ReviewEMBO reports2013
Programming cancer cells for high expression levels of Mcl1.
Review in EMBO reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed.
- Trial
- Development and validation of a small extracellular vesicle-derived RNA signature for early diagnosis of lung adenocarcinoma and prognosis in advanced stages.Molecular cancer · 2025Article
- Selective Cytotoxicity of Ochratoxin A: Pro-Apoptotic Effects on Healthy Immune Cells Compared to Leukemia Cells.Molecules (Basel, Switzerland) · 2025Article
- Identification of bicyclic compounds that act as dual inhibitors of Bcl-2 and Mcl-1.Molecular diversity · 2023Article
- Screening and Bioinformatics Analyses of Key miRNAs Associated with Toll-like Receptor Activation in Gastric Cancer Cells.Medicina (Kaunas, Lithuania) · 2023Article
- FOXO1 represses MCL1 transcription to regulate the function of vascular smooth muscle cells in intracranial aneurysm.Experimental brain research · 2022Article
- Targeting cancer stemness mediated by BMI1 and MCL1 for non-small cell lung cancer treatment.Journal of cellular and molecular medicine · 2022Article
- Skp2 stabilizes Mcl-1 and confers radioresistance in colorectal cancer.Cell death & disease · 2022Article
- Increased MCL-1 synthesis promotes irradiation-induced nasopharyngeal carcinoma radioresistance via regulation of the ROS/AKT loop.Cell death & disease · 2022Article
- Synergism of a novel MCL‑1 downregulator, acriflavine, with navitoclax (ABT‑263) in triple‑negative breast cancer, lung adenocarcinoma and glioblastoma multiforme.International journal of oncology · 2022Article
- Myeloid cell leukemia-1: a formidable barrier to anticancer therapeutics and the quest of targeting it.Exploration of targeted anti-tumor therapy · 2022Review
- Interplay between protein acetylation and ubiquitination controls MCL1 protein stability.Cell reports · 2021Article
- Therapeutic Synergy in Esophageal Cancer and Mesothelioma Is Predicted by Dynamic BH3 Profiling.Molecular cancer therapeutics · 2021Article
- Elevated USP9X drives early-to-late-stage oral tumorigenesis via stabilisation of anti-apoptotic MCL-1 protein and impacts outcome in oral cancers.British journal of cancer · 2021Article
- CircRNA DOCK1 Regulates miR-409-3p/MCL1 Axis to Modulate Proliferation and Apoptosis of Human Brain Vascular Smooth Muscle Cells.Frontiers in cell and developmental biology · 2021Article
- lncRNA PART1 mitigates MPPAmerican journal of translational research · 2021Article
- Advancement in research and therapy ofCancer cell international · 2020Review
- Allele-Specific Expression of CD4Genes · 2019Article
- Tyrosine Kinase Inhibitors Increase MCL1 Degradation and in Combination with BCLXL/BCL2 Inhibitors Drive Prostate Cancer Apoptosis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Dual inhibition of JAK1/2 kinases and BCL2: a promising therapeutic strategy for acute myeloid leukemia.Leukemia · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The Bcl2 pro-survival protein family has long been recognized for its important contributions to cancer. At elevated levels relative to pro-apoptotic effector members, the survival proteins prevent cancer cells from initiating apoptosis in the face of many intrinsic tumour-suppressing pathways and extrinsic therapeutic treatments aimed at controlling tumorigenesis. Recent studies, including genome-wide analyses, have begun to focus attention on a particularly enigmatic member of the family-myeloid cell leukaemia 1 (Mcl1). For reasons that are not clear, Mcl1 in cancer cells is turned over rapidly, eliminated primarily through the ubiquitin-proteasome pathway. Moreover, the mechanistic aspects of this constitutive membrane-associated protein have not been fully elucidated. As the pro-cancer activity of Mcl1 requires elevated expression levels of the protein, the cancer genome adapts to ensure either high levels of synthesis or evasion of degradation, or both. Here, we focus on the complex strategies at play and their therapeutic implications.
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What 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.