Evidence map›Paper›PMID 22329458›Full record

ReviewExpert opinion on investigational drugs2012

Sapacitabine for cancer.

Xiaojun Liu, Hagop Kantarjian, William Plunkett

Abstract readReview
In one paragraph

Review in Expert opinion on investigational drugs, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Therapeutic Advances in Oncology.International journal of molecular sciences · 2021
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. HDAC Inhibition Induces MicroRNA-182, which Targets RAD51 and Impairs HR Repair to Sensitize Cells to Sapacitabine in Acute Myelogenous Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  10. Article
  11. 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 1 institution in 1 country.

Xiaojun LiuThe University of Texas M.D. Anderson Cancer Center, Department of Experimental Therapeutics, Houston, TX, USA.
Hagop Kantarjian
William Plunkett
The University of Texas MD Anderson Cancer Center · US

Funding

Tissue CoreP01CA081534 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KIPPS, THOMAS J · 2000 to 2016
$59.5M
University of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DRAETTA, GIULIO FRANCESCO · 2003 to 2023
$43.7M
TOLERANCE INDUCTION BY MEGADOSE STEM CELL TRANSPLANTS IN CML--GVHD AND GVLP01CA049639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THALL, PETER F · 1990 to 2014
$41.8M
Tyrosine Kinases, Serine-Threonine Kinases,&Phosophatases in PathogenesisP01CA108631 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ESTEY, ELIHU · 2005 to 2009
$9.7M
BIOCHEMICAL BASIS FOR THERAPEUTIC ACTIVITYR01CA028596 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PLUNKETT, WILLIAM K · 1985 to 2015
$3.0M
Novel pharmacologic agents in CLLP20CA081534 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI KIPPS, THOMAS J. · 1999 to 1999
–
NCI NIH HHS CA100532NCI NIH HHS CA28596NCI NIH HHS CA81534NCI NIH HHS P01 CA049639NCI NIH HHS P01 CA081534NCI NIH HHS P01 CA108631NCI NIH HHS P20 CA081534NCI NIH HHS P50 CA100632NCI NIH HHS R01 CA028596
6 · The paper itself

Abstract

introductionSapacitabine is an orally bioavailable nucleoside analog prodrug that is in clinical trials for hematologic malignancies and solid tumors. The active metabolite of sapacitabine, CNDAC (2'-C-cyano-2'-deoxy-1-β-D-arabino-pentofuranosylcytosine), exhibits the unique mechanism of action of causing single-strand breaks (SSBs) after incorporation into DNA, which are converted into double-strand breaks (DSBs) when cells enter a second S-phase. CNDAC-induced DSBs are predominantly repaired through homologous recombination (HR). Cells deficient in HR components are greatly sensitized to CNDAC. Therefore, sapacitabine could be specifically effective against tumors that are deficient in this repair pathway. AREAS COVERED: This review summarizes results from supporting evidence for the mechanisms of action of sapacitabine, its preclinical activities and the current results of clinical trials in a variety of cancers. The novel action mechanism of sapacitabine is discussed, with a view to validate it as a chemotherapeutic drug targeting malignancies with defects in HR. EXPERT OPINION: Knowledge of CNDAC mechanism identifies tumors that may be sensitized to sapacitabine, thus enabling a personalized treatment strategy. It also creates the opportunity to overcome resistance to current front-line therapies and identify synergistic interactions with known anticancer drugs. The results of such investigations may provide rationales for the design of sapacitabine-based clinical trials.

Indexed as

AnimalsArabinonucleosidesCell CycleClinical Trials as TopicCytosineDNA DamageDrug Evaluation, PreclinicalHumansNeoplasmsProdrugsRandomized Controlled Trials as TopicArabinonucleosidesCytosineProdrugssapacitabine

Identifiers

PMID22329458
PMCPMC3366487
OpenAlexW1980207802

What OpenQuestion holds

Textmetadata
LicenceTDM
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.