BCR-ABL1 mutation ≠ ponatinib resistance.

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

4 citing papers in PubMed, 5 citations in OpenAlex.

1. Molecularly targeted therapy and immunotherapy in leukemias.Journal of hematology & oncology · 2026
   Review
2. Isoalantolactone mediates the degradation of BCR-ABL protein in imatinib-resistant CML cells by down-regulating survivin.Cell cycle (Georgetown, Tex.) · 2023
   Article
3. Assessing Measurable Residual Disease in Chronic Myeloid Leukemia. BCR-ABL1 IS in theFrontiers in oncology · 2019
   Article
4. Molecular biology as a tool for the treatment of cancer.Clinical and experimental medicine · 2018
   Review

Corrections and comments

• Comment on
  Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients.2016

Authors and funding

2 authors at 1 institution in 1 country.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

Indexed as