Evidence map›Paper›PMID 39305329›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2025

Potential promising of synthetic lethality in cancer research and treatment.

Mohsen Karami Fath, Behnam Najafiyan, Reza Morovatshoar, Mahdieh Khorsandi, Adib Dashtizadeh, Arash Kiani, Farnoosh Farzam, Kimia Sadat Kazemi, Mohsen Nabi Afjadi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. 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

9 authors.

Mohsen Karami FathDepartment of Cellular and Molecular Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran.
Behnam NajafiyanPharmaceutical Sciences Research Center, Faculty of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
Reza MorovatshoarMolecular Medicine Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
Mahdieh KhorsandiDepartment of Biotechnology, Faculty of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
Adib DashtizadehFaculty of Pharmacy, Zhengzhou University, Zhengzhou, China.
Arash KianiStudent Research Committee, Yasuj University of Medical Sciences, Yasuj, Iran.
Farnoosh FarzamDepartment of Biochemistry, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran.
Kimia Sadat KazemiFaculty of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran. kazemi.kimia@yahoo.com.
Mohsen Nabi AfjadiDepartment of Biochemistry, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran. mohsen.nabiafjadi@modares.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is a complex disease driven by multiple genetic changes, including mutations in oncogenes, tumor suppressor genes, DNA repair genes, and genes involved in cancer metabolism. Synthetic lethality (SL) is a promising approach in cancer research and treatment, where the simultaneous dysfunction of specific genes or pathways causes cell death. By targeting vulnerabilities created by these dysfunctions, SL therapies selectively kill cancer cells while sparing normal cells. SL therapies, such as PARP inhibitors, WEE1 inhibitors, ATR and ATM inhibitors, and DNA-PK inhibitors, offer a distinct approach to cancer treatment compared to conventional targeted therapies. Instead of directly inhibiting specific molecules or pathways, SL therapies exploit genetic or molecular vulnerabilities in cancer cells to induce selective cell death, offering benefits such as targeted therapy, enhanced treatment efficacy, and minimized harm to healthy tissues. SL therapies can be personalized based on each patient's unique genetic profile and combined with other treatment modalities to potentially achieve synergistic effects. They also broaden the effectiveness of treatment across different cancer types, potentially overcoming drug resistance and improving patient outcomes. This review offers an overview of the current understanding of SL mechanisms, advancements, and challenges, as well as the preclinical and clinical development of SL. It also discusses new directions and opportunities for utilizing SL in targeted therapy for anticancer treatment.

Indexed as

Antineoplastic AgentsNeoplasmsSynthetic Lethal MutationsAnimalsHumansMolecular Targeted TherapyAntineoplastic AgentsDNA repair genesPARP inhibitorsSynthetic lethalityTargeted therapy

Identifiers

What OpenQuestion holds

Textmetadata
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.