Evidence map›Paper›PMID 36371025›Full record

ReviewSeminars in cancer biology2022

Emerging role of chemokines in small cell lung cancer: Road signs for metastasis, heterogeneity, and immune response.

Parvez Khan, Mahek Fatima, Md Arafat Khan, Surinder Kumar Batra, Mohd Wasim Nasser

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
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  9. Article
  10. Observational
  11. State of the art in treatment of small cell lung cancer.Therapeutic advances in medical oncology · 2025
    Review
  12. Review
  13. Article
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  15. Article
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  17. Article
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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

5 authors.

Parvez KhanDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Mahek FatimaDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Md Arafat KhanDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Surinder Kumar BatraDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA; Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA; Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Mohd Wasim NasserDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA; Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA. Electronic address: wasim.nasser@unmc.edu.

Funding

Project 3: MUC16-Mediated Metabolic Reprograming Induces PC MetastasisP01CA217798 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI THAYER, SARAH P · 2018 to 2022
$8.1M
Modulation of Tumor Microenvironment for Improved Therapy of Pancreatic CancerR01CA247471 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K., JAIN, MANEESH · 2020 to 2024
$2.8M
Novel approach to attenuate small cell lung cancer growth and metastasisR01CA218545 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI NASSER, MOHD WASIM · 2018 to 2022
$2.6M
Targeting MUC5AC mucin in breast cancer brain metastasisR01CA241752 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI NASSER, MOHD WASIM · 2021 to 2025
$2.3M
Targeted Radiation Therapy for Pancreatic CancerR01CA195586 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K., JAIN, MANEESH · 2015 to 2019
$2.2M
NCI NIH HHS P01 CA217798NCI NIH HHS R01 CA195586NCI NIH HHS R01 CA218545NCI NIH HHS R01 CA241752NCI NIH HHS R01 CA247471
6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is a recalcitrant, relatively immune-cold, and deadly subtype of lung cancer. SCLC has been viewed as a single or homogenous disease that includes deletion or inactivation of the two major tumor suppressor genes (TP53 and RB1) as a key hallmark. However, recent sightings suggest the complexity of SCLC tumors that comprises highly dynamic multiple subtypes contributing to high intratumor heterogeneity. Furthermore, the absence of targeted therapies, the understudied tumor immune microenvironment (TIME), and subtype plasticity are also responsible for therapy resistance. Secretory chemokines play a crucial role in immunomodulation by trafficking immune cells to the tumors. Chemokines and cytokines modulate the anti-tumor immune response and wield a pro-/anti-tumorigenic effect on SCLC cells after binding to cognate receptors. In this review, we summarize and highlight recent findings that establish the role of chemokines in SCLC growth and metastasis, and sophisticated intratumor heterogeneity. We also discuss the chemokine networks that are putative targets or modulators for augmenting the anti-tumor immune responses in targeted or chemo-/immuno-therapeutic strategies, and how these combinations may be utilized to conquer SCLC.

Indexed as

Lung NeoplasmsSmall Cell Lung CarcinomaCarcinogenesisChemokinesHumansImmunityTumor MicroenvironmentChemokinesCCL5, neuroendocrine tumorsCXCL10CXCR4Small cell lung cancerSubtype switching

Identifiers

PMID36371025
PMCPMC10199458

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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.