Evidence map›Paper›PMID 15018632›Full record

ArticleBMC cancer2004

Chromosomal amplifications, 3q gain and deletions of 2q33-q37 are the frequent genetic changes in cervical carcinoma.

Pulivarthi H Rao, Hugo Arias-Pulido, Xin-Yan Lu, Charles P Harris, Hernan Vargas, Fang F Zhang, Gopeshwar Narayan, Achim Schneider, Mary Beth Terry, Vundavalli V V S Murty

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Low-coverage whole-genome sequencing for differentiating cervical cancer from cervical intraepithelial neoplasia and benign diseases.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025
    Article
  3. Thymopoietin-The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025
    Article
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  7. Expression ofFrontiers in genetics · 2021
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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

10 authors at 7 institutions in 3 countries.

Pulivarthi H RaoTexas Children's Cancer Center, Baylor College of Medicine, Houston, TX, USA. prao@bcm.tmc.edu
Hugo Arias-Pulido
Xin-Yan Lu
Charles P Harris
Hernan Vargas
Fang F Zhang
Gopeshwar Narayan
Achim Schneider
Mary Beth Terry
Vundavalli V V S Murty
Cancer Genetics (United States) · USChildren's Cancer Center · USColumbia University · USBaylor College of Medicine · USFriedrich Schiller University Jena · DEInstituto Nacional de Cancerología · COUniversity of New Mexico · US

Funding

Molecular Genetics of Cervical Cancer ProgressionR21CA095647 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI VUNDAVALLI, MURTY V V S · 2003 to 2004
$393k
NCI NIH HHS CA095647NCI NIH HHS R21 CA095647
6 · The paper itself

Abstract

backgroundCarcinoma of uterine cervix is the second most common cancers among women worldwide. Combined radiation and chemotherapy is the choice of treatment for advanced stages of the disease. The prognosis is poor, with a five-year survival rate ranging from about 20-65%, depending on stage of the disease. Therefore, genetic characterization is essential for understanding the biology and clinical heterogeneity in cervical cancer (CC).

methodsWe used a genome-wide screening method--comparative genomic hybridization (CGH) to identify DNA copy number changes in 77 patients with cervical cancer. We applied categorical and survival analyses to analyze whether chromosomal changes were related to clinico-pathologic characteristics and patients survival.

resultsThe CGH analysis revealed a loss of 2q33-q37 (57.1%), gain of 3q (54.5%) and chromosomal amplifications (20.77%) as frequent genetic changes. A total of 15 amplified chromosomal sites were detected in 16 cases that include 1p31, 2q32, 7q22, 8q21.2-q24, 9p22, 10q21, 10q24, 11q13, 11q21, 12q15, 14q12, 17p11.2, 17q22, 18p11.2, and 19q13.1. Recurrent amplified sites were noted at 11q13, 11q21, and 19q13.1. The genomic alterations were further evaluated for prognostic significance in CC patients, and we did not find any correlation with a number of clinical or histological parameters. The tumors harboring HPV18 exhibited higher genomic instability compared to tumors with HPV 16.

conclusionsThis study demonstrated that 2q33-q37 deletions, 3q gains and chromosomal amplifications as characteristic changes in invasive CC. These genetic alterations will aid in the identification of novel tumor suppressor gene(s) at 2q33-q37 and oncogenes at amplified chromosomal sites. Molecular characterization of these chromosomal changes utilizing the current genomic technologies will provide new insights into the biology and clinical behavior of CC.

Indexed as

Chromosome DeletionGene AmplificationAdenocarcinomaCarcinoma, Squamous CellChromosomes, Human, Pair 2Chromosomes, Human, Pair 3FemaleHumansNucleic Acid HybridizationPapillomaviridaeUterine Cervical Neoplasms

Identifiers

PMID15018632
PMCPMC356916
OpenAlexW1805947811

What OpenQuestion holds

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Registered trials

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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.