ReviewOncotarget2016
Multiple myeloma cancer stem cells.
Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed.
- Single-cell analysis of neoplastic plasma cells identifies myeloma pathobiology mediators and potential targets.Cell reports. Medicine · 2025Article
- Single-cell profiling uncovers PTPRG-driven stemness in malignant plasma cells and signatures of treatment failure in multiple myeloma.Frontiers in immunology · 2025Article
- CAR-T cell therapy in Multiple Myeloma: current status and future challenges.Blood cancer journal · 2024Review
- Pathways to therapy resistance: The sheltering effect of the bone marrow microenvironment to multiple myeloma cells.Heliyon · 2024Review
- Current Status of Hedgehog Signaling Inhibitors.Current topics in medicinal chemistry · 2024Review
- Past, Present, and a Glance into the Future of Multiple Myeloma Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Editorial: New immunotherapeutic and pharmacological targets and strategies in haematological malignancies.Frontiers in pharmacology · 2023Article
- A novel E-cadherin/SOX9 axis regulates cancer stem cells in multiple myeloma by activating Akt and MAPK pathways.Experimental hematology & oncology · 2022Article
- The Route of the Malignant Plasma Cell in Its Survival Niche: Exploring "Multiple Myelomas".Cancers · 2022Review
- CD24 Is a Prognostic Marker for Multiple Myeloma Progression and Survival.Journal of clinical medicine · 2022Article
- Understanding the Bioactivity and Prognostic Implication of Commonly Used Surface Antigens in Multiple Myeloma.Journal of clinical medicine · 2022Review
- Drug resistance in multiple myeloma: Soldiers and weapons in the bone marrow niche.Frontiers in oncology · 2022Review
- T cell landscape and dynamics in immunoglobulin light chain amyloidosis before and after daratumumab-based therapy.Clinical and translational medicine · 2021Article
- Review
- Cyclopamine sensitizes multiple myeloma cells to circularly permuted TRAIL-induced apoptosis.Oncology letters · 2021Article
- CAR T cell therapies for patients with multiple myeloma.Nature reviews. Clinical oncology · 2021Review
- Exosomal miR-1305 in the oncogenic activity of hypoxic multiple myeloma cells: a biomarker for predicting prognosis.Journal of Cancer · 2021Article
- Article
- A novel M phase blocker, DCZ3301 enhances the sensitivity of bortezomib in resistant multiple myeloma through DNA damage and mitotic catastrophe.Journal of experimental & clinical cancer research : CR · 2020Article
- Review
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
Multiple myeloma (MM) remains incurable despite much progress that has been made in the treatment of the disease. MM cancer stem cell (MMSC), a rare subpopulation of MM cells with the capacity for self-renewal and drug resistance, is considered to lead to disease relapse. Several markers such as side population (SP) and ALDH1+ have been used to identify MMSCs. However, ideally and more precisely, the identification of the MMSCs should rely on MMSCs phenotype. Unfortunately the MMSC phenotype has not been properly defined yet. Drug resistance is the most important property of MMSCs and contributes to disease relapse, but the mechanisms of drug resistance have not been fully understood. The major signaling pathways involved in the regulation of self-renewal and differentiation of MMSCs include Hedgehog (Hh), Wingless (Wnt), Notch and PI3K/Akt/mTOR. However, the precise role of these signaling pathways needs to be clarified. It has been reported that the microRNA profile of MMSCs is remarkably different than that of non-MMSCs. Therefore, the search for targeting MMSCs has also been focused on microRNAs. Complex and mutual interactions between the MMSC and the surrounding bone marrow (BM) microenvironment sustain self-renewal and survival of MMSC. However, the required molecules for the interaction of the MMSC and the surrounding BM microenvironment need to be further identified. In this review, we summarize the current state of knowledge of MMSCs regarding their phenotype, mechanisms of drug resistance, signaling pathways that regulate MMSCs self-renewal and differentiation, abnormal microRNAs expression, and their interactions with the BM microenvironment.
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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.