Evidence map›Paper›PMID 19095773›Full record

GuidelineThe Journal of molecular diagnostics : JMD2009

Laboratory practice guidelines for detecting and reporting BCR-ABL drug resistance mutations in chronic myelogenous leukemia and acute lymphoblastic leukemia: a report of the Association for Molecular Pathology.

Dan Jones, Suzanne Kamel-Reid, David Bahler, Henry Dong, Kojo Elenitoba-Johnson, Richard Press, Neil Quigley, Paul Rothberg, Dan Sabath, David Viswanatha and 2 more

Open access · bronzeAbstract readPractice Guideline
PubMed Full text at PMC Publisher
In one paragraph

Guideline in The Journal of molecular diagnostics : JMD, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009
    Guideline
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. CRISPR-Cas9-mediated saturated mutagenesis screen predicts clinical drug resistance with improved accuracy.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Imatinib mesylate resistance and mutations: An Indian experience.Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology · 2013
    Article
  17. Review
  18. Article
  19. Article
  20. Dasatinib in chronic myeloid leukemia: a review.Therapeutics and clinical risk management · 2009
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 11 institutions in 2 countries.

Dan JonesABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; University of Texas M. D. Anderson Cancer Center, Houston, Texas. Electronic address: dajones@mdanderson.org.
Suzanne Kamel-ReidABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; The University Health Network, Toronto, Canada.
David BahlerABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; ARUP Laboratories, Salt Lake City, Utah.
Henry DongABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; Genzyme Genetics, New York City, New York.
Kojo Elenitoba-JohnsonABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; University of Michigan Medical School, Ann Arbor, Michigan.
Richard PressABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; Oregon Health & Science University, Portland, Oregon.
Neil QuigleyABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; Molecular Pathology Laboratory Network, Inc., Maryville, Tennessee.
Paul RothbergABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; University of Rochester Medical Center, Rochester, New York.
Dan SabathABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; University of Washington, Seattle, Washington.
David ViswanathaABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; Mayo Clinic, Rochester, Minnesota.
Karen WeckABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; University of North Carolina, Chapel Hill, North Carolina.
James ZehnderABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; Stanford University, Stanford, California.
ARUP Laboratories (United States) · USMayo Clinic · USMolecular Pathology Laboratory Network (United States) · USOregon Health & Science University · USStanford University · USThe University of Texas MD Anderson Cancer Center · USUniversity Health Network · CAUniversity of Michigan–Ann Arbor · USUniversity of North Carolina at Chapel Hill · USUniversity of Rochester Medical Center · USUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The BCR-ABL tyrosine kinase produced by the t(9;22)(q34;q11) translocation, also known as the Philadelphia chromosome, is the initiating event in chronic myeloid leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL). Targeting of BCR-ABL with tyrosine kinase inhibitors (TKIs) has resulted in rapid clinical responses in the vast majority of patients with CML and Philadelphia chromosome+ ALL. However, long-term use of TKIs occasionally results in emergence of therapy resistance, in part through the selection of clones with mutations in the BCR-ABL kinase domain. We present here an overview of the current practice in monitoring for such mutations, including the methods used, the clinical and laboratory criteria for triggering mutational analysis, and the guidelines for reporting BCR-ABL mutations. We also present a proposal for a public database for correlating mutational status with in vitro and in vivo responses to different TKIs to aid in the interpretation of mutation studies.

Indexed as

MutationClinical Trials as TopicData CollectionDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositivePrecursor Cell Lymphoblastic Leukemia-LymphomaFusion Proteins, bcr-abl

Identifiers

PMID19095773
PMCPMC2607559
OpenAlexW1533032912

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.