ReviewInternational journal of hematology2004
Apoptosis of multiple myeloma.
Review in International journal of hematology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 57 citations in OpenAlex.
- Safety and effects of two mistletoe preparations on production of Interleukin-6 and other immune parameters - a placebo controlled clinical trial in healthy subjects.BMC complementary and alternative medicine · 2011Trial
- Regulated cell death plasticity in cancer: thresholds, reversibility, and therapeutic failure.Journal of translational medicine · 2026Review
- Article
- Antitumor effect of BC12-3 on multiple myeloma via proteasome inhibition.Medical oncology (Northwood, London, England) · 2025Article
- Acid ceramidase controls proteasome inhibitor resistance and is a novel therapeutic target for the treatment of relapsed/refractory multiple myeloma.Haematologica · 2025Article
- Mitochondrial metabolic determinants of multiple myeloma growth, survival, and therapy efficacy.Frontiers in oncology · 2022Review
- Review
- Proliferation to Apoptosis Tumor Cell Ratio as a Biomarker to Improve Clinical Management of Pre-Malignant and Symptomatic Plasma Cell Neoplasms.International journal of molecular sciences · 2021Article
- Blood-based risk stratification for pre-malignant and symptomatic plasma cell neoplasms to improve patient management.American journal of cancer research · 2021Article
- Pharmacodynamic Models of Differential Bortezomib Signaling Across Several Cell Lines of Multiple Myeloma.CPT: pharmacometrics & systems pharmacology · 2019Article
- Rational combination strategies to enhance venetoclax activity and overcome resistance in hematologic malignancies.Leukemia & lymphoma · 2018Review
- Flavopiridol enhances ABT-199 sensitivity in unfavourable-risk multiple myeloma cells in vitro and in vivo.British journal of cancer · 2018Article
- Cell Signaling Model Connects Vorinostat Pharmacokinetics and Tumor Growth Response in Multiple Myeloma Xenografts.CPT: pharmacometrics & systems pharmacology · 2017Article
- Article
- Dysfunction of microRNA-32 regulates ubiquitin ligase FBXW7 in multiple myeloma disease.OncoTargets and therapy · 2016Article
- Mature adipocytes in bone marrow protect myeloma cells against chemotherapy through autophagy activation.Oncotarget · 2015Article
- Logic-Based and Cellular Pharmacodynamic Modeling of Bortezomib Responses in U266 Human Myeloma Cells.The Journal of pharmacology and experimental therapeutics · 2015Article
- Icaritin suppresses multiple myeloma, by inhibiting IL-6/JAK2/STAT3.Oncotarget · 2015Article
- Lycorine induces programmed necrosis in the multiple myeloma cell line ARH-77.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Article
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 at 2 institutions in 1 country.
Funding
Abstract
Multiple myeloma (MM) is a malignancy of terminally differentiated plasma cells. MM cells localize to the bone marrow, where cell adhesion-mediated autocrine or paracrine activation of various cytokines, such as interleukin 6, insulin-like growth factor 1, and interferon alpha, results in their accumulation mainly because of loss of critical apoptotic controls. Resistance to apoptosis, a genetically regulated cell death process, may play a critical role in both pathogenesis and resistance to treatment of MM. Abnormalities in regulation and execution of apoptosis can contribute to tumor initiation, progression, as well as to tumor resistance to various therapeutic agents. Apoptosis is executed via 2 main pathways that lead to activation of caspases: the death receptor (extrinsic) pathway and the mitochondrial (intrinsic) pathway. Ionizing radiation and chemotherapeutic agents act primarily through the intrinsic pathway, in which mitochondria play the central role. Various therapeutic modalities that are effective in MM modulate levels of the proapoptotic and antiapoptotic Bcl-2 family of proteins and of inhibitors of apoptosis, expression of which is primarily regulated by p53, nuclear factor KB, and STAT (signal transducers and activators of transcription) factors. This review focuses on the key concepts and some of the most recent studies of signaling pathways regulated in MM and summarizes what is known about the clinical role of these pathways.
Indexed as
Identifiers
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.