ReviewJournal of biosciences2016
Therapeutic resistance and cancer recurrence mechanisms: Unfolding the story of tumour coming back.
Review in Journal of biosciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled 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.
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
29 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Patient-reported emotional responses and coping mechanisms in cancer recurrence: a systematic review of qualitative evidence.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025Pooled it
- CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer.Translational lung cancer research · 2026Article
- MULGONET: An interpretable neural network framework to integrate multi-omics data for cancer recurrence prediction and biomarker discovery.Fundamental research · 2026Article
- Computational insights into cancer stem cell dynamics and the urokinase plasminogen activation pathway.Journal of biosciences · 2026Article
- Advancements and challenges in brain cancer therapeutics.Exploration (Beijing, China) · 2024Review
- Clinical significance of ribosomal protein S15 expression in patients with colorectal cancer liver metastases.Journal of hepato-biliary-pancreatic sciences · 2024Article
- TGF-β Modulated Pathways in Colorectal Cancer: New Potential Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Article
- Cancer cell repopulation after therapy: which is the mechanism?Oncoscience · 2023Article
- The Interaction between DNMT1 and High-Mannose CD133 Maintains the Slow-Cycling State and Tumorigenic Potential of Glioma Stem Cell.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Stem cells from a malignant rat prostate cell line generate prostate cancersAmerican journal of clinical and experimental urology · 2022Article
- Irradiation-induced polyploid giant cancer cells are involved in tumor cell repopulation via neosis.Molecular oncology · 2021Article
- A Wnt-mediated phenotype switch along the epithelial-mesenchymal axis defines resistance and invasion downstream of ionising radiation in oral squamous cell carcinoma.British journal of cancer · 2021Article
- Review
- Links between Inflammation and Postoperative Cancer Recurrence.Journal of clinical medicine · 2021Review
- Non-coding RNAs underlying chemoresistance in gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- Review of cancer-associated fibroblasts and their microenvironment in post-chemotherapy recurrence.Human cell · 2020Review
- Intratumor Heterogeneity and Therapy Resistance: Contributions of Dormancy, Apoptosis Reversal (Anastasis) and Cell Fusion to Disease Recurrence.International journal of molecular sciences · 2020Review
- PODXL2 maintains cellular stemness and promotes breast cancer development through the Rac1/Akt pathway.International journal of medical sciences · 2020Article
- Necrosis in the Tumor Microenvironment and Its Role in Cancer Recurrence.Advances in experimental medicine and biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer recurrence is believed to be one of the major reasons for the failure of cancer treatment strategies. This biological phenomenon could arise from the incomplete eradication of tumour cells after chemo- and radiotherapy. Recent developments in the design of models reflecting cancer recurrence and in vivo imaging techniques have led researchers to gain a deeper and more detailed insight into the mechanisms underlying tumour relapse. Here, we provide an overview of three important drivers of recurrence including cancer stem cells (CSCs), neosis, and phoenix rising. The survival of cancer stem cells is well recognized as one of the primary causes of therapeutic resistance in malignant cells. CSCs have a relatively latent metabolism and show resistance to therapeutic agents through a variety of routes. Neosis has proven to be as an important mechanism behind tumour self-proliferation after treatment which gives rise to the expansion of tumour cells in the injured site via production of Raju cells. Phoenix rising is a prorecurrence pathway through which apoptotic cancer cells send strong signals to the neighbouring diseased cells leading to their multiplication. The mechanisms involved in therapeutic resistance and tumour recurrence have not yet been fully understood and mostly remain unexplained. Without doubt, an improved understanding of the cellular machinery contributing to recurrence will pave the way for the development of novel, sophisticated and effective antitumour therapeutic strategies which can eradicate tumour without the threat of relapse.
Indexed as
Identifiers
27581940What OpenQuestion holds
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.