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Добірка наукової літератури з теми "Multiple myeloma Chemotherapy"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 30 січня 2023

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Статті в журналах з теми "Multiple myeloma Chemotherapy"

1

Durie, Brian G. M. "Chemotherapy of multiple myeloma." Baillière's Clinical Haematology 4, no. 1 (January 1991): 181–95. http://dx.doi.org/10.1016/s0950-3536(05)80290-2.

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2

Kogan, Michael, and Adnan H. Siddiqui. "Intracranial Multiple Myeloma After Chemotherapy." Archives of Clinical and Medical Case Reports 01, no. 02 (2017): 42–44. http://dx.doi.org/10.26502/acmcr.9655008.

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3

Lokhorst, H. M., O. J. A. Th Meuwissen, E. J. E. G. Bast, and A. W. Dekker. "VAD chemotherapy for refractory multiple myeloma." British Journal of Haematology 71, no. 1 (January 1989): 25–30. http://dx.doi.org/10.1111/j.1365-2141.1989.tb06269.x.

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4

Peest, D., H. J. Schmoll, I. Schedel, S. Glück, K. Schumacher, and H. Deicher. "VBAMDex chemotherapy in advanced multiple myeloma*." European Journal of Haematology 40, no. 3 (April 24, 2009): 245–49. http://dx.doi.org/10.1111/j.1600-0609.1988.tb00831.x.

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5

Terrovitis, John V., Charis Matsouka, Athanassios Anagnostopoulos, Maria I. Anastasiou-Nana, and Athanassios Meletios Dimopoulos. "Hemophagocytic Lymphohistiocytosis After Chemotherapy for Multiple Myeloma." Clinical Lymphoma 5, no. 3 (December 2004): 194–96. http://dx.doi.org/10.3816/clm.2004.n.026.

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6

Alexanian, Raymond, Bart Barlogie, and Gerard Ventura. "Chemotherapy for resistant and relapsing multiple myeloma." European Journal of Haematology 43, S51 (April 24, 2009): 140–44. http://dx.doi.org/10.1111/j.1600-0609.1989.tb01507.x.

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7

Vidarsson, Brynjar, Svanhvit Olafsdottir, and Sigrun Reykdal. "VASP Chemotherapy in Patients with Multiple Myeloma." Blood 106, no. 11 (November 16, 2005): 5189. http://dx.doi.org/10.1182/blood.v106.11.5189.5189.

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Abstract Introduction: Multiple myeloma (MM) is a malignant disorder of plasma cells resistant to chemotherapy. Various chemotherapy protocols are available for patients with MM, including VAD (vincristine, adriamycin, prednisolon) and MP (melphalan, prednisolon). These therapies aim to slow disease progression and/or prepare the patient for stem cell transplantation (SCT), the standard of care for MM patients younger than 70. An additional regimen, VASP, consisting of etoposide 50mg/m2 IV on day 1 and 100mg/m2 PO on days 2–4, adriamycin 25mg/m2 IV on day 1, cyclophosphamide 500mg/m2 IV on day 1 and dexamethasone 40mg PO qd on days 1–4, has been used in Iceland for the past 18 years. Due to the advantage of outpatient administration of VASP compared to VAD (96 hour hospital admission or indwelling venous access device with risk of extravasation), VASP has increasingly become the preferred chemotherapeutic regimen for Icelandic MM patients. Although our experience shows that VASP is comparable to VAD with respect to efficacy and toxicity, we are unaware of previous studies in support of this. The aim of this study was therefore to evaluate the efficacy and toxicity of VASP chemotherapy as it has been used in Iceland. Patients and methods: Medical records of all MM patients treated with VASP chemotherapy over a 15-year period (1990–2004) were retrospectively analyzed. Baseline disease characteristics were assessed, as was information about disease progression and previous therapy. Response to VASP (CR, PR and NR; EBMT criteria) and toxicity was documented. Survival was evaluated by the Kaplan-Meier method. Results: Of the 26 patients receiving VASP chemotherapy, 22 (12 male, 10 female) were included in this study (4 records incomplete or absent). Mean age was 64 years (range 35–86). 14 patients had IgG, 7 IgA, and 1 patient had no measurable paraprotein. 15 of the 22 patients had previously been treated with 1–2 courses of chemotherapy including VAD. Each patient received on average 5,3 courses of VASP (range 1–11). A response was seen in 17 patients (77.3%) (2 CR, 15 PR) and 5 (22,7%) showed no response. Three patients not responding to initial VAD therapy demonstrated a subsequent PR to VASP. Of the 22 patients, 15 died during the 15 years of study, resulting in a mean overall survival (OS) of 3,8 years (0,9–10,5) from diagnosis of MM and 2,0 years after VASP therapy (0–3,4). 33 of 116 VASP courses resulted in hospitalization (28,4%). Neutropenia was seen after 38,8% of the courses (nadir 0.5 x 109/L; 77.3% after the first course) and G-CSF was used in 56% of cases. Neutropenic fever was seen after 10.6% of courses and infection was documented in 15,5% of patients (bacteremia 13.6%). Transfusion of PRBC’s was required after 25 of the 116 courses but platelets after only three. Conclusion: We present data supporting the efficacy and safety of VASP chemotherapy for MM patients. Our total response rate of 77,3% compares favorably with other therapies such as VAD, and survival and toxicity is also comparable to other therapies. Although small, this is the first study we are aware of on VASP therapy for MM. Further studies, preferably larger and prospective, are required to confirm the efficacy and toxicity of VASP chemotherapy for MM.

