Evidence map›Paper›PMID 27550448›Full record

ArticleCancer research2016

The Greater Genomic Landscape: The Heterogeneous Evolution of Cancer.

Luay M Almassalha, Greta M Bauer, John E Chandler, Scott Gladstein, Igal Szleifer, Hemant K Roy, Vadim Backman

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Luay M AlmassalhaDepartment of Biomedical Engineering, Northwestern University, Evanston, Illinois.
Greta M BauerDepartment of Biomedical Engineering, Northwestern University, Evanston, Illinois.
John E ChandlerDepartment of Biomedical Engineering, Northwestern University, Evanston, Illinois.
Scott GladsteinDepartment of Biomedical Engineering, Northwestern University, Evanston, Illinois.
Igal SzleiferDepartment of Biomedical Engineering, Northwestern University, Evanston, Illinois. Chemistry of Life Processes Institute, Northwestern University, Evanston, Illinois. v-backman@northwestern.edu igalsz@northwestern.edu hkroy@bu.edu.
Hemant K RoySection of Gastroenterology, Boston Medical Center/Boston University School of Medicine, Boston, Massachusetts. v-backman@northwestern.edu igalsz@northwestern.edu hkroy@bu.edu.
Vadim BackmanDepartment of Biomedical Engineering, Northwestern University, Evanston, Illinois. Chemistry of Life Processes Institute, Northwestern University, Evanston, Illinois. v-backman@northwestern.edu igalsz@northwestern.edu hkroy@bu.edu.
Northwestern University · USBoston Medical Center · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM008152 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARDEHALI, HOSSEIN · 1987 to 2021
$24.0M
Spatio-Temporal Organization of Chromatin and Information Transfer in CancerU54CA193419 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LICHT, JONATHAN D., O'HALLORAN, THOMAS V · 2015 to 2020
$10.4M
Training Program In Lung SciencesT32HL076139 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAREN M RIDGE, Jacob I Sznajder · 2004 to 2026
$9.6M
Nanoscale/Molecular analysis of Fecal Colonocytes for Colorectal Cancer ScreeningR01CA165309 · NCI · NORTHWESTERN UNIVERSITY · PI BACKMAN, VADIM, ROY, HEMANT K. · 2012 to 2016
$2.8M
Optical Nanoscale Analysis of Buccal Cells: Transforming Lung Cancer ScreeningR01CA155284 · NCI · NORTHWESTERN UNIVERSITY · PI BACKMAN, VADIM, ROY, HEMANT K. · 2011 to 2014
$2.3M
NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA155284NCI NIH HHS R01 CA165309NCI NIH HHS U54 CA193419NHLBI NIH HHS T32 HL076139NIGMS NIH HHS T32 GM008152
6 · The paper itself

Abstract

Results have historically shown a broad plasticity in the origin of tumors and their functions, with significant heterogeneity observed in both morphologies and functional capabilities. Largely unknown, however, are the mechanisms by which these variations occur and how these events influence tumor formation and behavior. Contemporary views on the origin of tumors focus mainly on the role of particular sets of driver transformations, mutational or epigenetic, with the occurrence of the observed heterogeneity as an accidental byproduct of oncogenesis. As such, we present a hypothesis that tumors form due to heterogeneous adaptive selection in response to environmental stress through intrinsic genomic sampling mechanisms. Specifically, we propose that eukaryotic cells intrinsically explore their available genomic information, the greater genomic landscape (GGL), in response to stress under normal conditions, long before the formation of a cancerous lesion. Finally, considering the influence of chromatin heterogeneity on the GGL, we propose a new class of compounds, chromatin-protective therapies (CPT), which target the physical variations in chromatin topology. In this approach, CPTs reduce the overall information space available to limit the formation of tumors or the development of drug-resistant phenotypes. Cancer Res; 76(19); 5605-9. ©2016 AACR.

Indexed as

ChromatinDrug Resistance, NeoplasmEvolution, MolecularGenomicsHumansNeoplasmsSelection, GeneticChromatin

Identifiers

PMID27550448
PMCPMC5084919
OpenAlexW2511185819

What OpenQuestion holds

Textmetadata
LicenceTDM
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.