Evidence map›Paper›PMID 28281554›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2017

Additional-structural-chromosomal aberrations are associated with inferior clinical outcome in patients with hyperdiploid multiple myeloma: a single-institution experience.

Adrian A Carballo-Zarate, L Jeffrey Medeiros, Lianghua Fang, Jatin J Shah, Donna M Weber, Sheeba K Thomas, Elisabet E Manasanch, Suyang Hao, Qi Shen, Robert Z Orlowski and 2 more

Open access · bronzeAbstract read
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In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. The survival impact of CKS1B gains or amplification is dependent on the background karyotype and TP53 deletion status in patients with myeloma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021
    Article
  6. Review
  7. Article
  8. Review
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

12 authors at 4 institutions in 2 countries.

Adrian A Carballo-ZarateDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
L Jeffrey MedeirosDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Lianghua FangDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jatin J ShahDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Donna M WeberDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Sheeba K ThomasDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Elisabet E ManasanchDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Suyang HaoDepartment of Pathology and Laboratory Medicine, The Methodist Hospital, Houston, TX, USA.
Qi ShenCentral Florida Pathology Associates, Orlando, FL, USA.
Robert Z OrlowskiDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Pei LinDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Xinyan LuDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · USFlorida Urology Associates · USMethodist Hospital · USNorthwestern University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
SWOG - Foreign Accrual under UMiU10CA032102 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BLANKE, CHARLES D. · 1985 to 2013
$141.3M
Role of TJP1 in Sensitivity and Resistance to Proteasome Inhibitors in MyelomaR01CA184464 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ORLOWSKI, ROBERT ZYGMUNT · 2015 to 2019
$1.8M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA184464NCI NIH HHS U10 CA032102
6 · The paper itself

Abstract

Multiple myeloma is cytogenetically heterogeneous and a hyperdiploid karyotype is considered currently to have standard risk. In this study, we investigated the clinical impact of additional-structural-chromosomal aberrations assessed by chromosome analysis in 284 patients with a hyperdiploid karyotype that were subdivided into four groups based on the complexity of additional-structural-chromosomal aberrations: group 1, no additional-structural-chromosomal aberrations (n=35); group 2, one additional-structural-chromosomal aberration (n=46); group 3, two additional-structural-chromosomal aberrations (n=39); group 4, ≥three additional-structural-chromosomal aberrations (n=164). Clinicopathological data among these groups showed no differences, except patients in group 1 had higher hemoglobin (P=0.031) and albumin (P=0.045) levels. The median follow-up was 55 months (range, 3-221). The median overall survival of patients in groups 1-4 was negatively correlated with the number of the additional-structural-chromosomal aberrations: 98, 76, 61, and 48 months, respectively (P<0.0001). In group 4, CKS1B gain, RB1, or TP53 deletions had no additional impact on overall survival; however, trisomy 3 or 15 conferred a much better overall survival, and monosomy 13 and 14 predicted a worse outcome. In addition, the overall survival of patients in groups 3 and 4 was similar to a subset of high-risk multiple myeloma cases (n=21) (P=0.387). About 192 (67.6%) patients who received stem cell transplantation did not show improved overall survival compared with non-stem cell transplantation patients (n=92; P=0.142) overall; however, they did show significantly improved overall survival in patients with refractory disease in group 4 (P=0.0084). Multivariate analysis showed that two or more additional-structural-chromosomal aberrations (P<0.0001), stages (P=0.02 and P=0.002) and relapsed disease (P=0.009) negatively impacted the overall survival. We conclude that hyperdiploid karyotypes in multiple myeloma are associated with additional-structural-chromosomal aberrations and a greater number of additional-structural-chromosomal aberrations predicts poorer clinical outcome. A hyperdiploid karyotype with ≥2 additional-structural-chromosomal aberrations at chromosomal level should be considered an independent high-risk factor.

Indexed as

Chromosome AberrationsDiploidyAdultAgedAged, 80 and overBiomarkers, TumorCDC2-CDC28 KinasesChromosomes, HumanFemaleGenetic Predisposition to DiseaseHumansIn Situ Hybridization, FluorescenceKaplan-Meier EstimateKaryotypeMaleMiddle AgedBiomarkers, TumorCDC2-CDC28 KinasesCKS1B protein, humanRB1 protein, humanRetinoblastoma Binding ProteinsTP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID28281554
OpenAlexW2593946176

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.