Evidence map›Paper›PMID 26113859›Full record

ReviewFrontiers in genetics2015

Targeting ATM-deficient CLL through interference with DNA repair pathways.

Gero Knittel, Paul Liedgens, Hans C Reinhardt

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Open life sciences · 2022
    Article
  5. Article
  6. Article
  7. Non-Coding RNAs as Cancer Hallmarks in Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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 2 institutions in 1 country.

Gero KnittelDepartment of Internal Medicine, University Hospital of Cologne Cologne, Germany ; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne Cologne, Germany.
Paul LiedgensDepartment of Internal Medicine, University Hospital of Cologne Cologne, Germany ; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne Cologne, Germany.
Hans C ReinhardtDepartment of Internal Medicine, University Hospital of Cologne Cologne, Germany ; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne Cologne, Germany.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) is the most common form of leukemia in the Western world and accounts for approximately 30% of adult leukemias and 25% of non-Hodgkin lymphomas. The median age at diagnosis is 72 years. During recent years numerous genetic aberrations have been identified that are associated with an aggressive course of the disease and resistance against genotoxic chemotherapies. The DNA damage-responsive proapoptotic ATM-CHK2-p53 signaling pathway is frequently mutationally inactivated in CLL either through large deletions on chromosome 11q (ATM) or 17p (TP53), or through protein-damaging mutations. Here, we focus on the role of ATM signaling for the immediate DNA damage response, DNA repair and leukemogenesis. We further discuss novel therapeutic concepts for the targeted treatment of ATM-defective CLLs. We specifically highlight the potential use of PARP1 and DNA-PKcs inhibitors for the treatment of ATM-mutant CLL clones. Lastly, we briefly discuss the current state of genetically engineered mouse models of the disease and emphasize the use of these preclinical tools as a common platform for the development and validation of novel therapeutic agents.

Indexed as

chronic lymphocytic leukemiaDNA damage responseDNA-PKcs inhibitorPARP inhibitorprecision medicine

Identifiers

PMID26113859
PMCPMC4461826
OpenAlexW1568312177

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.