ArticleCancer discovery2016
Molecular Mechanism of Mutant CALR-Mediated Transformation.
Article in Cancer discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Calreticulin Type 26 Mutation in Myelofibrosis: A Rare Variant With Diagnostic Challenges.Journal of clinical laboratory analysis · 2026Article
- FDX1 is associated with CALR abundance and JAK-STAT-related inflammatory signaling in myeloproliferative neoplasms.Frontiers in oncology · 2026Article
- The Contemporary Approach to CALR-Positive Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- Unfolding the Role of Calreticulin in Myeloproliferative Neoplasm Pathogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Review
- Emerging therapeutic targets in myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas.Expert opinion on therapeutic targets · 2018Review
Corrections and comments
- Comment on
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Elf and colleagues used an elegant series of functional and biochemical assays to investigate the molecular mechanism of mutant calreticulin (CALR)-driven cellular transformation in myeloproliferative neoplasms (MPN). Mutant CALR is sufficient to induce MPN in mouse transplantation experiments, and transformation is dependent upon physical interaction mediated by the positive electrostatic charge of the mutant CALR C-terminal domain and the thrombopoietin receptor MPL.
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.