Evidence map›Paper›PMID 21385932›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2011

Molecular karyotypes of Hodgkin and Reed-Sternberg cells at disease onset reveal distinct copy number alterations in chemosensitive versus refractory Hodgkin lymphoma.

Marilyn L Slovak, Victoria Bedell, Ya-Hsuan Hsu, Dolores B Estrine, Norma J Nowak, Maria L Delioukina, Lawrence M Weiss, David D Smith, Stephen J Forman

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

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  4. Genetic lesions and targeted therapy in Hodgkin lymphoma.Therapeutic advances in hematology · 2023
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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

9 authors at 3 institutions in 1 country.

Marilyn L SlovakCytogenetics Laboratory, Department of Hematology/Stem Cell Transplantation, City of Hope, Duarte, California 91010, USA.
Victoria Bedell
Ya-Hsuan Hsu
Dolores B Estrine
Norma J Nowak
Maria L Delioukina
Lawrence M Weiss
David D Smith
Stephen J Forman
Roswell Park Comprehensive Cancer Center · USCity Of Hope National Medical Center · USCity of Hope · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI STANLEY R. HAMILTON · 1985 to 2026
$86.3M
Transplant for Lymphoma:Therapy-Related LeukemiaP50CA107399 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI FORMAN, STEPHEN J, KWAK, LARRY W · 2004 to 2022
$35.5M
Vaccine-Induced Immunity to CMVP01CA030206 · NCI · CITY OF HOPE NATIONAL MEDICAL CENTER · PI FORMAN, STEPHEN J · 1985 to 2010
$31.8M
NCI NIH HHS CA016056NCI NIH HHS CA-30206NCI NIH HHS CA33572NCI NIH HHS P01 CA030206NCI NIH HHS P30 CA016056NCI NIH HHS P30 CA033572NCI NIH HHS P50 CA107399
6 · The paper itself

Abstract

purposeTo determine the recurring DNA copy number alterations (CNA) in classical Hodgkin lymphoma (HL) by microarray-based comparative genomic hybridization (aCGH) using laser capture microdissected CD30(+) Hodgkin and Reed-Sternberg (HRS) cells. EXPERIMENTAL

designArchived tissues from 27 CD30(+) HL plus control samples were analyzed by DNA microarrays. The HL molecular karyotypes were compared with the genomic profiles of germinal center B cells and treatment outcome (chemotherapy responsive vs. primary refractory disease).

resultsGains and losses observed in more than 35% of HL samples were localized to 22 and 12 chromosomal regions, respectively. Frequent gains (>65%) were associated with growth and proliferation, NF-κB activation, cell-cycle control, apoptosis, and immune and lymphoid development. Frequent losses (>40%) observed encompassed tumor suppressor genes (SPRY1, NELL1, and ID4, inhibitor of DNA binding 4), transcriptional repressors (TXNIP, thioredoxin interacting protein), SKP2 (S-phase kinase-associated protein 2; ubiquitin ligase component), and an antagonist of NF-κB activation (PPARGC1A). In comparison to the germinal center profiles, the most frequent imbalances in HL were losses in 5p13 (AMACR, GDNF, and SKP2), and gains in 7q36 (SHH, sonic hedgehog homolog) and 9q34 (ABL1, CDK9, LCN2, and PTGES). Gains (>35%) in the HL chemoresponsive patients housed genes known to regulate T-cell trafficking or NF-κB activation (CCL22, CX3CL1, CCL17, DOK4, and IL10), whereas the refractory samples showed frequent loss of 4q27 (interleukin; IL21/IL2) and 17p12, and gain of 19q13.3 (BCL3/RELB).

conclusionWe identified nonrandom CNAs in the molecular karyotypes of classical HL. Several recurring genetic lesions correlated with disease outcome. These findings may be useful prognostic markers in the counseling and management of patients and for the development of novel therapeutic approaches in primary refractory HL.

Indexed as

DNA Copy Number VariationsAdolescentAdultChildChild, PreschoolCohort StudiesComparative Genomic HybridizationDrug Resistance, NeoplasmEarly Detection of CancerFemaleGene Expression Regulation, NeoplasticHodgkin DiseaseHumansKaryotypingMaleMiddle Aged

Identifiers

PMID21385932
PMCPMC3096736
OpenAlexW2162223132

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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.