Evidence map›Paper›PMID 20924105›Full record

ArticleCancer research2010

Impact of stromal sensitivity on radiation response of tumors implanted in SCID hosts revisited.

Mónica García-Barros, Tin Htwe Thin, Jerzy Maj, Carlos Cordon-Cardo, Adriana Haimovitz-Friedman, Zvi Fuks, Richard Kolesnick

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 63 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Mónica García-BarrosLaboratory of Signal Transduction and Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center; Department of Pathology, Columbia University, New York, NY 10065, USA.
Tin Htwe Thin
Jerzy Maj
Carlos Cordon-Cardo
Adriana Haimovitz-Friedman
Zvi Fuks
Richard Kolesnick
Memorial Sloan Kettering Cancer Center · USColumbia University · US

Funding

MODULATION OF CERAMIDE INDUCED APOPTOSIS IN VIVOR01CA085704 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI KOLESNICK, RICHARD N · 2000 to 2009
$3.7M
Ceramide synthase as a therapy target in prostate cancerR01CA105125 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI HAIMOVITZ-FRIEDMAN, ADRIANA · 2005 to 2009
$1.6M
NCI NIH HHS R01 CA085704NCI NIH HHS R01 CA105125
6 · The paper itself

Abstract

Severe combined immunodeficient (SCID) mice carry a germ-line mutation in DNA-PK, associated with deficiency in recognition and repair DNA double-strand breaks. Thus, SCID cells and tissues display increased sensitivity to radiation-induced postmitotic (clonogenic) cell death. Nonetheless, the single-radiation doses required for 50% permanent local control (TCD(50)) of tumors implanted in SCID mice are not significantly different from the TCD(50) values of the same tumors in wild-type hosts. Whereas the tumor stroma is derived from the host, the observation that tumors implanted in SCID mice do not exhibit hypersensitivity to radiation might imply that stromal endothelial elements do not contribute substantially to tumor cure by ionizing radiation. Here, we challenge this notion, testing the hypothesis that ASMase-mediated endothelial apoptosis, which results from plasma membrane alterations, not DNA damage, is a crucial element in the cure of tumors in SCID mice by single-dose radiotherapy (SDRT). We show that the endothelium in MCA/129 fibrosarcomas and B16 melanomas exhibits a wild-type apoptotic phenotype in SCID hosts, abrogated in tumors in SCID(asmase-/-) littermates, which also acquire resistance to SDRT. Conversion into a radioresistant tumor phenotype when implanted in SCID(asmase-/-) hosts provides compelling evidence that cell membrane ASMase-mediated microvascular dysfunction, rather than DNA damage-mediated endothelial clonogenic lethality, plays a mandatory role in the complex pathophysiologic mechanism of tumor cure by SDRT, and provides an explanation for the wild-type SDRT responses reported in tumors implanted in SCID mice.

Indexed as

AnimalsApoptosisCell DeathCell DivisionCrosses, GeneticDNA DamageFibrosarcomaIn Situ Nick-End LabelingMelanoma, ExperimentalMiceMice, Inbred C57BLMice, SCIDMutationSevere Combined Immunodeficiency

Identifiers

PMID20924105
PMCPMC2976483
OpenAlexW2152237718

What OpenQuestion holds

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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.