Evidence map›Paper›PMID 38140100›Full record

ReviewPharmaceutics2023

DNA Damage by Radiopharmaceuticals and Mechanisms of Cellular Repair.

Yousef Khazaei Monfared, Pedram Heidari, Samuel J Klempner, Umar Mahmood, Aparna R Parikh, Theodore S Hong, Matthew R Strickland, Shadi A Esfahani

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Deciphering the phenotypic responses toEuropean journal of nuclear medicine and molecular imaging · 2026
    Article
  3. Review
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  5. Article
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  7. Review
  8. [European journal of nuclear medicine and molecular imaging · 2026
    Article
  9. Review
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  11. In Vivo Studies of [Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
    Article
  12. Review
  13. Combination therapy strategies in engineeredCell communication and signaling : CCS · 2026
    Review
  14. Review
  15. Review
  16. Article
  17. Article
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  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Yousef Khazaei MonfaredDivision of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.ORCID 0000-0002-1171-8670
Pedram HeidariDivision of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.ORCID 0000-0001-6383-465X
Samuel J KlempnerDivision of Hematology-Oncology, Department of Medicine, Mass General Cancer Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Umar MahmoodDivision of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.ORCID 0000-0001-7414-6123
Aparna R ParikhDivision of Hematology-Oncology, Department of Medicine, Mass General Cancer Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Theodore S HongDepartment of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Matthew R StricklandDivision of Hematology-Oncology, Department of Medicine, Mass General Cancer Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Shadi A EsfahaniDivision of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Harvard University · US

Funding

Molecular Imaging of Fibrosis for Improved Treatment Planning of Pancreatic Ductal AdenocarcinomaK08CA259626 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI Shadi Abdar Esfahani · 2022 to 2026
$1.3M
NCI NIH HHS K08 CA259626
6 · The paper itself

Abstract

DNA is an organic molecule that is highly vulnerable to chemical alterations and breaks caused by both internal and external factors. Cells possess complex and advanced mechanisms, including DNA repair, damage tolerance, cell cycle checkpoints, and cell death pathways, which together minimize the potentially harmful effects of DNA damage. However, in cancer cells, the normal DNA damage tolerance and response processes are disrupted or deregulated. This results in increased mutagenesis and genomic instability within the cancer cells, a known driver of cancer progression and therapeutic resistance. On the other hand, the inherent instability of the genome in rapidly dividing cancer cells can be exploited as a tool to kill by imposing DNA damage with radiopharmaceuticals. As the field of targeted radiopharmaceutical therapy (RPT) is rapidly growing in oncology, it is crucial to have a deep understanding of the impact of systemic radiation delivery by radiopharmaceuticals on the DNA of tumors and healthy tissues. The distribution and activation of DNA damage and repair pathways caused by RPT can be different based on the characteristics of the radioisotope and molecular target. Here we provide a comprehensive discussion of the biological effects of RPTs, with the main focus on the role of varying radioisotopes in inducing direct and indirect DNA damage and activating DNA repair pathways.

Indexed as

cancerDNA damageDNA repairradioisotoperadiopharmaceuticals

Identifiers

PMID38140100
PMCPMC10748326
OpenAlexW4389617830

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.