Evidence map›Paper›PMID 28825045›Full record

ArticleNPJ precision oncology2017

Targeting the duality of cancer.

Jack L Arbiser, Michael Y Bonner, Linda C Gilbert

Open access · goldAbstract read
In one paragraph

Article in NPJ precision oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed, 71 citations in OpenAlex.

  1. Chemoresistance: The hidden barrier in cancer treatment.Cancer pathogenesis and therapy · 2026
    Review
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  8. Identification of ANXA1 as a Novel Upstream Negative Regulator of Notch1 Function in AML.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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  10. Diterpenoids from the Aerial Parts ofMolecules (Basel, Switzerland) · 2024
    Article
  11. Globospiramine fromCells · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Review
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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

3 authors at 2 institutions in 1 country.

Jack L ArbiserDepartment of Dermatology, Emory University School of Medicine, Atlanta Veterans Administration Medical Center, Winship Cancer Institute, Atlanta, GA, USA.
Michael Y BonnerDepartment of Dermatology, Emory University School of Medicine, Atlanta Veterans Administration Medical Center, Winship Cancer Institute, Atlanta, GA, USA.
Linda C GilbertDepartment of Dermatology, Emory University School of Medicine, Atlanta Veterans Administration Medical Center, Winship Cancer Institute, Atlanta, GA, USA.
Winship Cancer InstituteEmory University · US

Funding

Cutaneous Hemangiomas and Signal TransductionR01AR047901 · NIAMS · EMORY UNIVERSITY · PI ARBISER, JACK L · 2001 to 2018
$4.3M
UV light and the cutaneous neurosensory systemP30AR042687 · NIAMS · EMORY UNIVERSITY · PI CAUGHMAN, STEWART W · 1994 to 2003
$2.5M
Role of microRNAs in the regulation of CML stem cell survival and self renewalR01CA163800 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI PERROTTI, DANILO · 2012 to 2017
$1.6M
Palladium based nanoparticles for the treatment of advanced melanomaI01BX002926 · VA · VETERANS HEALTH ADMINISTRATION · PI ARBISER, JACK L · 2016 to 2019
–
BLRD VA I01 BX002926NCI NIH HHS R01 CA163800NIAMS NIH HHS P30 AR042687NIAMS NIH HHS R01 AR047901
6 · The paper itself

Abstract

Cancer is the second leading cause of death in the United States, and is an increasing cause of death in the developing world. While there is great heterogeneity in the anatomic site and mutations involved in human cancer, there are common features, including immortal growth, angiogenesis, apoptosis evasion, and other features, that are common to most if not all cancers. However, new features of human cancers have been found as a result of clinical use of novel "targeted therapies," angiogenesis inhibitors, and immunotherapies, including checkpoint inhibitors. These findings indicate that cancer is a moving target, which can change signaling and metabolic features based upon the therapies offered. It is well-known that there is significant heterogeneity within a tumor and it is possible that treatment might reduce the heterogeneity as a tumor adapts to therapy and, thus, a tumor might be synchronized, even if there is no major clinical response. Understanding this concept is important, as concurrent and sequential therapies might lead to improved tumor responses and cures. We posit that the repertoire of tumor responses is both predictable and limited, thus giving hope that eventually we can be more effective against solid tumors. Currently, among solid tumors, we observe a response of 1/3 of tumors to immunotherapy, perhaps less to angiogenesis inhibition, a varied response to targeted therapies, with relapse and resistance being the rule, and a large fraction being insensitive to all of these therapies, thus requiring the older therapies of chemotherapy, surgery, and radiation. Tumor phenotypes can be seen as a continuum between binary extremes, which will be discussed further. The biology of cancer is undoubtedly more complex than duality, but thinking of cancer as a duality may help scientists and oncologists discover optimal treatments that can be given either simultaneously or sequentially.

Identifiers

PMID28825045
PMCPMC5559615
OpenAlexW2626666302

What OpenQuestion holds

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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.