Evidence map›Paper›PMID 39055715›Full record

ArticleFrontiers in immunology2024

Differential tumor immune microenvironment coupled with tumor progression or tumor eradication in HPV-antigen expressing squamous cell carcinoma (SCC) models.

Arpitha H Shivarudrappa, Jessy John, Monika Vashisht, Huaibin Ge, Silvia Liu, Jingxin Chen, Karen Siddoway, Rui Dong, Zhangguo Chen, Jing H Wang

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 2 pooled it
–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

5 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
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

10 authors.

Arpitha H ShivarudrappaUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Jessy JohnUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Monika VashishtUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Huaibin GeUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Silvia LiuDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Jingxin ChenUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Karen SiddowayUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Rui DongUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Zhangguo ChenUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Jing H WangUniversity of Pittsburgh Medical Center UPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 1988 to 2026
$158.0M
Identifying cellular and molecular signatures from distinct T cell receptor clonotypes associated with favorable immune checkpoint inhibitor responses in HNSCCsR01DE031947 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Robert L. Ferris, Lazar Vujanovic · 2022 to 2026
$3.6M
Elucidating Mechanism of Immune Evasion in Head and Neck CancersR01DE027329 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WANG, JING HONG, WANG, XIAO-JING · 2018 to 2022
$2.8M
Mechanisms of Dual Inhibition of TGFbeta/PD-L1 in HNSCCR01DE028420 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI WANG, JING HONG, WANG, XIAO-JING · 2019 to 2023
$2.7M
Mechanistic connection between HPV-specific TCRs and therapeutic responses to ICI in HPV+ HNSCCR01CA282074 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Robert L. Ferris, Jing Hong Wang · 2024 to 2026
$2.0M
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA282074NIDCR NIH HHS R01 DE027329NIDCR NIH HHS R01 DE028420NIDCR NIH HHS R01 DE031947
6 · The paper itself

Abstract

Human papilloma virus (HPV) is an etiological factor of head and neck squamous cell carcinoma (HNSCC). To investigate the role of HPV antigen in anti-tumor immunity, we established mouse models by expressing HPV16 E6 and E7 in a SCC tumor cell line. We obtained two HPV antigen-expressing clones (C-225 and C-100) transplantable into C57BL/6 recipients. We found that C-225 elicited complete eradication in C57BL/6 mice (eradicated), whereas C-100 grew progressively (growing). We examined immune tumor microenvironment (TME) using flow cytometry and found that eradicated or growing tumors exhibited differential immune profiles that may influence the outcome of anti-tumor immunity. Surprisingly, the percentage of CD8 and CD4 tumor-infiltrating lymphocytes (TILs) was much higher in growing (C-100) than eradicated (C-225) tumor. However, the TILs upregulated PD-1 and LAG-3 more potently and exhibited impaired effector functions in growing tumor compared to their counterparts in eradicated tumor. C-225 TME is highly enriched with myeloid cells, especially polymorphonuclear (PMN) myeloid-derived suppressor cells (MDSC), whereas the percentage of M-MDSC and tumor-associated macrophages (TAMs) was much higher in C-100 TME, especially M2-TAMs (CD206

Indexed as

Disease Models, AnimalLymphocytes, Tumor-InfiltratingMice, Inbred C57BLOncogene Proteins, ViralPapillomavirus E7 ProteinsPapillomavirus InfectionsTumor MicroenvironmentAnimalsCD8-Positive T-LymphocytesCell Line, TumorDisease ProgressionFemaleHead and Neck NeoplasmsHuman papillomavirus 16HumansLymphocyte Activation Gene 3 ProteinE6 protein, Human papillomavirus type 16Lag3 protein, mouseLymphocyte Activation Gene 3 Proteinoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsProgrammed Cell Death 1 ReceptorRepressor Proteinshead and neck squamous cell carcinomaimmunological heterogeneityindividualized anti-tumor immune responsesT cell receptortumor immune microenvironment

Identifiers

PMID39055715
PMCPMC11269233

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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.