ArticleBlood2012
Dendritic cell-mediated activation-induced cytidine deaminase (AID)-dependent induction of genomic instability in human myeloma.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- Mechanistic insights into bone destruction in multiple myeloma: Cellular and molecular perspectives.Journal of bone oncology · 2025Review
- Inflammation and aging-related disease: A transdisciplinary inflammaging framework.GeroScience · 2025Review
- Rebuilding the microenvironment of primary tumors in humans: a focus on stroma.Experimental & molecular medicine · 2024Review
- The Complexities of Diagnosis with Co-Existing Gaucher Disease and Hemato-Oncology-A Case Report and Review of the Literature.Journal of clinical medicine · 2023Review
- The immune system in multiple myeloma and precursor states: Lessons and implications for immunotherapy and interception.American journal of hematology · 2023Review
- Dissecting molecular mechanisms of immune microenvironment dysfunction in multiple myeloma and precursor conditions.Journal of cancer metastasis and treatment · 2023Article
- Role of the mechanisms for antibody repertoire diversification in monoclonal light chain deposition disorders: when a friend becomes foe.Frontiers in immunology · 2023Review
- Potent high-avidity neutralizing antibodies and T cell responses after COVID-19 vaccination in individuals with B cell lymphoma and multiple myeloma.Nature cancer · 2023Observational
- An elevated systemic inflammation index is related to an inferior response to pomalidomide and dexamethasone treatment in patients with relapsed and refractory multiple myeloma.Contemporary oncology (Poznan, Poland) · 2023Article
- Inflammation and infection in plasma cell disorders: how pathogens shape the fate of patients.Leukemia · 2022Review
- Role of Sphingolipids in Multiple Myeloma Progression, Drug Resistance, and Their Potential as Therapeutic Targets.Frontiers in oncology · 2022Review
- Mechanisms of Immune Evasion in Multiple Myeloma: Open Questions and Therapeutic Opportunities.Cancers · 2021Review
- Review
- Co-evolution of Immune Response in Multiple Myeloma: Implications for Immune Prevention.Frontiers in immunology · 2021Review
- Multiple Myeloma: Molecular Pathogenesis and Disease Evolution.Oncology research and treatment · 2021Review
- Transcription factor binding at Ig enhancers is linked to somatic hypermutation targeting.European journal of immunology · 2020Article
- Game of Bones: How Myeloma Manipulates Its Microenvironment.Frontiers in oncology · 2020Review
- Endogenous APOBEC3B Overexpression Constitutively Generates DNA Substitutions and Deletions in Myeloma Cells.Scientific reports · 2019Article
- Germline Risk Contribution to Genomic Instability in Multiple Myeloma.Frontiers in genetics · 2019Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor microenvironment (TME) is commonly implicated in regulating the growth of tumors, but whether it can directly alter the genetics of tumors is not known. Genomic instability and dendritic cell (DC) infiltration are common features of several cancers, including multiple myeloma (MM). Mechanisms underlying genomic instability in MM are largely unknown. Here, we show that interaction between myeloma and DCs, but not monocytes, leads to rapid induction of the genomic mutator activation-induced cytidine deaminase (AID) and AID-dependent DNA double-strand breaks (DSBs) in myeloma cell lines as well as primary MM cells. Both myeloid as well as plasmacytoid DCs have the capacity to induce AID in tumor cells. The induction of AID and DSBs in tumor cells by DCs requires DC-tumor contact and is inhibited by blockade of receptor activator of NF-κB/receptor activator of NF-κB ligand (RANKL) interactions. AID-mediated genomic damage led to altered tumorigenicity and indolent behavior of tumor cells in vivo. These data show a novel pathway for the capacity of DCs in the TME to regulate genomic integrity. DC-mediated induction of AID and resultant genomic damage may therefore serve as a double-edged sword and be targeted by approaches such as RANKL inhibition already in the clinic.
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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.