The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
The MAPK pathway across different malignancies: A new perspective
Open accessAbstract
The mitogen‐activated protein kinase/extracellular signal‐regulated (MAPK/ERK) pathway is activated by upstream genomic events and/or activation of multiple signaling events in which information coalesces at this important nodal pathway point. This pathway is tightly regulated under normal conditions by phosphatases and bidirectional communication with other pathways, like the protein kinase B/mammalian target of rapamycin (AKT/m‐TOR) pathway. Recent evidence indicates that the MAPK/ERK signaling node can function as a tumor suppressor as well as the more common pro‐oncogenic signal. The effect that predominates depends on the intensity of the signal and the context or tissue in which the signal is aberrantly activated. Genomic profiling of tumors has revealed common mutations in MAPK/ERK pathway components, such as v‐raf murine sarcoma viral oncogene homolog B1 (BRAF). Currently approved for the treatment of melanoma, inhibitors of BRAF kinase are being studied alone and in combination with inhibitors of the MAPK and other pathways to optimize the treatment of many tumor types. Therapies targeted toward MAPK/ERK components have various response rates when used in different solid tumors, such as colorectal cancer and ovarian cancer. Understanding the differential nature of activation of the MAPK/ERK pathway in each tumor type is critical in developing single and combination regimens, because different tumors have unique mechanisms of primary and secondary signaling and subsequent sensitivity to drugs. Cancer 2014;120:3446–3456. © 2014 American Cancer Society.
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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
Lynch, T. J., Bell, D. W., Sordella, R., Gurubhagavatula, S., Okimoto, R. A., Brannigan, B. W., Harris, P. L., Haserlat, S. M., Supko, J. G., Haluska, F. G., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040938 · Cited by 11,486
Mutations of the BRAF gene in human cancer
Davies, H., Bignell, G. R., Cox, C., Stephens, P., Edkins, S., Clegg, S., Teague, J., Woffendin, H., Garnett, M. J., Bottomley, W., et al. (2002) · Nature · doi:10.1038/nature00766 · Cited by 10,674
Comprehensive molecular characterization of human colon and rectal cancer
The Cancer Genome Atlas Network (2012) · Nature · doi:10.1038/nature11252 · Cited by 8,499
Vogelstein, B., Papadopoulos, N., Velculescu, V. E., Zhou, S., Diaz, L. A., & Kinzler, K. W. (2013) · Science · doi:10.1126/science.1235122 · Cited by 7,863
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 1×
“Senescence involves the inhibition of cell proliferation through terminal cell cycle arrest.(29) Abnormal activation of MAPK/ ERK by RAS causes degradation of proteins required for both migration and progression through the cell cycle, as demonstrated in a model of normal fibroblasts and validated in benign prostate t…”
BackgroundMET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
Engelman, J. A., Zejnullahu, K., Mitsudomi, T., Song, Y., Hyland, C., Park, J. O., Lindeman, N., Gale, C.-M., Zhao, X., Christensen, J., et al. (2007) · Science · doi:10.1126/science.1141478 · Cited by 4,496
Pao, W., Miller, V. A., Politi, K. A., Riely, G. J., Somwar, R., Zakowski, M. F., Kris, M. G., & Varmus, H. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020073 · Cited by 3,527
Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors
Sequist, L. V., Waltman, B. A., Dias-Santagata, D., Digumarthy, S., Turke, A. B., Fidias, P., Bergethon, K., Shaw, A. T., Gettinger, S., Cosper, A. K., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002003 · Cited by 3,499
Combined BRAF and MEK inhibition in melanoma with BRAF V600 mutations
Flaherty, K. T., Infante, J. R., Daud, A., Gonzalez, R., Kefford, R. F., Sosman, J., Hamid, O., Schuchter, L., Cebon, J., Ibrahim, N., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1210093 · Cited by 2,810
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Targeting autophagy to sensitive glioma to temozolomide treatment
Yan, Y., Xu, Z., Dai, S., Qian, L., Sun, L., & Gong, Z. (2016) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-016-0303-5 · Cited by 299
Jackson, M., Marks, L., May, G. H. W., & Wilson, J. B. (2018) · Essays in Biochemistry · doi:10.1042/ebc20170053 · Cited by 295
Lau, T.-S., Chan, L. K.-Y., Wong, E. C.-H., Hui, C. W.-C., Sneddon, K., Cheung, T.-H., Yim, S.-F., Lee, J. H.-S., Yeung, C. S.-Y., Chung, T. K.-H., et al. (2017) · Oncogene · doi:10.1038/onc.2016.509 · Cited by 88
Self-citationClinical protein science in translational medicine targeting malignant melanoma
Gil, J., Betancourt, L. H., Pla, I., Sanchez, A., Appelqvist, R., Miliotis, T., Kuras, M., Oskolas, H., Kim, Y., Horvath, Z., et al. (2019) · Cell Biology and Toxicology · doi:10.1007/s10565-019-09468-6 · Cited by 45
Metadata
- Authors
- Burotto, M., Chiou, V. L., Lee, J., & Kohn, E. C.
- Venue
- Cancer
- Publisher
- Wiley
- Published
- 2014-06-19
- Volume
- 120
- Issue
- 22
- Pages
- 3446-3456
- ISSN
- 0008-543X (ISSN-L)
- 1097-0142
- OpenAlex
- W1490956705
- Cited by
- 956
- References
- 22
- FWCI
- 13.63
- Type
- journal article
- Language
- en
- Open access
- bronze
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