Evidence map›Paper›PMID 18473727›Full record

ReviewAnti-cancer agents in medicinal chemistry2008

BRCA-FA pathway as a target for anti-tumor drugs.

Rachel Litman, Rigu Gupta, Robert M Brosh, Sharon B Cantor

Abstract readReview
In one paragraph

Review in Anti-cancer agents in medicinal chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. CD10Cell death & disease · 2017
    Article
  6. Curcumin reverses cisplatin resistance in cisplatin-resistant lung caner cells by inhibiting FA/BRCA pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  7. Article
  8. Fanconi anaemia: from a monogenic disease to sporadic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2011
    Review
  9. Article
  10. Susceptibility pathways in Fanconi's anemia and breast cancer.The New England journal of medicine · 2010
    Review
  11. Targeting DNA damage and repair by curcumin.Breast cancer : basic and clinical research · 2010
    Article
  12. Article
  13. Article
  14. Review
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

4 authors.

Rachel LitmanDepartment of Cancer Biology, University of Massachusetts Medical School, 364 Plantation St., Worcester, MA 01605, USA.
Rigu Gupta
Robert M Brosh
Sharon B Cantor

Funding

Roles Of DNA Helicases In Pathways Required For Maintenance Of Genomic StabilityZIAAG000741 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$7.6M
Fanconi Anemia PathwayZIAAG000753 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$4.3M
Roles Of Dna Helicases:Pathways Required For MaintenanceZ01AG000741 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT M · 2001 to 2008
$1.1M
Intramural NIH HHS Z01 AG000741
6 · The paper itself

Abstract

Promising research on DNA repair signaling pathways predicts a new age of anti-tumor drugs. This research was initiated through the discovery and characterization of proteins that functioned together in signaling pathways to sense, respond, and repair DNA damage. It was realized that tumor cells often lacked distinct DNA repair pathways, but simultaneously relied heavily on compensating pathways. More recently, researchers have begun to manipulate these compensating pathways to reign in and kill tumor cells. In a striking example it was shown that tumors derived from mutations in the DNA repair genes, of BRCA-FA pathway, were selectively sensitive to inhibition of the base excision repair pathway. These findings suggest that tumors derived from defects in DNA repair genes will be easier to treat clinically, providing a streamlined and targeted therapy that spares healthy cells. In the future, identifying patients with susceptible tumors and discovering additional DNA repair targets amenable to anti-tumor drugs will have a major impact on the course of cancer treatment.

Indexed as

AnimalsAntineoplastic AgentsBRCA1 ProteinCell Line, TumorDNA DamageDNA RepairFanconi Anemia Complementation Group ProteinsHumansNeoplasmsSignal TransductionAntineoplastic AgentsBRCA1 ProteinFanconi Anemia Complementation Group Proteins

Identifiers

PMID18473727
PMCPMC2564853

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.