Evidence map›Paper›PMID 25051364›Full record

ArticleOncotarget2014

Macrophages are recruited to hypoxic tumor areas and acquire a pro-angiogenic M2-polarized phenotype via hypoxic cancer cell derived cytokines Oncostatin M and Eotaxin.

Chakrapani Tripathi, Brij Nath Tewari, Ranjana Kumari Kanchan, Khemraj Singh Baghel, Naveen Nautiyal, Richa Shrivastava, Harbeer Kaur, Madan Lal Bramha Bhatt, Smrati Bhadauria

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.

0numbers the graph read from it
0cells of the map it votes in
135citing 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

135 citing papers in PubMed, 220 citations in OpenAlex.

  1. Reprogramming the Immune Landscape of Inflammatory Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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75 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

9 authors at 3 institutions in 1 country.

Chakrapani TripathiDivision of Toxicology, Central Drug Research Institute, (CSIR) Lucknow, India; Academy of Scientific Innovative Research, (AcSIR) India.
Brij Nath TewariDepartment of Surgical Oncology, King George Medical University, Lucknow, India.
Ranjana Kumari KanchanDivision of Toxicology, Central Drug Research Institute, (CSIR) Lucknow, India.
Khemraj Singh BaghelDivision of Toxicology, Central Drug Research Institute, (CSIR) Lucknow, India.
Naveen NautiyalDivision of Toxicology, Central Drug Research Institute, (CSIR) Lucknow, India.
Richa ShrivastavaDivision of Toxicology, Central Drug Research Institute, (CSIR) Lucknow, India; Academy of Scientific Innovative Research, (AcSIR) India.
Harbeer KaurDivision of Toxicology, Central Drug Research Institute, (CSIR) Lucknow, India.
Madan Lal Bramha BhattDepartment of Radiotherapy, King George Medical University, Lucknow, India.
Smrati BhadauriaDivision of Toxicology, Central Drug Research Institute, (CSIR) Lucknow, India; Academy of Scientific Innovative Research, (AcSIR) India.
Central Drug Research Institute · INAcademy of Scientific and Innovative Research · INKing George's Medical University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TAMs, a unique and distinct M2-skewed myeloid population of tumor stroma, exhibiting pro-tumor functions is fast emerging as a potential target for anti-cancer immunotherapy. Macrophage-recruitment and M2-polarization represent key TAMs-related phenomenon that are amenable to therapeutic intervention. However successful translation of these approaches into effective therapeutic regimen requires better characterization of tumor-microenvironment derived signals that regulate macrophage recruitment and their polarization. Owing to hypoxic milieu being a persistent feature of tumor-microenvironment and a major contributor to malignancy and treatment resistance, the current study was planned with an aim to decipher tumor cell responses to hypoxia vis-a-vis macrophage homing and phenotype switching. Here, we show that hypoxia-primed cancer cells chemoattract and polarize macrophages to pro-angiogenic M2-polarized subtype via Eotaxin and Oncostatin M. Concordantly, hypoxic regions of human breast-cancer specimen exhibited elevated Eotaxin and Oncostatin M levels with concurrently elevated M2-macrophage content. Blockade of Eotaxin/Oncostatin M not only prevented hypoxic breast-cancer cells from recruiting and polarizing macrophages towards an M2-polarized phenotype and retarded tumor progression in 4T1/BALB/c-syngenic-mice-model of breast-cancer but also enhanced the efficacy of anti-angiogenic Bevacizumab. The findings established these two cytokines as novel targets for devising effective anticancer therapy particularly for tumors that are refractory or develop resistance to anti-angiogenic therapeutics.

Indexed as

AnimalsBreast NeoplasmsCell HypoxiaCell Line, TumorChemokine CCL11FemaleHumansMacrophagesMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, Inbred BALB CNeovascularization, PathologicOncostatin MPhenotypeRandom AllocationChemokine CCL11Oncostatin M

Identifiers

PMID25051364
PMCPMC4170629
OpenAlexW2112740421

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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.