Evidence map›Paper›PMID 24786206›Full record

ArticleCancer discovery2014

SPSB1 promotes breast cancer recurrence by potentiating c-MET signaling.

Yi Feng, Tien-Chi Pan, Dhruv K Pant, Kristi R Chakrabarti, James V Alvarez, Jason R Ruth, Lewis A Chodosh

Open access · greenAbstract read
In one paragraph

Article in Cancer discovery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

32 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
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  6. Testis-enrichedAmerican journal of translational research · 2025
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  10. Dormancy in Breast Cancer.Cold Spring Harbor perspectives in medicine · 2023
    Review
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  17. Cancer classification and biomarker selection via a penalized logsum network-based logistic regression model.Technology and health care : official journal of the European Society for Engineering and Medicine · 2021
    Article
  18. Gene expression profiling after LINC00472 overexpression in an NSCLC cell line1.Cancer biomarkers : section A of Disease markers · 2021
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Yi FengAuthors' Affiliations: Departments of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Tien-Chi PanAuthors' Affiliations: Departments of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Dhruv K PantAuthors' Affiliations: Departments of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Kristi R ChakrabartiAuthors' Affiliations: Departments of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
James V AlvarezAuthors' Affiliations: Departments of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Jason R RuthAuthors' Affiliations: Departments of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Lewis A ChodoshAuthors' Affiliations: Departments of Cancer Biology and Medicine; and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania chodosh@mail.med.upenn.edu.
Cancer Research Institute · USUniversity of Pennsylvania · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
In Vivo Ras-induced Senescence and TumorigenesisR01CA098371 · NCI · UNIVERSITY OF PENNSYLVANIA · PI LEWIS A CHODOSH · 2003 to 2026
$7.4M
Mechanisms of breast cancer progressionU01CA105490 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CHODOSH, LEWIS A · 2004 to 2013
$6.7M
Novel PET imaging agents for understanding glutamine addiction in cancerR01CA164490 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CHODOSH, LEWIS A, KUNG, HANK F · 2011 to 2015
$4.0M
Minimal Residual Disease and Mechanisms of Breast Cancer RecurrenceR01CA143296 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CHODOSH, LEWIS A · 2010 to 2022
$3.5M
Survival and Recurrence of Dormant Cancer CellsR01CA148774 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CHODOSH, LEWIS A · 2010 to 2022
$3.4M
NCI NIH HHS CA10549NCI NIH HHS CA143296NCI NIH HHS CA148774NCI NIH HHS CA164490NCI NIH HHS CA98371NCI NIH HHS P30 CA016520NCI NIH HHS R01 CA098371NCI NIH HHS R01 CA143296NCI NIH HHS R01 CA148774NCI NIH HHS R01 CA164490NCI NIH HHS U01 CA105490
6 · The paper itself

Abstract

unlabelledBreast cancer mortality is principally due to tumor recurrence; however, the molecular mechanisms underlying this process are poorly understood. We now demonstrate that the suppressor of cytokine signaling protein SPSB1 is spontaneously upregulated during mammary tumor recurrence and is both necessary and sufficient to promote tumor recurrence in genetically engineered mouse models. The recurrence-promoting effects of SPSB1 result from its ability to protect cells from apoptosis induced by HER2/neu pathway inhibition or chemotherapy. This, in turn, is attributable to SPSB1 potentiation of c-MET signaling, such that preexisting SPSB1-overexpressing tumor cells are selected for following HER2/neu downregulation. Consistent with this, SPSB1 expression is positively correlated with c-MET activity in human breast cancers and with an increased risk of relapse in patients with breast cancer in a manner that is dependent upon c-MET activity. Our findings define a novel pathway that contributes to breast cancer recurrence and provide the first evidence implicating SPSB proteins in cancer. SIGNIFICANCE: The principal cause of death from breast cancer is recurrence. This study identifies SPSB1 as a critical mediator of breast cancer recurrence, suggests activation of the SPSB1-c-MET pathway as an important mechanism of therapeutic resistance in breast cancers, and emphasizes that pharmacologic targets for recurrence may be unique to this stage of tumor progression.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMammary Neoplasms, ExperimentalMiceNeoplasm Recurrence, LocalOligonucleotide Array Sequence AnalysisProto-Oncogene Proteins c-metSignal TransductionSuppressor of Cytokine Signaling ProteinsProto-Oncogene Proteins c-metSuppressor of Cytokine Signaling Proteins

Identifiers

PMID24786206
PMCPMC4121738
OpenAlexW2159503436

What OpenQuestion holds

Textmetadata
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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.