ReviewClinical & developmental immunology2012
Targeting multiple-myeloma-induced immune dysfunction to improve immunotherapy outcomes.
Review in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 41 citations in OpenAlex.
- Therapeutic strategies to enhance immune response induced by multiple myeloma cells.Frontiers in immunology · 2023Review
- The Leading Role of the Immune Microenvironment in Multiple Myeloma: A New Target with a Great Prognostic and Clinical Value.Journal of clinical medicine · 2022Review
- Dendritic Cell-Based Immunotherapy in Multiple Myeloma: Challenges, Opportunities, and Future Directions.International journal of molecular sciences · 2022Review
- Immune microenvironment characteristics in multiple myeloma progression from transcriptome profiling.Frontiers in oncology · 2022Article
- Immune-based therapies in the management of multiple myeloma.Blood cancer journal · 2020Review
- Deregulation of Adaptive T Cell Immunity in Multiple Myeloma: Insights Into Mechanisms and Therapeutic Opportunities.Frontiers in oncology · 2020Review
- Oncolytic immunotherapy and bortezomib synergy improves survival of refractory multiple myeloma in a preclinical model.Blood advances · 2019Article
- Article
- Activation of NK cells and disruption of PD-L1/PD-1 axis: two different ways for lenalidomide to block myeloma progression.Oncotarget · 2017Review
- Variation and significance of secretory immunoglobulin A, interleukin 6 and dendritic cells in oral cancer.Oncology letters · 2017Article
- Docosahexaenoic acid (DHA) promotes immunogenic apoptosis in human multiple myeloma cells, induces autophagy and inhibits STAT3 in both tumor and dendritic cells.Genes & cancer · 2017Article
- Immune checkpoint blockade for hematologic malignancies: a review.Stem cell investigation · 2017Review
- Myeloid-derived suppressor cells: The green light for myeloma immune escape.Blood reviews · 2016Review
- Immunotherapy for Multiple Myeloma, Past, Present, and Future: Monoclonal Antibodies, Vaccines, and Cellular Therapies.Current hematologic malignancy reports · 2015Review
- Immunotherapy in Multiple Myeloma Using Cancer-Testis Antigens.Iranian journal of cancer prevention · 2015Review
- Multiple myeloma induces Mcl-1 expression and survival of myeloid-derived suppressor cells.Oncotarget · 2015Article
- Article
- Coinhibitory molecule PD-1 as a potential target for the immunotherapy of multiple myeloma.Leukemia · 2014Review
- Myeloid-derived suppressor cells as therapeutic target in hematological malignancies.Frontiers in oncology · 2014Review
- Monitoring NK cell activity in patients with hematological malignancies.Oncoimmunology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is a plasma cell malignancy associated with high levels of monoclonal (M) protein in the blood and/or serum. MM can occur de novo or evolve from benign monoclonal gammopathy of undetermined significance (MGUS). Current translational research into MM focuses on the development of combination therapies directed against molecularly defined targets and that are aimed at achieving durable clinical responses. MM cells have a unique ability to evade immunosurveillance through several mechanisms including, among others, expansion of regulatory T cells (Treg), reduced T-cell cytotoxic activity and responsiveness to IL-2, defects in B-cell immunity, and induction of dendritic cell (DC) dysfunction. Immune defects could be a major cause of failure of the recent immunotherapy trials in MM. This article summarizes our current knowledge on the molecular determinants of immune evasion in patients with MM and highlights how these pathways can be targeted to improve patients' clinical outcome.
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.