Evidence map›Paper›PMID 27391340›Full record

ArticleOncotarget2016

Notch pathway activation is essential for maintenance of stem-like cells in early tongue cancer.

Pawan Upadhyay, Sudhir Nair, Ekjot Kaur, Jyotirmoi Aich, Prachi Dani, Vidyalakshmi Sethunath, Nilesh Gardi, Pratik Chandrani, Mukul Godbole, Kavita Sonawane and 7 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  14. Review
  15. HPVTranslational oncology · 2021
    Review
  16. Review
  17. Trop2 Promotes Multidrug Resistance by Regulating Notch1 Signaling Pathway in Gastric Cancer Cells.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  18. Article
  19. Article
  20. 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

17 authors at 2 institutions in 1 country.

Pawan UpadhyayIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Sudhir NairDivision of Head and Neck Oncology, Department of Surgical Oncology, Tata Memorial Hospital, Tata Memorial Centre, Mumbai- 4100012, India.
Ekjot KaurShilpee Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Jyotirmoi AichIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Prachi DaniIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Vidyalakshmi SethunathIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Nilesh GardiIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Pratik ChandraniIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Mukul GodboleIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Kavita SonawaneDivision of Head and Neck Oncology, Department of Surgical Oncology, Tata Memorial Hospital, Tata Memorial Centre, Mumbai- 4100012, India.
Ratnam PrasadIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Sadhana KannanAdvanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Beamon AgarwalDepartment of Pathology, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Shubhada KaneDepartment of Pathology, Tata Memorial Hospital, Tata Memorial Centre, Mumbai- 400012, India.
Sudeep GuptaDepartment of Medical Oncology, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Mumbai- 400012, India.
Shilpee DuttShilpee Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Amit DuttIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education In Cancer, Tata Memorial Centre, Navi Mumbai- 410210, India.
Tata Memorial Hospital · INAdvanced Centre for Treatment, Research and Education in Cancer · IN

Funding

DBT-Wellcome Trust India Alliance IA/I/11/2500278
6 · The paper itself

Abstract

backgroundNotch pathway plays a complex role depending on cellular contexts: promotes stem cell maintenance or induces terminal differentiation in potential cancer-initiating cells; acts as an oncogene in lymphocytes and mammary tissue or plays a growth-suppressive role in leukemia, liver, skin, and head and neck cancer. Here, we present a novel clinical and functional significance of NOTCH1 alterations in early stage tongue squamous cell carcinoma (TSCC). PATIENTS AND

methodsWe analyzed the Notch signaling pathway in 68 early stage TSCC primary tumor samples by whole exome and transcriptome sequencing, real-time PCR based copy number, expression, immuno-histochemical, followed by cell based biochemical and functional assays.

resultsWe show, unlike TCGA HNSCC data set, NOTCH1 harbors significantly lower frequency of inactivating mutations (4%); is somatically amplified; and, overexpressed in 31% and 37% of early stage TSCC patients, respectively. HNSCC cell lines over expressing NOTCH1, when plated in the absence of attachment, are enriched in stem cell markers and form spheroids. Furthermore, we show that inhibition of NOTCH activation by gamma secretase inhibitor or shRNA mediated knockdown of NOTCH1 inhibits spheroid forming capacity, transformation, survival and migration of the HNSCC cells suggesting an oncogenic role of NOTCH1 in TSCC. Clinically, Notch pathway activation is higher in tumors of non-smokers compared to smokers (50% Vs 18%, respectively, P=0.026) and is also associated with greater nodal positivity compared to its non-activation (93% Vs 64%, respectively, P=0.029).

conclusionWe anticipate that these results could form the basis for therapeutic targeting of NOTCH1 in tongue cancer.

Indexed as

AdultAgedCarcinoma, Squamous CellCell DifferentiationCell Line, TumorCell MovementCell ProliferationCell SurvivalExomeFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedMutationNeoplastic Stem CellsNOTCH1 protein, humanReceptor, Notch1cancer stem cell-like featureearly stage tongue cancerexome and transcriptome sequencingIHC based expression analysisNotch pathway inhibitors

Identifiers

PMID27391340
PMCPMC5226594
OpenAlexW2464045293

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.