Evidence map›Paper›PMID 37266436›Full record

ReviewFrontiers in immunology2023

New molecular targets in Hodgkin and Reed-Sternberg cells.

Hummaira Sadaf, Maciej Ambroziak, Robert Binkowski, Jakkapong Kluebsoongnoen, Ewa Paszkiewicz-Kozik, Jaroslaw Steciuk, Sergiusz Markowicz, Jan Walewski, Elzbieta Sarnowska, Tomasz Jacek Sarnowski and 1 more

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

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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

11 authors.

Hummaira SadafDepartment of Experimental Immunotherapy, Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, Poland.
Maciej AmbroziakDepartment of Experimental Immunotherapy, Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, Poland.
Robert BinkowskiInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw, Poland.
Jakkapong KluebsoongnoenInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw, Poland.
Ewa Paszkiewicz-KozikDepartment of Lymphoid Malignancies, Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, Poland.
Jaroslaw SteciukInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw, Poland.
Sergiusz MarkowiczDepartment of Experimental Immunotherapy, Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, Poland.
Jan WalewskiDepartment of Lymphoid Malignancies, Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, Poland.
Elzbieta SarnowskaDepartment of Experimental Immunotherapy, Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, Poland.
Tomasz Jacek SarnowskiInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw, Poland.
Ryszard KonopinskiDepartment of Experimental Immunotherapy, Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent discoveries shed light on molecular mechanisms responsible for classical Hodgkin lymphoma (HL) development and progression, along with features of Hodgkin - Reed and Sternberg cells (HRS). Here, we summarize current knowledge on characteristic molecular alterations in HL, as well as existing targeted therapies and potential novel treatments for this disease. We discuss the importance of cluster of differentiation molecule 30 (CD30) and the programmed cell death-1 protein (PD-1) and ligands (PD-L1/2), and other molecules involved in immune modulation in HL. We highlight emerging evidence indicating that the altered function of SWI/SNF-type chromatin remodeling complexes, PRC2, and other epigenetic modifiers, contribute to variations in chromatin status, which are typical for HL. We postulate that despite of the existence of plentiful molecular data, the understanding of HL development remains incomplete. We therefore propose research directions involving analysis of reverse signaling in the PD-1/PD-L1 mechanism, chromatin remodeling, and epigenetics-related alterations, in order to identify HL features at the molecular level. Such attempts may lead to the identification of new molecular targets, and thus will likely substantially contribute to the future development of more effective targeted therapies.

Indexed as

Hodgkin DiseaseReed-Sternberg CellsB7-H1 AntigenHumansProgrammed Cell Death 1 ReceptorSignal TransductionB7-H1 AntigenProgrammed Cell Death 1 ReceptorCD30chromatin remodelingHodgkin lymphomancRNAPD-1PD-L1Reed-Sternberg cells

Identifiers

PMID37266436
PMCPMC10230546

What Socratic holds

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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 Socratic graph.