ReviewHematology. American Society of Hematology. Education Program2011
Many multiple myelomas: making more of the molecular mayhem.
Review in Hematology. American Society of Hematology. Education Program, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 53 citations in OpenAlex.
- GP130 activation induces myeloma and collaborates with MYC.The Journal of clinical investigation · 2014Trial
- The FGF/FGFR/c-Myc axis as a promising therapeutic target in multiple myeloma.Journal of experimental & clinical cancer research : CR · 2024Review
- Biological relapse in multiple myeloma: Outcome and treatment strategies in a Spanish real-world setting.HemaSphere · 2024Article
- Review
- Cryopreservation Preserves Cell-Type Composition and Gene Expression Profiles in Bone Marrow Aspirates From Multiple Myeloma Patients.Frontiers in genetics · 2021Article
- Multiple Myeloma as a Bone Disease? The Tissue Disruption-Induced Cell Stochasticity (TiDiS) Theory.Cancers · 2020Article
- Activated gp130 signaling selectively targets B cell differentiation to induce mature lymphoma and plasmacytoma.JCI insight · 2019Article
- Discovery platform for inhibitors of IgH gene enhancer activity.Cancer biology & therapy · 2019Article
- Old and Young Actors Playing Novel Roles in the Drama of Multiple Myeloma Bone Marrow Microenvironment Dependent Drug Resistance.International journal of molecular sciences · 2018Review
- Extracellular matrix and the myeloid-in-myeloma compartment: balancing tolerogenic and immunogenic inflammation in the myeloma niche.Journal of leukocyte biology · 2017Review
- Article
- Molecular mechanisms in multiple myeloma drug resistance.Journal of clinical pathology · 2016Review
- Chromatin structure, transcriptional activity and DNA repair efficiency affect the outcome of chemotherapy in multiple myeloma.British journal of cancer · 2014Article
- Plasmacytomagenesis in Eμ-v-abl transgenic mice is accelerated when apoptosis is restrained.Blood · 2014Article
- A DNA repair pathway score predicts survival in human multiple myeloma: the potential for therapeutic strategy.Oncotarget · 2014Article
- Progressive changes in chromatin structure and DNA damage response signals in bone marrow and peripheral blood during myelomagenesis.Leukemia · 2014Article
- GSK3-mediated MAF phosphorylation in multiple myeloma as a potential therapeutic target.Blood cancer journal · 2014Article
- Observational
- Article
- Plasma cell formation, secretion, and persistence: the short and the long of it.Critical reviews in immunology · 2014Review
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 1 institution in 1 country.
Funding
Abstract
Multiple myeloma (MM) is malignancy of isotype-switched, BM-localized plasma cells that frequently results in bone destruction, BM failure, and death. Important molecular subgroups are identified by three classes of recurrent immunoglobulin gene translocations and hyperdiploidy, both of which affect disease course. From a clinical standpoint, it is critical to identify MM patients carrying the t(4;14) translocation, which is present in 15% of myelomas and is associated with dysregulation of WHSC1/MMSET and often FGFR3. These patients should all receive bortezomib as part of their initial induction treatment because this has been shown to significantly prolong survival. In contrast, patients with translocations affecting the MAF family of transcription factors, del17p, or gene-expression profiling (GEP)-defined high-risk disease appear to have a worse prognosis that is not dramatically improved by any intervention. These patients should be enrolled in innovative clinical trials. The remaining patients with cyclin D translocations or hyperdiploidy do well with most therapies, and the goal should be to control disease while minimizing toxicity.
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.