Evidence map›Paper›PMID 38927982›Full record

ArticleCancers2024

The Histogenetic Origin of Malignant Cells Predicts Their Susceptibility towards Synthetic Lethality Utilizing the

Fabian Bernhard Pallasch, Vera Freytag, Malte Kriegs, Dennis Gatzemeier, Thomas Mair, Hannah Voss, Kristoffer Riecken, Mona Dawood, Boris Fehse, Thomas Efferth and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Fabian Bernhard PallaschInstitute of Anatomy and Experimental Morphology, Center for Experimental Medicine, University Cancer Center, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Vera FreytagInstitute of Anatomy and Experimental Morphology, Center for Experimental Medicine, University Cancer Center, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Malte KriegsDepartment of Radiotherapy and Radiation Oncology, Hubertus Wald Tumorzentrum-University Cancer Center Hamburg (UCCH), University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany.
Dennis GatzemeierSection Mass Spectrometric and Proteomics, Center of Diagnostics, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Thomas MairSection Mass Spectrometric and Proteomics, Center of Diagnostics, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.ORCID 0000-0002-8886-7498
Hannah VossSection Mass Spectrometric and Proteomics, Center of Diagnostics, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Kristoffer RieckenResearch Department Cell and Gene Therapy, Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.ORCID 0000-0001-9050-6766
Mona DawoodDepartment of Pharmaceutical Biology, Institute of Pharmaceutical and Biomedical Sciences, Johannes Gutenberg University, Staudinger Weg 5, 55128 Mainz, Germany.
Boris FehseResearch Department Cell and Gene Therapy, Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.ORCID 0000-0001-9780-7211
Thomas EfferthDepartment of Pharmaceutical Biology, Institute of Pharmaceutical and Biomedical Sciences, Johannes Gutenberg University, Staudinger Weg 5, 55128 Mainz, Germany.ORCID 0000-0002-2637-1681
Hartmut SchlüterSection Mass Spectrometric and Proteomics, Center of Diagnostics, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.ORCID 0000-0002-9358-7036
Udo SchumacherInstitute of Anatomy and Experimental Morphology, Center for Experimental Medicine, University Cancer Center, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.

Funding

Open Access Publication Fund of the University of Freiburg. X
6 · The paper itself

Abstract

backgroundRemarkable differences exist in the outcome of systemic cancer therapies. Lymphomas and leukemias generally respond well to systemic chemotherapies, while solid cancers often fail. We engineered different human cancer cells lines to uniformly express a modified herpes simplex virus thymidine kinase TK.007 as a suicide gene when ganciclovir (GCV) is applied, thus in theory achieving a similar response in all cell lines.

methodsFifteen different cell lines were engineered to express the

resultsGCV potency varied among cell lines, with lymphoma and leukemia cells showing higher susceptibility than solid cancer cells. Functional kinome profiling implies a contribution of the SRC family kinases and decreased overall kinase activity. mRNA sequencing highlighted alterations in the MAPK pathways and bottom-up proteomics showed differences in apoptotic and epithelial junction signaling proteins.

conclusionsThe histogenetic origin of cells influenced the susceptibility of human malignant cells towards cytotoxic agents with leukemias and lymphomas being more sensitive than solid cancer cells.

Indexed as

chemotherapydrug resistancefunctional kinome profilingganciclovirherpes simplex virus thymidine kinasesuicide gene transduction

Identifiers

PMID38927982
PMCPMC11202008

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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.