Evidence map›Paper›PMID 36111352›Full record

ArticleAging cell2022

Age alters the oncogenic trajectory toward luminal mammary tumors that activate unfolded proteins responses.

Edmund Charles Jenkins, Mrittika Chattopadhyay, Maria Gomez, Denis Torre, Avi Ma'ayan, Miguel Torres-Martin, Daniela Sia, Doris Germain

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. 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 at 4 institutions in 2 countries.

Edmund Charles JenkinsDepartment of Medicine, Division of Hematology/Oncology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Mrittika ChattopadhyayDepartment of Medicine, Division of Hematology/Oncology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Maria GomezRutgers Cancer Institute of New Jersey, New Brunswick, New Jersey, USA.
Denis TorreDepartment of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID 0000-0003-4615-223X
Avi Ma'ayanDepartment of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID 0000-0002-6904-1017
Miguel Torres-MartinClinical Genomics Research Group, Germans Trias I Pujol Research Institute (IGTP), Barcelona, Spain.
Daniela SiaDepartment of Medicine, Division of Liver Diseases, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Doris GermainDepartment of Medicine, Division of Hematology/Oncology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID 0000-0001-6597-0196
Tisch Hospital · USIcahn School of Medicine at Mount Sinai · USInstitut d'Investigació en Ciències de la Salut Germans Trias i Pujol · ESRutgers, The State University of New Jersey · US

Funding

Understanding the role of mitochondrial UPR-activating mtDNA landscapes in health and longevity.R01AG059635 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GERMAIN, DORIS A · 2018 to 2022
$2.2M
Post-doctoral Training Program in Cancer Metabolism and Tumor-host InteractionsT32CA257957 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI KANG, YIBIN, ZONG, WEI-XING · 2021 to 2025
$1.2M
NCI NIH HHS T32 CA257957NIA NIH HHS R01 AG059635
6 · The paper itself

Abstract

A major limitation in the use of mouse models in breast cancer research is that most mice develop estrogen receptor-alpha (ERα)-negative mammary tumors, while in humans, the majority of breast cancers are ERα-positive. Therefore, developing mouse models that best mimic the disease in humans is of fundamental need. Here, using an inducible MMTV-rtTA/TetO-NeuNT mouse model, we show that despite being driven by the same oncogene, mammary tumors in young mice are ERα-negative, while they are ERα-positive in aged mice. To further elucidate the mechanisms for this observation, we performed RNAseq analysis and identified genes that are uniquely expressed in aged female-derived mammary tumors. We found these genes to be involved in the activation of the ERα axis of the mitochondrial UPR and the ERα-mediated regulation of XBP-1s, a gene involved in the endoplasmic reticulum UPR. Collectively, our results indicate that aging alters the oncogenic trajectory towards the ERα-positive subtype of breast cancers, and that mammary tumors in aged mice are characterized by the upregulation of multiple UPR stress responses regulated by the ERα.

Indexed as

Estrogen Receptor alphaReceptors, EstrogenAgedAnimalsCarcinogenesisFemaleHumansMiceOncogenesUnfolded Protein ResponseEstrogen Receptor alphaReceptors, Estrogenaged mammary glandagingendoplasmic reticulumER stressestrogen receptor-alphamitochondrial UPRunfolded protein responseXBP-1

Identifiers

PMID36111352
PMCPMC9577951
OpenAlexW4296035303

What OpenQuestion holds

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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.