Evidence map›Paper›PMID 35791509›Full record

ReviewCancer communications (London, England)2022

Cytokine- and chemokine-induced inflammatory colorectal tumor microenvironment: Emerging avenue for targeted therapy.

Ajaz A Bhat, Sabah Nisar, Mayank Singh, Bazella Ashraf, Tariq Masoodi, Chandra P Prasad, Atul Sharma, Selma Maacha, Thasni Karedath, Sheema Hashem and 8 more

Open access · goldAbstract readReview
In one paragraph

Review in Cancer communications (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 2 pooled it
20.2field-weighted citation impact, top 1% 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

136 citing papers in PubMed, 2 syntheses or guidelines pooled it, 211 citations in OpenAlex.

  1. Pooled it
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  3. Evolution of SPP1Cell reports. Medicine · 2026
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76 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

18 authors at 10 institutions in 3 countries.

Ajaz A BhatLaboratory of Molecular and Metabolic Imaging, Cancer Research Department, Sidra Medicine, Doha, 26999, Qatar.
Sabah NisarLaboratory of Molecular and Metabolic Imaging, Cancer Research Department, Sidra Medicine, Doha, 26999, Qatar.
Mayank SinghDepartment of Medical Oncology, Dr. B. R. Ambedkar Institute Rotary Cancer Hospital, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India.
Bazella AshrafDepartment of Biotechnology, School of Life Sciences, Central University of Kashmir, Ganderbal, Jammu & Kashmir, 191201, India.
Tariq MasoodiLaboratory of Molecular and Metabolic Imaging, Cancer Research Department, Sidra Medicine, Doha, 26999, Qatar.
Chandra P PrasadDepartment of Medical Oncology, Dr. B. R. Ambedkar Institute Rotary Cancer Hospital, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India.
Atul SharmaDepartment of Medical Oncology, Dr. B. R. Ambedkar Institute Rotary Cancer Hospital, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India.
Selma MaachaDivision of Translational Medicine, Research Branch, Sidra Medicine, Doha, 26999, Qatar.
Thasni KaredathGenomics Core Facility, QBRI, Qatar Foundation, Doha, 34110, Qatar.
Sheema HashemLaboratory of Molecular and Metabolic Imaging, Cancer Research Department, Sidra Medicine, Doha, 26999, Qatar.
Syed Besina YasinDepartment of Pathology, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu & Kashmir, 190011, India.
Puneet BaggaDepartment of Diagnostic Imaging, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Ravinder ReddyCenter for Advanced Metabolic Imaging in Precision Medicine, Department of Radiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, 19104, USA.
Michael P FrennauxAcademic Health System, Hamad Medical Corporation, Doha, 3050, Qatar.
Shahab UddinTranslational Research Institute, Hamad Medical Corporation, Doha, 3050, Qatar.
Punita DhawanDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
Mohammad HarisLaboratory of Molecular and Metabolic Imaging, Cancer Research Department, Sidra Medicine, Doha, 26999, Qatar.
Muzafar A MachaWatson-Crick Centre for Molecular Medicine, Islamic University of Science and Technology, Awantipora, Jammu & Kashmir, 192122, India.
Sidra Medical and Research Center · QAAll India Institute of Medical Sciences Raipur · INHamad Medical Corporation · QACentral University of Kashmir · INIslamic University of Science and Technology · INQatar Foundation · QASher-i-Kashmir Institute of Medical Sciences · INSt. Jude Children's Research Hospital · USUniversity of Nebraska Medical Center · USUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is a predominant life-threatening cancer, with liver and peritoneal metastases as the primary causes of death. Intestinal inflammation, a known CRC risk factor, nurtures a local inflammatory environment enriched with tumor cells, endothelial cells, immune cells, cancer-associated fibroblasts, immunosuppressive cells, and secretory growth factors. The complex interactions of aberrantly expressed cytokines, chemokines, growth factors, and matrix-remodeling enzymes promote CRC pathogenesis and evoke systemic responses that affect disease outcomes. Mounting evidence suggests that these cytokines and chemokines play a role in the progression of CRC through immunosuppression and modulation of the tumor microenvironment, which is partly achieved by the recruitment of immunosuppressive cells. These cells impart features such as cancer stem cell-like properties, drug resistance, invasion, and formation of the premetastatic niche in distant organs, promoting metastasis and aggressive CRC growth. A deeper understanding of the cytokine- and chemokine-mediated signaling networks that link tumor progression and metastasis will provide insights into the mechanistic details of disease aggressiveness and facilitate the development of novel therapeutics for CRC. Here, we summarized the current knowledge of cytokine- and chemokine-mediated crosstalk in the inflammatory tumor microenvironment, which drives immunosuppression, resistance to therapeutics, and metastasis during CRC progression. We also outlined the potential of this crosstalk as a novel therapeutic target for CRC. The major cytokine/chemokine pathways involved in cancer immunotherapy are also discussed in this review.

Indexed as

Colorectal NeoplasmsCytokinesChemokinesEndothelial CellsHumansTumor MicroenvironmentChemokinesCytokineschemokinecolorectal cancercytokinedrug resistanceepithelial-mesenchymal transitionimmunosuppressionimmunotherapyinflammationmetastasistumor microenvironment

Identifiers

PMID35791509
PMCPMC9395317
OpenAlexW4283826714

What OpenQuestion holds

Textmetadata
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.