Evidence map›Paper›PMID 7706497›Full record

ArticleThe Journal of clinical investigation1995

Apoptosis induced by an anti-epidermal growth factor receptor monoclonal antibody in a human colorectal carcinoma cell line and its delay by insulin.

X Wu, Z Fan, H Masui, N Rosen, J Mendelsohn

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
10.4field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 386 citations in OpenAlex.

  1. Pooled it
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  4. Insulin, glucose, insulin resistance, and incident colorectal cancer in male smokers.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2006
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26 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

5 authors at 2 institutions in 1 country.

X WuDepartment of Medicine, Memorial Sloan-Kettering Cancer Center, New York, USA.
Z Fan
H Masui
N Rosen
J Mendelsohn
Cornell University · USMemorial Sloan Kettering Cancer Center · US

Funding

ANTITUMOR ACTIVITIES OF ANTIRECEPTOR ANTIBODIESR01CA042060 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI KUMAR, RAKESH · 1985 to 1988
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ANTITUMOR ACTIVITIES OF ANTIRECEPTOR ANTIBODIESR37CA042060 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI MENDELSOHN, JOHN · 1989 to 1996
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ANTIRECEPTOR MONOCLONAL ANTIBODY IN CANCER TREATMENTU01CA037641 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI KUMAR, RAKESH · 1985 to 1994
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EFFICACY AND TOXICITY OF IRON DEPRIVATION TREATMENTU19CA037641 · NCI · UNIVERSITY OF ARIZONA · PI REISFELD, RALPH A. · 1995 to 1997
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NCI NIH HHS CA-37641NCI NIH HHS CA-42060
6 · The paper itself

Abstract

Both EGF and insulin, or IGF, stimulate the growth of many cell types by activating receptors that contain tyrosine kinase activities. A monoclonal antibody (mAb 225) against the EGF receptor produced in this laboratory has been shown to competitively inhibit EGF binding and block activation of receptor tyrosine kinase. Here we report that a human colorectal carcinoma cell line, DiFi, which expresses high levels of EGF receptors on plasma membranes, can be induced to undergo G1 cell cycle arrest and programmed cell death (apoptosis) when cultured with mAb 225 at concentrations that saturate EGF receptors. Addition of IGF-1 or high concentrations of insulin can delay apoptosis induced by mAb 225, while the G1 arrest cannot be reversed by either IGF-1 or insulin. Insulin/IGF-1 cannot activate EGF receptor tyrosine kinase that has been inhibited by mAb 225. Moreover, an mAb against the IGF-1 receptor, which has little direct effect on DiFi cell growth, can block the capacity of insulin/IGF-1 to delay apoptosis induced by mAb 225, suggesting that the insulin/IGF-1-mediated delay of apoptosis is acting through the IGF-1 receptor. In contrast, insulin/IGF-1 cannot delay the apoptosis caused by the DNA damaging agent, cisplatin. The results indicate that EGF receptor activation is required both for cell cycle progression and for prevention of apoptosis in DiFi cells, and that a signal transduction pathway shared by receptors for insulin/IGF-1 and EGF may be involved in regulating apoptosis triggered by blockade of the EGF receptor.

Indexed as

Antibodies, MonoclonalApoptosisCarcinomaCell CycleCisplatinColorectal NeoplasmsDrug InteractionsErbB ReceptorsHumansInsulinInsulin-Like Growth Factor IPhosphorylationReceptor, IGF Type 1Retinoblastoma ProteinTumor Cells, CulturedAntibodies, MonoclonalCisplatinErbB ReceptorsInsulinInsulin-Like Growth Factor IReceptor, IGF Type 1Retinoblastoma Protein

Identifiers

PMID7706497
PMCPMC295734
OpenAlexW2038882649

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.