Evidence map›Paper›PMID 26208433›Full record

ArticleCancer letters2015

Simultaneous suppression of the MAP kinase and NF-κB pathways provides a robust therapeutic potential for thyroid cancer.

Koji Tsumagari, Zakaria Y Abd Elmageed, Andrew B Sholl, Paul Friedlander, Mohamed Abdraboh, Mingzhao Xing, A Hamid Boulares, Emad Kandil

Abstract read
In one paragraph

Article in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. NF-κB in Thyroid Cancer: An Update.International journal of molecular sciences · 2024
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Nuclear interaction of Arp2/3 complex and BRAFAmerican journal of cancer research · 2022
    Article
  8. Article
  9. Article
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  12. Article
  13. Article
  14. A possible role of GDDR in the development of Helicobacter pylori-associated gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  15. Article
  16. Article
  17. Article
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

8 authors.

Koji TsumagariDepartments of Surgery, Tulane University School of Medicine, New Orleans, LA 70112, USA; Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Zakaria Y Abd ElmageedDepartments of Surgery, Tulane University School of Medicine, New Orleans, LA 70112, USA; Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Andrew B ShollDepartments of Pathology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Paul FriedlanderDepartments of Otolaryngology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Mohamed AbdrabohDepartments of Surgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Mingzhao XingDivision of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
A Hamid BoularesThe Stanley Scott Cancer Center, Department of Pharmacology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA.
Emad KandilDepartments of Surgery, Tulane University School of Medicine, New Orleans, LA 70112, USA; Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA. Electronic address: ekandil@tulane.edu.

Funding

PARTICIPATION OF PARP-1 IN THE PATHOGENESIS OF ASTHMAR01HL072889 · NHLBI · LSU HEALTH SCIENCES CENTER · PI BOULARES, HAMID · 2004 to 2015
$3.4M
NHLBI NIH HHS HL072889NHLBI NIH HHS R01 HL072889
6 · The paper itself

Abstract

The MAP kinase and NF-κB signaling pathways play an important role in thyroid cancer tumorigenesis. We aimed to examine the therapeutic potential of dually targeting the two pathways using AZD6244 and Bortezomib in combination. We evaluated their effects on cell proliferation, cell-cycle progression, apoptosis, cell migration assay, and the activation of the MAPK pathway in vitro and the in vivo using tumor size and immunohistochemical changes of Ki67 and ppRB. We found inhibition of cell growth rate by 10%, 20%, and 56% (p <0.05), migration to 55%, 61%, and 29% (p <0.05), and induction of apoptosis to 10%, 15%, and 38% (p <0.05) with AZD6244, Bortezomib, or combination, respectively. Induction of cell cycle arrest occurred only with drug combination. Dual drug treatment in the xenograft model caused a 94% reduction in tumor size (p <0.05) versus 15% with AZD6244 and 34% with Bortezomib (p < 0.05) and also reduced proliferative marker Ki67, and increased pRb dephosphorylation. Our results demonstrate a robust therapeutic potential of combining AZD6244 and Bortezomib as an effective strategy to overcome drug resistance encountered in monotherapy in the treatment of thyroid cancer, strongly supporting clinical trials to further test this strategy.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBenzimidazolesBortezomibCell CycleCell Line, TumorCell MovementCell ProliferationDose-Response Relationship, DrugHumansMaleMice, Inbred BALB CMice, NudeMitogen-Activated Protein KinasesMutationAZD 6244BenzimidazolesBortezomibBRAF protein, humanMitogen-Activated Protein KinasesNF-kappa BProto-Oncogene Proteins B-rafAZD6244BortezomibMAPKNF-κBThyroid cancer

Identifiers

PMID26208433
PMCPMC4555189

What OpenQuestion holds

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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.