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Stable suppression of tumorigenicity by virus-mediated RNA interference
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Continued reliance on mutant RAS signaling is required for tumor maintenance after neoplastic initiation.
“the continued reliance on mutant RAS signaling for tumor maintenance”
From A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution (2017) · cites this paper as Brummelkamp et al., 2002
The Significance passage reports that suppressing mutant K-RAS V12 in human pancreatic carcinoma cells caused loss of tumorigenicity, indicating that this oncogene remained necessary late in tumorigenesis. The Abstract reports the same result. These passages support continued dependence in that setting, but not an unqualified requirement for mutant RAS signaling in tumors generally. (LLM, conf=0.84)
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Metadata
- Authors
- Brummelkamp, T. R., Bernards, R., & Agami, R.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2002-09
- Volume
- 2
- Issue
- 3
- Pages
- 243-247
- ISSN
- 1535-6108
- Cited by
- 886
- References
- 3
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 3972 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
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