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Minařík, Jiří, and Sabina Ševčíková. "Immunomodulatory Agents for Multiple Myeloma." Cancers 14, no. 23 (November 23, 2022): 5759. http://dx.doi.org/10.3390/cancers14235759.

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The treatment of multiple myeloma (MM) has undergone a significant paradigm shift in the last 20 years, from conventional chemotherapy to more tumor-specific treatments, based on the interference with pathogenesis of the malignant clone as well as the bone microenvironment [...]

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9

Katagiri, Daisuke, Eisei Noiri, and Fumihiko Hinoshita. "Multiple Myeloma and Kidney Disease." Scientific World Journal 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/487285.

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Multiple myeloma (MM) has a high incidence rate in the elderly. Responsiveness to treatments differs considerably among patients because of high heterogeneity of MM. Chronic kidney disease (CKD) is a common clinical feature in MM patients, and treatment-related mortality and morbidity are higher in MM patients with CKD than in patients with normal renal function. Recent advances in diagnostic tests, chemotherapy agents, and dialysis techniques are providing clinicians with novel approaches for the management of MM patients with CKD. Once reversible factors, such as hypercalcemia, have been corrected, the most common cause of severe acute kidney injury (AKI) in MM patients is tubulointerstitial nephropathy, which results from very high circulating concentrations of monoclonal immunoglobulin free light chains (FLC). In the setting of AKI, an early reduction of serum FLC concentration is related to kidney function recovery. The combination of extended high cutoff hemodialysis and chemotherapy results in sustained reductions in serum FLC concentration in the majority of patients and a high rate of independence from dialysis.

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10

Bensinger, William I. "Hematopoietic Cell Transplantation for Multiple Myeloma." Cancer Control 5, no. 3 (May 1998): 235–42. http://dx.doi.org/10.1177/107327489800500304.

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Background Multiple myeloma (MM) is a malignant plasma cell disorder with a median survival of three years. Despite the development of numerous conventional chemotherapy regimens and interferons, there has been little progress in improving the survival of patients with MM. Very high-dose chemoradiotherapy and autologous or allogeneic hematopoetic stem cell transplantation (HSCT) can result in high complete remission rates, even in patients with advanced disease. Methods A prospective, randomized study has shown that autologous HSCT results in superior response rates, progression-free survival, and disease-free survival compared with conventional chemotherapy. This is the first real advance in the treatment of this disease in 30 years. Unfortunately, few, if any, patients with MM who receive autologous HSCT are cured. Results Allogeneic HSCT can be curative for a fraction of patients with MM. However, very high transplant-related morbidity and mortality limit the application of allografts to younger patients with compatible donors. Conclusions Challenges for the future include the development of less intensive or more disease-specific chemotherapy regimens that preserve the antitumor activity but are less toxic, improvement in the control of graft-vs-host disease in the case of allografts and, for autologous graft recipients, the development of vaccines and cytotoxic lymphocytes to augment a graft vs myeloma effect.

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Дисертації з теми "Multiple myeloma Chemotherapy"

1

Turner, Joel G. "Drug resistance to topoisomerase directed chemotherapy in human multiple myeloma." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002446.

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2

Redzepovic, Jasmina [Verfasser]. "Meta-analysis in context : Chemotherapy versus chemotherapy combined with bisphosphonate therapy in multiple myeloma patients / Jasmina Redzepovic." Berlin : Freie Universität Berlin, 2009. http://d-nb.info/1023664585/34.

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3

Viziteu, Elena. "RECQ1 Helicase Involvement in the Resistance to Replication Stress and Chemotherapy in Multiple Myeloma Myélome Multiple." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT008.

