Evidence map›Paper›PMID 31954172›Full record

ReviewSeminars in cancer biology2020

Overcoming immunotherapeutic resistance by targeting the cancer inflammation cycle.

Max M Wattenberg, Gregory L Beatty

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 50 citations in OpenAlex.

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  18. Sestrin2 in cancer: a foe or a friend?Biomarker research · 2022
    Review
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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

2 authors at 1 institution in 1 country.

Max M WattenbergAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States; Division of Hematology-Oncology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States.
Gregory L BeattyAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States; Division of Hematology-Oncology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States. Electronic address: Gregory.Beatty@pennmedicine.upenn.edu.
University of Pennsylvania · US

Funding

HEMATOLOGY CLINICAL RESEARCH TRAINING PROGRAMT32HL007439 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LAWRENCE F BRASS, PETER S KLEIN · 1985 to 2026
$17.1M
Targeting the liver for immunotherapy in pancreatic cancerR01CA197916 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Gregory L Beatty · 2016 to 2026
$3.7M
Stopping PDA progression using inhibitors of CSC dissemination and immunotherapyU01CA224193 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HINGORANI, SUNIL R · 2017 to 2021
$3.3M
Mechanisms and therapeutic targets of cancer metastasisR01CA245323 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BEATTY, GREGORY L · 2020 to 2024
$1.8M
NCI NIH HHS R01 CA197916NCI NIH HHS R01 CA245323NCI NIH HHS U01 CA224193NHLBI NIH HHS T32 HL007439
6 · The paper itself

Abstract

Inflammation is a hallmark of cancer and supports tumor growth, proliferation, and metastasis, but also inhibits T cell immunosurveillance and the efficacy of immunotherapy. The biology of cancer inflammation is defined by a cycle of distinct immunological steps that begins during disease conception with the release of inflammatory soluble factors. These factors communicate with host organs to trigger bone marrow mobilization of myeloid cells, trafficking of myeloid cells to the tumor, and differentiation of myeloid cells within the tumor bed. Tumor-infiltrating myeloid cells then orchestrate an immunosuppressive microenvironment and assist in sustaining a vicious cycle of inflammation that co-evolves with tumor cells. This Cancer-Inflammation Cycle acts as a rheostat or "inflammostat" that impinges upon T cell immunosurveillance and prevents the development of productive anti-tumor immunity. Here, we define the major nodes of the Cancer-Inflammation Cycle and describe their impact on T cell immunosurveillance in cancer. Additionally, we discuss emerging pre-clinical and clinical data suggesting that intervening upon the Cancer-Inflammation Cycle will be a necessary step for broadening the potential of immunotherapy in cancer.

Indexed as

Cell MovementDrug Resistance, NeoplasmHumansImmunotherapyInflammationMyeloid CellsNeoplasmsT-LymphocytesTumor MicroenvironmentCancerImmunotherapyInflammationInflammostatMacrophageMyeloid cellsT cells

Identifiers

PMID31954172
PMCPMC7363515
OpenAlexW2998856333

What OpenQuestion holds

Textmetadata
LicenceTDM
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.