Evidence map›Paper›PMID 26645663›Full record

ReviewPharmacology & therapeutics2016

AKT signaling in ERBB2-amplified breast cancer.

F Javier Carmona, Filippo Montemurro, Srinivasaraghavan Kannan, Valentina Rossi, Chandra Verma, José Baselga, Maurizio Scaltriti

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

43 citing papers in PubMed, 68 citations in OpenAlex.

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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

7 authors at 4 institutions in 3 countries.

F Javier CarmonaMemorial Sloan Kettering Cancer Center (MSKCC), Human Oncology and Pathogenesis Program (HOPP), NY, USA.
Filippo MontemurroUnit of Investigative Clinical Oncology, Institute for Cancer Research and Treatment, Candiolo, Italy.
Srinivasaraghavan KannanBioinformatics Institute (A*STAR), #07-01 Matrix, 30 Biopolis Street #07-01, 138671, Singapore.
Valentina RossiMedical Oncology, Ospedale Civile di Saluzzo, Saluzzo, Italy.
Chandra VermaBioinformatics Institute (A*STAR), #07-01 Matrix, 30 Biopolis Street #07-01, 138671, Singapore; Department of Biological Sciences, National University of Singapore, 14 Science Drive 4, 117543, Singapore; School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551, Singapore.
José BaselgaMemorial Sloan Kettering Cancer Center (MSKCC), Human Oncology and Pathogenesis Program (HOPP), NY, USA; Department of Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, NY 10065, USA.
Maurizio ScaltritiMemorial Sloan Kettering Cancer Center (MSKCC), Human Oncology and Pathogenesis Program (HOPP), NY, USA. Electronic address: scaltrim@mskcc.org.
Memorial Sloan Kettering Cancer Center · USAgency for Science, Technology and Research · SGCandiolo Cancer Institute · ITNanyang Technological University · SG

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
The possible role of the novel Akt 3 R247C mutation in opposing to anti-HER2 therR03CA187094 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SCALTRITI, MAURIZIO · 2014 to 2015
$176k
NCI NIH HHS P30 CA008748NCI NIH HHS R03 CA187094NCI NIH HHS R03CA187094-01
6 · The paper itself

Abstract

The PI3K/AKT pathway is the focus of several targeted therapeutic agents for a variety of malignancies. In ERBB2-amplified breast cancer, the hyperactivation of this signaling cascade is associated with resistance to ERBB2-targeted therapy. This can occur through gain-of-function alterations or compensatory mechanisms that enter into play upon pharmacological pressure. The strong rationale in combining anti-ERBB2 agents with PI3K/AKT inhibitors, together with the identification of genomic alterations conferring sensitivity to targeted inhibition, are guiding the design of clinical studies aimed at preventing the emergence of drug resistance and achieving more durable response. In the present review, we describe the involvement of this pathway in breast cancer pathogenesis, with an emphasis on AKT kinases, and provide insight into currently available targeted agents for the treatment of ERBB2-amplified breast cancer. Finally, we provide preliminary data on a novel AKT3 mutation detected in the context of resistance to anti-ERBB2 therapy as an example of genomics-based approaches towards uncovering novel actionable targets in this setting.

Indexed as

AnimalsBreast NeoplasmsDrug Resistance, NeoplasmFemaleGenes, erbB-2HumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKT3Drug resistancemTORPI3KTargeted therapyTrastuzumab

Identifiers

PMID26645663
PMCPMC4747800
OpenAlexW2185621054

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.