ArticleMethods in molecular biology (Clifton, N.J.)2021
Mathematical Modeling to Study KRAS Mutant-Specific Responses to Pathway Inhibition.
Article in Methods in molecular biology (Clifton, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- A guide to ERK dynamics, part 2: downstream decoding.The Biochemical journal · 2023Article
- Computational Random Mutagenesis to Investigate RAS Mutant Signaling.Methods in molecular biology (Clifton, N.J.) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
This chapter will describe how mathematical modeling allows the RAS pathway to be studied with computational experiments. The mathematical model utilized simulates the biochemical reactions that regulate RAS signaling. This type of model incorporates knowledge of reaction mechanisms, including measured quantitative parameters that characterize these reactions for both wild-type and mutant RAS proteins. For an illustrative example, this chapter focuses on how modeling provided new insights that helped solve a problem that challenged the RAS community for nearly a decade: why do colorectal cancers with the KRAS G13D mutation, but not the other common KRAS mutations, benefit from EGFR inhibition? The methods described include computational dose-response experiments and the use of "computational chimeric" RAS mutants.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.