
“Mutations at codons 12, 13, and 61 of KRAS protein are common, and notably, the G12D and G12C are more frequent mutations [4, 5].”
BackgroundThe interplay between obesity and cancer: a fly view
Hirabayashi, S. (2016) · Disease Models & Mechanisms · doi:10.1242/dmm.025320 · Cited by 17
“Ras-family proteins are frequently mutated and activated in various human cancers (Prior et al., 2012).”
Matson, D. R., Xu, J., Huffman, L. B., Barroilhet, L. M., Accola, M. A., Rehrauer, W. M., & Weisman, P. S. (2017) · American Journal of Case Reports · doi:10.12659/ajcr.903581 · Cited by 17
“Mutation of KRAS at G12 greatly reduces GTP hydrolysis, leading to constitutive KRAS activity [15].”
BackgroundKaushal, N., Tiruchinapally, G., Durmaz, Y. Y., Bao, L., Gilani, R. A., Merajver, S. D., & ElSayed, M. E. H. (2018) · Journal of Controlled Release · doi:10.1016/j.jconrel.2018.07.042 · Cited by 17
Thabet, N. A., El-Guendy, N., Mohamed, M. M., & Shouman, S. A. (2019) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2019.114773 · Cited by 17
Prognostic implications of RAS alterations in diverse malignancies and impact of targeted therapies
Kato, S., Okamura, R., Sicklick, J., Daniels, G., Hong, D., Goodman, A., Weihe, E., Lee, S., Khalid, N., Collier, R., et al. (2019) · International Journal of Cancer · doi:10.1002/ijc.32813 · Cited by 16
“Among different RAS alterations, KRAS is the isoform most frequently altered (86% of all RAS alterations), followed by NRAS (11%) and HRAS (3%).(4,5) The frequency of alterations in RAS”
BackgroundNRAS Mutations May Be Involved in the Pathogenesis of Cutaneous Rosai Dorfman Disease: A Pilot Study
Wu, K., Li, S.-H., Liao, J.-B., Chiou, C.-C., Wu, C., & Chen, C. (2021) · Biology · doi:10.3390/biology10050396 · Cited by 17
“To our knowledge, this is the first study to demonstrate gene mutations in cutaneous RDD. NRAS mutation was frequent in cutaneous RDD, especially at NRAS A146T.”
BackgroundInfluentialHigh-Throughput Dual Screening Method for Ras Activities and Inhibitors
Kopra, K., van Adrichem, A. J., Salo‐Ahen, O. M. H., Peltonen, J. T. K., Wennerberg, K., & Härmä, H. (2017) · Analytical Chemistry · doi:10.1021/acs.analchem.6b04904 · Cited by 17
Bisulfite-converted duplexes for the strand-specific detection and quantification of rare mutations
Mattox, A. K., Wang, Y., Springer, S. U., Cohen, J. D., Yegnasubramanian, S., Nelson, W. G., Kinzler, K. W., Vogelstein, B., & Papadopoulos, N. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1701382114 · Cited by 17
“6% of these cancers, respectively (47).”
The protonation states of GTP and GppNHp in Ras proteins
Mann, D., Güldenhaupt, J., Schartner, J., Gerwert, K. B., & Kötting, C. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra117.001110 · Cited by 17
“The importance of these signaling proteins is well known, as about 20% of all human cancers show a mutation in Ras genes (3).”
BackgroundAvicin G is a potent sphingomyelinase inhibitor and blocks oncogenic K- and H-Ras signaling
Garrido, C. M., Henkels, K. M., Rehl, K. M., Hong, L., Zhou, Y., Gutterman, J. U., & Cho, K. (2020) · Scientific Reports · doi:10.1038/s41598-020-65882-5 · Cited by 16
Site-specific monoubiquitination activates Ras by impeding GTPase-activating protein function
Hobbs, G. A., Gunawardena, H. P., Baker, R., Chen, X., & Campbell, S. L. (2013) · Small GTPases · doi:10.4161/sgtp.26270 · Cited by 17
“Monoubiquitination of Ras may be activated in a similar manner to common GAP-defective oncogenic Ras mutations at positions 12, 13, and 61.(2) It is unclear how mUb of Ras impairs GAP-mediated hydrolysis while retaining the intrinsic rate of GTP hydrolysis.”
Correlation of O2 transport on the micro and macro scale.