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Le myélome multiple (MM) est une néoplasie B caractérisée par l’accumulation d’un clone plasmocytaire dans la moelle osseuse. Des études ont démontré que les modifications épigénétiques comme la méthylation de l’ADN jouent un rôle dans la régulation d’expression de différents gènes associés au cancer. Dans une étude récente, nous avons pu décrire un score génique de méthylation de l’ADN permettant de prédire la sensibilité des cellules de MM aux inhibiteurs de DNMT (DNA methyltranfexrase) (Moreaux, et al 2012). Parmi les gènes dont l’expression est inhibée par les inhibiteurs de DNMT et associés avec un pronostic péjoratif chez les patients atteints de MM, nous avons identifié RECQ1. RECQ1 est une hélicase de la famille RECQ qui s’associe aux origines de réplication durant la phase S du cycle cellulaire et joue un rôle important dans l’élongation des fourches de réplication. RECQ1 est fortement exprimé dans différents types de tumeurs solides et l’inhibition de RECQ1 conduit à la catastrophe mitotique et inhibe la croissance de tumeurs solides. Le but de notre projet a été de caractériser la fonction de RECQ1 dans la physiopathologie du MM et les mécanismes de résistance aux traitements. Afin d’étudier le rôle biologique de RECQ1 dans les plasmocytes tumoraux, nous avons utilisé des vecteurs lentiviraux pour induire de façon inductible la surexpression ou l'inhibition de RECQ1. La déplétion de RECQ1 dans les cellules de MM entraîne une inhibition de la croissance, une induction significative d’apoptose et la formation de foyers 53BP1 indiquant la présence de cassures d’ADN double brin. Une forte expression de RECQ1 étant associée à un mauvais pronostic et la déplétion de RECQ1 conduisant à une induction de cassures d’ADN double brin, nous nous sommes demandé si l’inhibition de l’expression de RECQ1 pourrait sensibiliser les cellules de MM aux agents génotoxiques utilisés dans le traitement du MM. La déplétion de RECQ1 sensibilise, de façon significative, les cellules de MM au melphalan suggérant que l’association d’un inhibiteur de DNMT pour cibler RECQ1 et du melphalan pourrait avoir un effet synergique chez les patients RECQ1++. La surexpression de RECQ1 protège les lignées cellulaires de myélome contra l'apoptose induite par melphalan et bortézomib. De plus, l'épuisement RECQ1 sensibilise les cellules de myélome de traitement est démontré que RECQ1 interagit avec des protéines impliquées dans différentes voies de réparation des dommages de l’ADN : PARP1 (NHEJ/BER), RAD51 (HR), MSH2 et MSH6 (Mismatch repair). RECQ1 interagit avec PARP1 dans la fraction chromatinienne des cellules de MM mais pas avec RAD51 ni MSH2. Cette interaction est significativement induite en présence de melphalan. Des inhibiteurs de PARP sont actuellement en développement préclinique ou en essai clinique. De façon intéressante, la déplétion de RECQ1 sensibilise significativement les cellules de MM à un inhibiteur de PARP in vitro suggérant que l’association d’un inhibiteur de DNMT pour cibler RECQ1 et d’un inhibiteur de PARP pourrait avoir un intérêt thérapeutique dans le MM. Nous avons également confirmé que des doses sous-létales d’inhibiteur de DNMT sensibilisent les cellules de MM au melphalan in vitro
Multiple myeloma (MM) is a plasma cell cancer with poor survival, characterized by the clonal expansion of multiple myeloma cells (MMCs), primarily in the bone marrow. Using a microarray-based genome-wide screen for genes responding to DNA methyltransferases (DNMT) inhibition in MM cells, we identified RECQ1 among the genes downregulated by DNMT inhibitor. RECQ helicase are DNA unwinding enzymes involved in the maintenance of chromosome stability. RECQ1 silencing in cancer cells results in mitotic catastrophe and prevents tumor growth in murine models. RECQ1 is significantly overexpressed in primary myeloma cells compared to normal plasma cells and in myeloma cell lines compared to primary myeloma cells of patients. High RECQ1 expression is associated with a poor prognosis in two independent cohorts of patients. RECQ1 knock down inhibits growth of myeloma cells and induces apoptosis. Given the known role of RECQ1 in replication and DNA repair activation, the effect of RECQ1 depletion in DNA damage response was investigated. RECQ1 depletion induced spontaneous accumulation of DNA double strand breaks (DSBs) evidenced by the phosphorylation of ATM and H2AX histone and detection of 53BP1 foci. Using an alkaline comet assay, a significant increase in DNA strand breaks was confirmed in RECQ1 depleted cell lines compared to control. RECQ1 depletion was associated with CHK1 and CHK2 phosphorylation in MM cells. Since RECQ1 depletion is associated with DNA damage response activation and DNA strand breaks formation, a link between RECQ1 expression and drug sensitivity was hypothesized. RECQ1 overexpression significantly protects myeloma cell lines from melphalan and bortezomib-induced apoptosis. Furthermore, RECQ1 depletion sensitizes myeloma cells to treatment. Using immunoprecipitation, RECQ1 was shown to interact with PARP1 but not RAD51 or MSH2. An increased association of the two proteins was found upon DNA damages induced by melphalan. In agreement, RECQ1 depletion sensitizes myeloma cell lines to PARP inhibitor. We identified RECQ1 as a miR-203 target. Interestingly, aberrant methylation of miR-203 was reported in MM cells and treatment with 5-aza-2’-deoxycitidine led to promoter demethylation and miR-203 re-expression. Furthermore, anti-miR-203 treatment induced a significant increase of RECQ1 mRNA level in MM cells.In conclusion, RECQ1 represent a biomarker of drug resistance in MM, which is targeted by DNMT inhibitors. This suggests association of alkylating agents and/or PARP inhibitors with DNMT inhibitor may represent a therapeutic approach in RECQ1high patients associated with a poor prognosis

