Evidence map›Paper›PMID 18473726›Full record

ReviewAnti-cancer agents in medicinal chemistry2008

DNA repair proteins as molecular targets for cancer therapeutics.

Mark R Kelley, Melissa L Fishel

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 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

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

  1. Pooled it
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  4. Novel Peptide-Drug Conjugates with Dual Anticancer Activity.International journal of molecular sciences · 2024
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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

2 authors.

Mark R KelleyDepartment of Pediatrics, Section of Hematology/Oncology, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, 1044 W Walnut St. R4-W302C, Indianapolis, IN 46202, USA. mkelley@iupui.edu
Melissa L Fishel

Funding

Functions of MRP2 and MRP3 in Drug DispositionR01CA114574 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GALLO, JAMES M. · 2006 to 2011
$1.6M
Imbalancing DNA BER to enhance Ovarian Tumor SensitivityR01CA106298 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KELLEY, MARK R. · 2004 to 2008
$1.5M
Mechanism of Redox Regulation by Ape1/Ref-1R01CA114571 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI GEORGIADIS, MILLIE M · 2006 to 2010
$1.2M
Therapeutic/Mechanistic Role of Ape1 in Germ Cell TumorsR01CA094025 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KELLEY, MARK R. · 2003 to 2007
$1.1M
Chemosensitization of Pancreatic Tumors via Inhibition of a DNA BER Enzyme, Ape1R21CA122298 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FISHEL, MELISSA L. · 2007 to 2008
$333k
NCI NIH HHS CA 094025NCI NIH HHS CA 106298NCI NIH HHS CA 114574NCI NIH HHS R01 CA094025NCI NIH HHS R01 CA106298NCI NIH HHS R01 CA114571NCI NIH HHS R01 CA114574NCI NIH HHS R21 CA122298
6 · The paper itself

Abstract

Cancer therapeutics include an ever-increasing array of tools at the disposal of clinicians in their treatment of this disease. However, cancer is a tough opponent in this battle and current treatments which typically include radiotherapy, chemotherapy and surgery are not often enough to rid the patient of his or her cancer. Cancer cells can become resistant to the treatments directed at them and overcoming this drug resistance is an important research focus. Additionally, increasing discussion and research is centering on targeted and individualized therapy. While a number of approaches have undergone intensive and close scrutiny as potential approaches to treat and kill cancer (signaling pathways, multidrug resistance, cell cycle checkpoints, anti-angiogenesis, etc.), much less work has focused on blocking the ability of a cancer cell to recognize and repair the damaged DNA which primarily results from the front line cancer treatments; chemotherapy and radiation. More recent studies on a number of DNA repair targets have produced proof-of-concept results showing that selective targeting of these DNA repair enzymes has the potential to enhance and augment the currently used chemotherapeutic agents and radiation as well as overcoming drug resistance. Some of the targets identified result in the development of effective single-agent anti-tumor molecules. While it is inherently convoluted to think that inhibiting DNA repair processes would be a likely approach to kill cancer cells, careful identification of specific DNA repair proteins is increasingly appearing to be a viable approach in the cancer therapeutic cache.

Indexed as

Antineoplastic AgentsEnzyme InhibitorsAnimalsDNA DamageDNA RepairDNA Repair EnzymesHumansNeoplasmsAntineoplastic AgentsDNA Repair EnzymesEnzyme Inhibitors

Identifiers

PMID18473726
PMCPMC2430594

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.