Evidence map›Paper›PMID 22237395›Full record

ReviewNature reviews. Cancer2012

Balancing repair and tolerance of DNA damage caused by alkylating agents.

Dragony Fu, Jennifer A Calvo, Leona D Samson

2 registry-linked trialsOpen access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 504 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
504citing papers in PubMed, 3 pooled it
0.8field-weighted citation impact, top 30% 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.

NCT04689347 phase1 / phase2recruitingnot on this mapstarted 2021, after this paper: background citation

Phase 1b/2 Trial of 5-fluorouracil, Leucovorin, Irinotecan in Combination With Temozolomide (FLIRT) and Bevacizumab for the First-line Treatment of Patients With MGMT Silenced, Microsatellite Stable Metastatic Colorectal Cancer.

TypeinterventionalSponsorFondazione IRCCS Istituto Nazionale dei Tumori, MilanoRan2021 to 2027Enrolled27ConditionsMetastatic Colorectal CancerArmsBevacizumab, Irinotecan, Leucovorin, 5Fluorouracil, Temozolomide
NCT05031975 phase2unknown statusnot on this mapstarted 2022, after this paper: background citation

Temozolomide and Irinotecan Consolidation in Patients With MGMT Silenced, Microsatellite Stable Colorectal Cancer With Persistence of Minimal Residual Disease in Liquid Biopsy After Standard Adjuvant Chemotherapy: the ERASE-TMZ Study

TypeinterventionalSponsorFondazione IRCCS Istituto Nazionale dei Tumori, MilanoRan2022 to 2024Enrolled35ConditionsColorectal CancerArmsIrinotecan, Temozolomide
3 · Its place in the literature

Who cites it

504 citing papers in PubMed, 3 syntheses or guidelines pooled it, 30 citations in OpenAlex.

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444 more citing papers are in PubMed but not listed here.

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.

Dragony FuDepartment of Biological Engineering, Center for Environmental Health Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Jennifer A Calvo
Leona D Samson
Massachusetts Institute of Technology · US

Funding

TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FOX, JAMES G · 1985 to 2020
$25.6M
IN VIVO ROLE OF DNA ALKYLATION REPAIRR01CA075576 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1997 to 2011
$4.9M
EUKARYTIC DNA ALKYLATION REPAIRR01CA055042 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1991 to 2010
$4.8M
Developing novel methods to measure DNA repair capacity in human populationsDP1OD006422 · OD · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 2009 to 2011
$2.5M
The influence of DNA repair on inflammation associated carcinogenesisR01CA149261 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 2010 to 2014
$1.7M
Developing novel methods to measure DNA repair capacity in human populationsDP1ES022576 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 2012 to 2013
$1.6M
NCI NIH HHS CA055042NCI NIH HHS CA075576NCI NIH HHS CA112967NCI NIH HHS CA149261NCI NIH HHS R01 CA055042NCI NIH HHS R01 CA075576NCI NIH HHS R01 CA149261NIEHS NIH HHS DP1 ES022576NIEHS NIH HHS ES002109NIEHS NIH HHS P30 ES002109NIH HHS DP1 OD006422NIH HHS DP1-OD006422
6 · The paper itself

Abstract

Alkylating agents constitute a major class of frontline chemotherapeutic drugs that inflict cytotoxic DNA damage as their main mode of action, in addition to collateral mutagenic damage. Numerous cellular pathways, including direct DNA damage reversal, base excision repair (BER) and mismatch repair (MMR), respond to alkylation damage to defend against alkylation-induced cell death or mutation. However, maintaining a proper balance of activity both within and between these pathways is crucial for a favourable response of an organism to alkylating agents. Furthermore, the response of an individual to alkylating agents can vary considerably from tissue to tissue and from person to person, pointing to genetic and epigenetic mechanisms that modulate alkylating agent toxicity.

Indexed as

DNA DamageDNA RepairAlkylating AgentsBase Pair MismatchHumansAlkylating Agents

Identifiers

PMID22237395
PMCPMC3586545
OpenAlexW1530962156

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.