Evidence map›Paper›PMID 34354944›Full record

ArticleFrontiers in oncology2021

Dual Inhibition of PARP and the Intra-S/G2 Cell Cycle Checkpoints Results in Highly Effective Radiosensitization of HPV-Positive HNSCC Cells.

Katharina Hintelmann, Thomas Berenz, Malte Kriegs, Sabrina Christiansen, Fruzsina Gatzemeier, Nina Struve, Cordula Petersen, Christian Betz, Kai Rothkamm, Agnes Oetting and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

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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 at 3 institutions in 1 country.

Katharina HintelmannDepartment of Otorhinolaryngology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Thomas BerenzDepartment of Otorhinolaryngology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Malte KriegsDepartment of Radiotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Sabrina ChristiansenDepartment of Otorhinolaryngology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Fruzsina GatzemeierDepartment of Otorhinolaryngology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Nina StruveDepartment of Radiotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Cordula PetersenDepartment of Radiotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Christian BetzDepartment of Otorhinolaryngology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Kai RothkammDepartment of Radiotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Agnes OettingDepartment of Otorhinolaryngology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Thorsten RieckmannDepartment of Otorhinolaryngology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Universität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEUniversity Cancer Center Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In head and neck squamous cell carcinoma (HNSCC), tumors positive for human papillomavirus (HPV) represent a distinct biological entity with favorable prognosis. An enhanced radiation sensitivity of these tumors is evident in the clinic and on the cellular level when comparing HPV-positive and HPV-negative HNSCC cell lines. We could show that the underlying mechanism is a defect in DNA double-strand break repair associated with a profound and sustained G2 arrest. This defect can be exploited by molecular targeting approaches additionally compromising the DNA damage response to further enhance their radiation sensitivity, which may offer new opportunities in the setting of future de-intensified regimes. Against this background, we tested combined targeting of PARP and the DNA damage-induced intra-S/G2 cell cycle checkpoints to achieve effective radiosensitization. Enhancing CDK1/2 activity through the Wee1 inhibitor adavosertib or a combination of Wee1 and Chk1 inhibition resulted in an abrogation of the radiation-induced G2 cell cycle arrest and induction of replication stress as assessed by

Indexed as

Chk1head and neck cancerhuman papillomavirus (HPV)molecular targetingPARPradiosensitizationradiotherapyWee1

Identifiers

PMID34354944
PMCPMC8329549
OpenAlexW3183583786

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.