ArticleOncotarget2012
Residual malignant and normal plasma cells shortly after high dose melphalan and stem cell transplantation. Highlight of a putative therapeutic window in Multiple Myeloma?
Article in Oncotarget, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Clinical significance of the lymphocyte-to-monocyte ratio in multiple myeloma patients with negative minimal residual disease: a single-center retrospective analysis.International journal of hematology · 2021Article
- Treatment Strategies Considering Micro-Environment and Clonal Evolution in Multiple Myeloma.Cancers · 2021Review
- Antioxidant Defenses Confer Resistance to High Dose Melphalan in Multiple Myeloma Cells.Cancers · 2019Article
- Loss of Stromal Galectin-1 Enhances Multiple Myeloma Development: Emphasis on a Role in Osteoclasts.Cancers · 2019Article
- Treatment May Be Harmful: Mechanisms/Prediction/Prevention of Drug-Induced DNA Damage and Repair in Multiple Myeloma.Frontiers in genetics · 2019Review
- Article
- Inhibiting the anaphase promoting complex/cyclosome induces a metaphase arrest and cell death in multiple myeloma cells.Oncotarget · 2016Article
- Targeted Therapies in Adult B-Cell Malignancies.BioMed research international · 2015Review
- The role of DNA damage and repair in decitabine-mediated apoptosis in multiple myeloma.Oncotarget · 2014Article
- DNA repair pathways in human multiple myeloma: role in oncogenesis and potential targets for treatment.Cell cycle (Georgetown, Tex.) · 2013Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple Myeloma (MM) is an incurable malignant plasma cell disorder. We have evaluated the counts of Multiple Myeloma Cells (MMCs) and normal plasma cells (N-PCs), seven days after high-dose melphalan (HDM) and autologous stem transplantation (ASCT). Two third of patients had detectable minimal residual disease (MRD+) (71.7 MMCs/µL) after induction treatment with dexamethasone and proteasome inhibitor. MMC counts were reduced by 92% (P ≤ .05) but not eradicated 7 days after HDM+ASCT. Post-HDM+ASCT MMCs were viable and bathed in a burst of MMC growth factors, linked with post-HDM aplasia. In one third of patients (MRD- patients), MMCs were not detectable after induction treatment and remained undetectable after HDM+ASCT. Major difference between MRD- and MRD+ patients is that N-PC counts were increased 3 fold (P〈.05) by HDM+ASCT in MRD- patients, but were unaffected in MRD+ patients. Possible explanation could be that clearance of MMCs in MRD- patients makes more niches available for N-PCs. Thus, MMCs are not fully eradicated shortly after HDM, are bathed in high concentrations of MMC growth factors in an almost desert BM, are viable in short-term culture, which suggests providing additional therapies shortly after HDM to kill resistant MMCs before full repair of lesions.
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