Honig, C. R., & Gayeski, T. E. (1982) · PubMed · Cited by 17
Tabernero, J., Taieb, J., Fakih, M., Prager, G. W., Van Cutsem, E., Ciardiello, F., Mayer, R. J., Amellal, N., Skanji, D., Calleja, E., et al. (2024) · ESMO Open · doi:10.1016/j.esmoop.2024.102945 · Cited by 18
Discovery of INCB159020, an Orally Bioavailable KRAS G12D Inhibitor
Ye, Q., Shvartsbart, A., Li, Z., Gan, P., Policarpo, R. L., Qi, C., Roach, J. J., Zhu, W., McCammant, M. S., Hu, B., et al. (2025) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.4c02662 · Cited by 17
Novel approaches for the development of direct KRAS inhibitors: structural insights and drug design
Haider, K., Sharma, A., Yar, M. S., Yakkala, P. A., Shafi, S., & Kamal, Ä. (2022) · Expert Opinion on Drug Discovery · doi:10.1080/17460441.2022.2029842 · Cited by 16
“mutations mainly occur at codon G12, G13, and Q61 sites, which mostly depends on the type of cancer [10].”
BackgroundNaoumi, N., Michaelidou, K., Papadakis, G., Simaiaki, A. E., Fernández, R., Calero, M., Arnau, A., Tsortos, A., Agelaki, S., & Gizeli, E. (2022) · ACS Sensors · doi:10.1021/acssensors.1c02245 · Cited by 16
Therapeutic Potential of Intrabodies for Cancer Immunotherapy: Current Status and Future Directions
Böldicke, T. W. (2022) · Antibodies · doi:10.3390/antib11030049 · Cited by 18
“This anti-Ras mutant antibody was engineered from a human antibody previously generated and is internalized through clathrin-mediated endocytosis using heparan sulfate proteoglycan (HSPG) as a receptor and escapes from early endosomes into the cytosol [84].”
BackgroundMarkov State Models Reconcile Conformational Plasticity of GTPase with Its Substrate Binding Event
Dandekar, B. R., Ahalawat, N., Sinha, S., & Mondal, J. (2023) · JACS Au · doi:10.1021/jacsau.3c00151 · Cited by 16
Methylation of KRAS by SETD7 promotes KRAS degradation in non-small cell lung cancer
Chiang, C.-Y., Fan, S., Zheng, H., Guo, W., Zheng, Z., Sun, Y., Zhong, C., Zeng, J., Li, S., Zhang, M., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.113003 · Cited by 16
Computational design and validation of effective siRNAs to silence oncogenic KRAS
Ramalingam, P. S., & Arumugam, S. (2023) · 3 Biotech · doi:10.1007/s13205-023-03767-w · Cited by 18
“KRAS is a 166 AA length protein that has higher mutation frequencies at 12th, 13th, and 61st residue positions as mutational hotspots with 89%, 9%, and 1% respectively (Prior et al. 2012).”
BackgroundYang, Q., To, K. K. W., Hu, G., Fu, K., Yang, C. H., Zhu, S., Pan, C., Wang, F., Luo, K.-W., & Fu, L. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01698-4 · Cited by 16
Crowley, E. H., Arena, S., Lamba, S., Nicolantonio, F. D., & Bardelli, A. (2013) · Human Mutation · doi:10.1002/humu.22487 · Cited by 17
“Consequently, we investigated the role of the silent polymorphism rs61764370 that is located in the 3′ untranslated region (UTR) of Kirsten rat sarcoma viral oncogene homolog (KRAS; HGNC: 6407; MIM #190070) that is the most frequently mutated oncogene in cancer [Prior et al., 2012].”
BackgroundJang, E. K., Kim, W. G., Kim, E. Y., Kwon, H., Choi, Y. M., Jeon, M. J., Baek, J. H., Lee, J. H., Kim, T. Y., Shong, Y. K., et al. (2015) · Endocrine · doi:10.1007/s12020-015-0773-9 · Cited by 16
Inhibitors of K-Ras Plasma Membrane Localization
Cho, K.-J., van der Hoeven, D., & Hancock, J. F. (2013) · The Enzymes · doi:10.1016/b978-0-12-416749-0.00011-7 · Cited by 16
Hušková, H., Ardin, M., Weninger, A., Vargová, K., Ghamry-Barrin, S., Villar, S., Olivier, M., Stopka, T., Herceg, Z., Hollstein, M., et al. (2017) · Oncogene · doi:10.1038/onc.2017.215 · Cited by 16
“41 The observed Ras hotspot mutations provide support to the notion that the MEF BBCE protocol can speci fi cally select for cancer-associated genetic alterations.”
