ReviewJournal of cell communication and signaling2018
Tumor cell-intrinsic phenotypic plasticity facilitates adaptive cellular reprogramming driving acquired drug resistance.
Review in Journal of cell communication and signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
- Adaptive epithelial-mesenchymal bi-directional transition: A key invasive plasticity for tumor metastasis.iScience · 2026Review
- The Shape-Shifting Myeloma: Adaptive Plasticity as a Hallmark of Relapse and Refractoriness.Cancers · 2026Review
- Review
- Lipidomics in Melanoma: Insights into Disease Progression and Therapeutical Targets.International journal of molecular sciences · 2026Review
- Drug-tolerant persister cells in lymphoid malignancies: from mechanisms to therapeutic opportunities.Frontiers in oncology · 2026Review
- Contrasting Impacts of Targeted Disruption of the Cancer Stem Cell Marker CD133 and Its Epigenetic Regulator TRIM28 in Colorectal Cancer Cells.International journal of molecular sciences · 2025Article
- Employing nullclines to balance treatment efficacy and neurotoxicity for sustained tumor control.Mathematical biosciences · 2025Article
- Lipidomic changes in persister cancer cells drive enhanced ferroptosis sensitivity.Ferroptosis and oxidative stress · 2025Article
- Phenotypically plastic drug-resistant chronic myeloid leukaemia cell line displays enhanced cellular dynamics in a zebrafish xenograft model.Journal of cellular and molecular medicine · 2024Article
- Article
- Pharmacological agents targeting drug-tolerant persister cells in cancer.Pharmacological research · 2024Review
- Dedifferentiated Leiomyosarcoma of the Uterine Corpus with Heterologous Component: Clinicopathological Analysis of Five Consecutive Cases from a Single Institution and Comprehensive Literature Review.Diagnostics (Basel, Switzerland) · 2024Article
- St-N, a novel alkaline derivative of stevioside, reverses docetaxel resistance by targeting lysosomes in vitro and in vivo.PloS one · 2024Article
- H3K4me3 remodeling induced acquired resistance through O-GlcNAc transferase.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2023Article
- Targeting drug-tolerant cells: A promising strategy for overcoming acquired drug resistance in cancer cells.MedComm · 2023Review
- Effective dose window for containing tumor burden under tolerable level.NPJ systems biology and applications · 2023Article
- Metabolic Reprogramming in Colon Cancer Cells Persistently Infected with Newcastle Disease Virus.Cancers · 2023Article
- Characteristics and molecular mechanism of drug-tolerant cells in cancer: a review.Frontiers in oncology · 2023Review
- Transcription factor binding process is the primary driver of noise in gene expression.PLoS genetics · 2022Article
- Regulatory chromatin rewiring promotes metabolic switching during adaptation to oncogenic receptor tyrosine kinase inhibition.Oncogene · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The enthusiasm about successful novel therapeutic strategies in cancer is often quickly dampened by the development of drug resistance. This is true for targeted therapies using tyrosine kinase inhibitors for EGFR or BRAF mutant cancers, but is also an increasingly recognized problem for immunotherapies. One of the major obstacles of successful cancer therapy is tumor heterogeneity of genotypic and phenotypic features. Historically, drivers for drug resistance have been suspected and found on the genetic level, with mutations either being pre-existing in a subset of cancer cells or emerging de novo to mediate drug resistance. In contrast to that, our group and others identified a non-mutational adaptive response, resulting in a reversible, drug tolerant, slow cycling phenotype that precedes the emergence of permanent drug resistance and is triggered by prolonged drug exposure. More recently, studies described the importance of initially reversible transcriptional reprogramming for the development of acquired drug resistance, identified factors important for the survival of the slow cycling phenotype and investigated the relationship of mutational and non-mutational resistance mechanisms. However, the connection and relative importance of mutational and adaptive drug resistance in relation to the in vitro models at hand and the clinically observed response patterns remains poorly defined. In this review we focus on adaptive intrinsic phenotypic plasticity in cancer cells that leads to the drug tolerant slow cycling state, which eventually transitions to permanent resistance, and propose a general model based on current literature, to describe the development of acquired drug resistance.
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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.