ReviewCancer gene therapy2026
Defining treatment-resistant brain cancer: Genetic screening to identify oncogene-driven immunomodulation and therapy resistance.
Review in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- A spatiotemporal state-inference framework for adaptive immunotherapy in glioblastoma.Frontiers in oncology · 2026Review
- Targeting replication stress in glioblastoma: From genotoxic treatment and inhibitors of the DNA damage response to immunotherapy.Neuro-oncology advancesReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is an extremely aggressive brain tumor characterized by rapid progression, poor prognosis, and limited potential for remission. A contributing factor to the aggressiveness of GBM is the high genetic and phenotypic variability of the tumor caused by the accumulation of beneficial mutations over time. Screening methodologies utilizing genetic tools such as clustered regulatory interspaced short palindromic repeats (CRISPR) and ribonucleic acid (RNA) interference (RNAi) have proven effective in identifying oncogenic driver genes in GBM. Here, we analyze and summarize these studies. Analysis of hits emerging from genetic screens in GBM has revealed key factors with the capacity for regulating deoxyribonucleic acid (DNA) repair, cell cycle, or metabolism of the cancer. The genetic programs which endow GBM a high degree of aggressiveness also contribute to outcompeting immune cells associated with tumor cell clearance. Genes identified in genetic screens influence the receptor landscape on the surface of both GBM and immune cells, as well as the soluble factors within the tumor microenvironment (TME). These soluble factors and surface receptors regulate function of immune cells, in particular natural killer (NK) cells. This systematic review links genetic drivers of GBM identified through screening approaches and their documented roles. As will be discussed, these genes were shown in literature to encode molecular programs that confer a competitive advantage to GBM in contexts such as chemotherapy and radiotherapy.
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Registered trials
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.