BackgroundCoia, H., Ma, N., Hou, Y., Dyba, M. D., Fu, Y., Cruz, M. I., Benitez, C., Graham, G. T., McCutcheon, J. N., Zheng, Y., et al. (2018) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-18-0160 · Cited by 16
“We did identify mutations at codon 61 in HRAS, a mutation hotspot of certain human cancers (30), in the liver tumors obtained from5of 9 mice, among them three are G>T mutation.”
BackgroundMicrobubble-Mediated Delivery for Cancer Therapy
Browning, R. J., & Stride, E. (2018) · Fluids · doi:10.3390/fluids3040074 · Cited by 17
“Progressive accumulation of genetic mutations is necessary for solid tumour development, leading to the growth of a mass of cells in a discrete location within an organ or tissue [4,5].”
BackgroundTargeting Mutant KRAS for Anticancer Therapy
Chen, F., Alphonse, M. P., Liu, Y., & Liu, Q. (2019) · Current Topics in Medicinal Chemistry · doi:10.2174/1568026619666190902151307 · Cited by 15
GSK-3 and miRs: Master regulators of therapeutic sensitivity of cancer cells
Duda, P., Akula, S. M., Abrams, S. L., Steelman, L. S., Gizak, A., Rakus, D., & McCubrey, J. A. (2020) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2020.118770 · Cited by 16
KRAS oncogene may be another target conquered in non‐small cell lung cancer ( NSCLC )
Chen, H., & Zhao, J. (2020) · Thoracic Cancer · doi:10.1111/1759-7714.13538 · Cited by 16
Otake, S., Itoh, Y., Omata, C., Saitoh, M., & Miyazawa, K. (2020) · Cancer Science · doi:10.1111/cas.14701 · Cited by 16
Cutting the Brakes on Ras—Cytoplasmic GAPs as Targets of Inactivation in Cancer
Bellazzo, A., & Collavin, L. (2020) · Cancers · doi:10.3390/cancers12103066 · Cited by 16
“Similarly, evidence of activated Ras signaling is consistently found in liver cancer and myeloma, tumors that have a lower RAS mutation rate compared to other cancers [4,5,9,10].”
BackgroundKRAS-G12C covalent inhibitors: A game changer in the scene of cancer therapies
Naim, N., Moukheiber, S., Daou, S., & Kourié, H. R. (2021) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2021.103524 · Cited by 16
Lu, H., & Martı́, J. (2022) · Nanoscale · doi:10.1039/d1nr07622a · Cited by 14
Discovery of ARS-1620 analogs as KRas G12C inhibitors with high in vivo antitumor activity
Zhao, H., Li, L., Liu, J., Mai, R., Chen, J., & Chen, J. (2022) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2022.105652 · Cited by 16
The Research Progress of Direct KRAS G12C Mutation Inhibitors
Yang, A., Li, M., & Fang, M. (2021) · Pathology and Oncology Research · doi:10.3389/pore.2021.631095 · Cited by 15
“However, mutations at codons 12 and 13 in RAS proteins impair GAP-stimulated GTP hydrolysis, leaving RAS predominantly in the GTP-bound state, the active state [3].”
Background
Metadata
- Authors
- Prior, I. A., Lewis, P. D., & Mattos, C.
- Affiliations
- Northeastern University (US)
- Corresponding author
- Prior, Ian A.
- Venue
- Cancer Research
- Published
- 2012-05-14
- Volume
- 72
- Issue
- 10
- Pages
- 2457-2467
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC3354961
- OpenAlex
- W2135184154
- Cited by
- 2,063
- References
- 67
- Citations by year
- 2026: 114 · 2025: 154 · 2024: 169 · 2023: 203 · 2022: 189 · 2021: 223 · 2020: 203 · 2019: 164 · 2018: 162 · 2017: 144 · 2016: 110 · 2015: 111 · 2014: 52 · 2013: 47 · 2012: 13
- FWCI
- 23.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Wellcome Trust (067398)
- Cancer Research UK (A6672)
- Biotechnology and Biological Sciences Research Council (BB/G018162/1)
- National Cancer Institute (R56CA096867)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- RAS mutations, KRAS, H-Ras, NRAS, Ras isoforms, codon 12 mutation, mutational spectra, carcinogenesis, epigenetic mechanisms, Ras signaling
- MeSH terms
- Cell Transformation, Neoplastic, Codon, Humans, Models, Molecular, Molecular Conformation, Neoplasms, Genes, ras, Signal Transduction, Point Mutation, ras Proteins, Protein Isoforms, Catalytic Domain, Databases, Genetic, Epigenesis, Genetic
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