Evidence map›Paper›PMID 29309058›Full record

ArticleNature medicine2018

Diverse genetic-driven immune landscapes dictate tumor progression through distinct mechanisms.

Marco Bezzi, Nina Seitzer, Tomoki Ishikawa, Markus Reschke, Ming Chen, Guocan Wang, Caitlin Mitchell, Christopher Ng, Jesse Katon, Andrea Lunardi and 4 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed
8.0field-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

119 citing papers in PubMed, 175 citations in OpenAlex.

  1. Journal for immunotherapy of cancer · 2025
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59 more citing papers are in PubMed but not listed here.

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

14 authors at 3 institutions in 2 countries.

Marco BezziCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Nina SeitzerCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Tomoki IshikawaCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Markus ReschkeCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Ming ChenCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Guocan WangCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Caitlin MitchellCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Christopher NgCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Jesse KatonCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Andrea LunardiCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Sabina SignorettiDepartment of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
John G ClohessyCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Jiangwen ZhangSchool of Biological Sciences, University of Hong Kong, Hong Kong SAR, China.
Pier Paolo PandolfiCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0002-5352-5295
Beth Israel Deaconess Medical Center · USBrigham and Women's Hospital · USUniversity of Hong Kong · HK

Funding

Targeting Tumor Suppressive Pathways for Cancer TherapyR35CA197529 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PANDOLFI, PIER PAOLO · 2015 to 2019
$4.6M
Role of POZ-zinc in hemopoietic malignaciesR01CA102142 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 2004 to 2014
$3.3M
NIH HHS R01 CA102142NIH HHS R35 CA197529
6 · The paper itself

Abstract

Multiple immune-cell types can infiltrate tumors and promote progression and metastasis through different mechanisms, including immunosuppression. How distinct genetic alterations in tumors affect the composition of the immune landscape is currently unclear. Here, we characterized the immune-cell composition of prostate cancers driven by the loss of the critical tumor suppressor gene Pten, either alone or in combination with the loss of Trp53, Zbtb7a or Pml. We observed a striking quantitative and qualitative heterogeneity that was directly dependent on the specific genetic events in the tumor and ranged from 'cold', noninflamed tumors to massively infiltrated landscapes-results with important therapeutic implications. Further, we showed these qualitative differences in transcriptomic analysis of human prostate cancer samples. These data suggest that patient stratification on the basis of integrated genotypic-immunophenotypic analyses may be necessary for successful clinical trials and tailored precision immunological therapies.

Indexed as

DNA-Binding ProteinsProstatic NeoplasmsPTEN PhosphohydrolaseTranscription FactorsTumor Suppressor Protein p53AnimalsB-LymphocytesDisease Models, AnimalGene Expression Regulation, NeoplasticGenetic HeterogeneityGenotypeHumansImmunotherapyLymphocytes, Tumor-InfiltratingMacrophagesMaleDNA-Binding ProteinsPml protein, mousePromyelocytic Leukemia ProteinPTEN PhosphohydrolaseTranscription FactorsTrp53 protein, mouseTumor Suppressor Protein p53Zbtb7a protein, mouse

Identifiers

PMID29309058
OpenAlexW2782798328

What OpenQuestion holds

Textmetadata
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.