Evidence map›Paper›PMID 26968398›Full record

ReviewBreast cancer research and treatment2016

Developmental signaling pathways regulating mammary stem cells and contributing to the etiology of triple-negative breast cancer.

Maria Cristina Rangel, Daniel Bertolette, Nadia P Castro, Malgorzata Klauzinska, Frank Cuttitta, David S Salomon

Open access · hybridAbstract readReview
In one paragraph

Review in Breast cancer research and treatment, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

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  20. Dll1Nature communications · 2021
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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

6 authors at 4 institutions in 1 country.

Maria Cristina RangelTumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Building 560, Room 32-40B, 1050 Boyles Street, Ft. Detrick, Frederick, MD, 21702, USA.
Daniel BertoletteTumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Building 560, Room 32-40B, 1050 Boyles Street, Ft. Detrick, Frederick, MD, 21702, USA.
Nadia P CastroTumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Building 560, Room 32-40B, 1050 Boyles Street, Ft. Detrick, Frederick, MD, 21702, USA.
Malgorzata KlauzinskaTumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Building 560, Room 32-40B, 1050 Boyles Street, Ft. Detrick, Frederick, MD, 21702, USA.
Frank CuttittaTumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Building 560, Room 32-40B, 1050 Boyles Street, Ft. Detrick, Frederick, MD, 21702, USA.
David S SalomonTumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Building 560, Room 32-40B, 1050 Boyles Street, Ft. Detrick, Frederick, MD, 21702, USA. salomond@mail.nih.gov.
Center for Cancer Research · USFrederick National Laboratory for Cancer Research · USCancer Genetics (United States) · USNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer has been considered as temporal and spatial aberrations of normal development in tissues. Similarities between mammary embryonic development and cell transformation suggest that the underlying processes required for mammary gland development are also those perturbed during various stages of mammary tumorigenesis and breast cancer (BC) development. The master regulators of embryonic development Cripto-1, Notch/CSL, and Wnt/β-catenin play key roles in modulating mammary gland morphogenesis and cell fate specification in the embryo through fetal mammary stem cells (fMaSC) and in the adult organism particularly within the adult mammary stem cells (aMaSC), which determine mammary progenitor cell lineages that generate the basal/myoepithelial and luminal compartments of the adult mammary gland. Together with recognized transcription factors and embryonic stem cell markers, these embryonic regulatory molecules can be inappropriately augmented during tumorigenesis to support the tumor-initiating cell (TIC)/cancer stem cell (CSC) compartment, and the effects of their deregulation may contribute for the etiology of BC, in particular the most aggressive subtype of BC, triple-negative breast cancer (TNBC). This in depth review will present evidence of the involvement of Cripto-1, Notch/CSL, and Wnt/β-catenin in the normal mammary gland morphogenesis and tumorigenesis, from fMaSC/aMaSC regulation to TIC generation and maintenance in TNBC. Specific therapies for treating TNBC by targeting these embryonic pathways in TICs will be further discussed, providing new opportunities to destroy not only the bulk tumor, but also TICs that initiate and promote the metastatic spread and recurrence of this aggressive subtype of BC.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsFemaleGene Expression Regulation, NeoplasticHumansMammary Glands, HumanNeoplastic Stem CellsTranscription FactorsTriple Negative Breast NeoplasmsAntineoplastic AgentsTranscription FactorsCripto-1fMaSC/aMaSCNotch/CSLTIC/CSCTNBCWnt/β-catenin

Identifiers

PMID26968398
PMCPMC4819564
OpenAlexW2296347968

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.