The treatment of newly diagnosed multiple myeloma has changed dramatically over the past 20 years, from near uniform application of chemotherapy to a patient performance status- and risk-based approach. Furthermore, initiation of treatment criteria have evolved from a pure end-organ damage-based definition to include risk factors of transformation to frank myeloma. Besides, the mainly cytogenetically defined Multiple Myeloma (MM) risk status, transplant eligibility of patients still serves primarily to allocate patients within a rational treatment algorithm. While all transplant-eligible MM patients should receive a triplet induction therapy followed by autologous transplantation and, in most cases, lenalidomide maintenance, other therapeutic elements (e. g., other maintenance strategies, consolidation, tandem transplantation,..) have to be decided on an individualized appraisal of risk and toxicities. Standard-risk patients should never be undertreated, as they derive the highest relative benefit from using the best available registered therapies. However, high-risk patients should be preferentially treated inside clinical trials testing additive innovative treatments, as the improvement in the prognosis of this group of patients by standard therapies has been underwhelming. Furthermore, the evaluation process of non-transplant-eligible patients should always comprise an evaluation of performance status, frailty, and comorbidities (e. g., a comprehensive geriatric assessment) to facilitate the allocation of individualized therapies.
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http://dx.doi.org/10.1007/s12254-018-0383-3 | DOI Listing |
Cancer Med
December 2024
Department of Hematology, Peking University First Hospital, Beijing, People's Republic of China.
Background: An effective urine-based method for the diagnosis, differential diagnosis and prognosis of multiple myeloma (MM) has not yet been developed. Urine cell-free DNA (cfDNA) carrying cancer-specific genetic and epigenetic aberrations may enable a noninvasive "liquid biopsy" for diagnosis and monitoring of cancer.
Methods: We first identified MM-specific hydroxymethylcytosine signatures by comparing 64 MM patients, 23 amyloidosis (AM) patients and 59 healthy cohort.
Biomaterials
December 2024
School of Engineering, Vanderbilt University, Nashville, TN, 37235, USA. Electronic address:
Multiple myeloma (MM), a cancer of bone marrow plasma cells, is the second-most common hematological malignancy. However, despite immunotherapies like chimeric antigen receptor (CAR)-T cells, relapse is nearly universal. The bone marrow (BM) microenvironment influences how MM cells survive, proliferate, and resist treatment.
View Article and Find Full Text PDFLeuk Lymphoma
December 2024
Division of Hematology, Mayo Clinic, Rochester, MN, USA.
Over the past two decades, new agents for multiple myeloma (MM) have significantly improved patient outcomes, particularly for those with standard-risk disease, who now have a median overall survival of over a decade. However, this benefit is less pronounced in high-risk and ultra-high-risk MM, where median survival ranges from 3 to 5 years. The definition of HRMM continues to evolve and is driven by the genomic features, disease burden, and medical comorbidities.
View Article and Find Full Text PDFClin Lymphoma Myeloma Leuk
November 2024
Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX. Electronic address:
Background: The prognosis of multiple myeloma involving the central nervous system (CNS-MM) is poor. We report outcomes of CNS-MM treated with CNS-directed radiation therapy (RT).
Methods: We retrospectively reviewed patients with CNS-MM treated with CNS-directed RT from 2015 to 2024.
Mol Biol Rep
December 2024
Department of Histology, Medical University of Gdańsk, Dębinki 1, 80-211, Gdańsk, Poland.
Multiple myeloma (MM), also referred to as Kahler's disease, is a cancer characterized by the uncontrolled growth of abnormal plasma cells and is associated with alterations in the bone tissue microenvironment. Bone marrow adipose tissue (BMAT), which comprises approximately ten percent of total body fat, can influence the progression, survival, and drug resistance of MM cells through paracrine, hormonal, and metabolic pathways. Obesity can lead to an increase in BMAT mass, which not only disrupts bone metabolism but also reduces bone density, potentially progressing from monoclonal gammopathy of undetermined significance, a benign condition, to MM.
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