Evidence map›Paper›PMID 38749609›Full record

ArticleThe American journal of pathology2024

Isolation and Characterization of a Novel Mammary Adenocarcinoma, MCa-P1362, with Hormone Receptor Expression, Human Epidermal Growth Factor Receptor 2 Positivity, and Enrichment in Cancer and Mesenchymal Stem Cells.

Samir Jana, Wende Li, Pin-Ji Lei, Zixiong Wang, Shaye Kibara, Peigen Huang, Dennis Jones

Abstract read
In one paragraph

Article in The American journal of pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

7 authors.

Samir JanaDepartment of Pathology and Laboratory Medicine, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts.
Wende LiEdwin L. Steele Laboratories for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Pin-Ji LeiEdwin L. Steele Laboratories for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Zixiong WangDepartment of Pathology and Laboratory Medicine, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts.
Shaye KibaraDepartment of Pathology and Laboratory Medicine, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts.
Peigen HuangEdwin L. Steele Laboratories for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. Electronic address: phuang2@mgh.harvard.edu.
Dennis JonesDepartment of Pathology and Laboratory Medicine, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts. Electronic address: djones1@bu.edu.

Funding

Understanding the mechanisms of immune suppression in lymph node metastasesK22CA230315 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI JONES, DENNIS · 2018 to 2020
$566k
NCI NIH HHS K22 CA230315
6 · The paper itself

Abstract

Preclinical models that display spontaneous metastasis are necessary to improve the therapeutic options for hormone receptor-positive breast cancers. Within this study, detailed cellular and molecular characterization was conducted on MCa-P1362, a newly established mouse model of metastatic breast cancer that is syngeneic in BALB/c mice. MCa-P1362 cancer cells express estrogen receptor, progesterone receptor, and the human epidermal growth factor receptor 2. MCa-P1362 cancer cells proliferate in vitro and in vivo in response to estrogen, yet do not depend on steroid hormones for growth and tumor progression. Analysis of MCa-P1362 tumor explants revealed the tumors contained a mixture of cancer cells and mesenchymal stromal cells. Through transcriptomic and functional analyses of both cancer and stromal cells, stem cells were detected within both populations. Functional studies demonstrated that MCa-P1362 cancer stem cells drove tumor initiation, whereas stromal cells from these tumors contributed to drug resistance. MCa-P1362 may serve as a useful preclinical model to investigate the cellular and molecular basis of breast tumor progression and therapeutic resistance.

Indexed as

AdenocarcinomaErb-b2 Receptor Tyrosine KinasesMesenchymal Stem CellsMice, Inbred BALB CReceptors, EstrogenAnimalsBreast NeoplasmsCell Line, TumorFemaleHumansMammary Neoplasms, ExperimentalMiceNeoplastic Stem CellsReceptors, ProgesteroneErb-b2 Receptor Tyrosine KinasesReceptors, EstrogenReceptors, Progesterone

Identifiers

PMID38749609
PMCPMC11156160

What OpenQuestion holds

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Registered trials

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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.