Evidence map›Paper›PMID 24157582›Full record

ReviewLeukemia2014

Immunotherapy for chronic lymphocytic leukemia in the era of BTK inhibitors.

M A Kharfan-Dabaja, W G Wierda, L J N Cooper

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Immunomodulation in leukemia: cellular aspects of anti-leukemic properties.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Outcomes of Patients With Chronic Lymphocytic Leukemia and Richter's Transformation After Transplantation Failure.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015
    Article
  9. Review
  10. Review
  11. Review
  12. 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

3 authors at 3 institutions in 1 country.

M A Kharfan-Dabaja1] Department of Blood and Marrow Transplantation, H. Lee Moffitt Cancer Center, Tampa, FL, USA [2] Department of Oncologic Sciences, H. Lee Moffitt Cancer Center, University of South Florida College of Medicine, Tampa, FL, USA.
W G WierdaDepartment of Leukemia, MD Anderson Cancer Center, University of Texas, Houston, TX, USA.
L J N Cooper1] Graduate School of Biomedical Sciences, University of Texas, Houston, TX, USA [2] Division of Pediatrics, MD Anderson Cancer Center, University of Texas, Houston, TX, USA.
Moffitt Cancer Center · USThe University of Texas MD Anderson Cancer Center · USUniversity of Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
6 · The paper itself

Abstract

Understanding the pathogenesis of CLL has uncovered a plethora of novel targets for human application of monoclonal antibodies, engineered T cells, or inhibitors of signal transduction pathways. The B-cell receptor signaling pathway is being actively explored as a therapeutic target in CLL. Ibrutinib, an inhibitor of Bruton's tyrosine kinase is showing impressive responses in heavily pre-treated high-risk CLL, whether alone or in combination with MoAbs or chemotherapy. Other key components of the BCR pathway, namely PI3K-δ, are also being targeted with novel therapies with promising results as well. Future trials would likely evaluate ibrutinib in the front-line setting. Moreover, improvements in allogeneic HCT mostly by continuing to reduce associated toxicity as well as incorporating cellular therapies such as autologous CLL tumor vaccines, among others, will continue to expand. This is also the case for the next generation of chimeric antigen receptor therapy for CLL once genetically modified T cells are available at broad scale and with improved efficacy. As our ability to further refine and integrate these therapies continues to improve, and we gain further knowledge from gene sequencing, we anticipate that treatment algorithms will continue to be revised to a more personalized approach to treat this disease with improved efficacy and devoid of unnecessary toxicity.

Indexed as

ImmunotherapyAgammaglobulinaemia Tyrosine KinaseCell TransplantationHematopoietic Stem Cell TransplantationHumansImmune ToleranceLenalidomideLeukemia, Lymphocytic, Chronic, B-CellProtein Kinase InhibitorsProtein-Tyrosine KinasesThalidomideAgammaglobulinaemia Tyrosine KinaseBTK protein, humanLenalidomideProtein Kinase InhibitorsProtein-Tyrosine KinasesThalidomide

Identifiers

PMID24157582
OpenAlexW1996083006

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.