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4

Pan, Beiqing. "Mechanisms of skeletal disease mediated by haematological malignancies /." Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09php1871.pdf.

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Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine and The Hanson Centre, Institute of Medical and Veterinary Science, 2004.
"August 2004" Errata inside front cover. Bibliography: leaves 126-159.

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5

Pan, Beiqing. "Molecular and cellular studies of zoledronic acid : a potent inhibitor of multiple myeloma-induced osteolysis." Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09MSM/09msmp187.pdf.

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Bibliography: leaves 86-103. Investigates the effect of zoledronic acid on myeloma cells and osteoblast-like cells to establish the molecular and cellular mechanisms responsible for the clinical effectiveness of bisphosphonates in the treatment of patients with myelomatosis. Concludes that zoledronic acid inhibits myelomatosis-induced osteolysis thorugh the mechanisms of myeloma cell death and proliferation and maturation of osteoblasts.

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6

Nikolich‐Zugich, Tijana. "Effects of High Vs. Reduced‐Dose Melphalan For Autologous Bone Marrow Transplantation in Multiple Myeloma On Pulmonary Function: A Longitudinal Study." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/623514.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
Bone marrow transplants (BMT, also hematopoietic stem cell transplants or HSCT/SCT) are one of the greatest medical achievements of the 20th century. They offer a treatment for a host of malignant and nonmalignant hematopoietic disorders, genetic diseases and solid tumors that could otherwise be fatal. Studies have found that 60% of patients undergoing BMT develop pulmonary complications (PC), and 1/3 of those require intensive care after transplantation. Despite the potential pneumotoxicity of induction agents, to date there have been no longitudinal studies following pulmonary function in this high‐risk patient population. This study reviewed patient who underwent autogeneic bone marrow transplant for multiple myeloma at Banner University Medical Center – Tucson (formerly University of Arizona Health Network) from January 1, 2003 through December 31, 2013. Pretransplant evaluatin and pulmonary function testing data were obtained and stratified between high dose (standard) Melphalan (200 mg/ms2) and reduced dose (140 mg/ms2). Statistically significant differences were present between the 2 groups at baseline for DLCO but disappeared at 6 and 12‐month followup, while a statistically significant difference for FEV1/FVC ratio was seen at baseline and 6 months but disappeared at 12‐month follow‐up. There were no statistically significant differences seen with FEV1 between the two groups. Given there is no difference in mortality and relapse outcomes between the groups, the standard of care dosing for Melphalan is not associated with an increase in pulmonary morbidity.

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7

Sezer, Orhan. "Angiogenese und Knochenstoffwechsel beim multiplen Myelom." Doctoral thesis, [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963183303.

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8

Andrews, S. W. "Genotoxicity and functionality assessment of a bone marrow stromal cell line following chemotherapy exposure in an in vitro model of multiple myeloma." Thesis, University of the West of England, Bristol, 2017. http://eprints.uwe.ac.uk/30035/.

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Multiple myeloma (MM) is a haematological malignancy characterized by terminally differentiated plasma cells and their accumulation in the bone marrow (BM). Despite significant advances in therapeutic strategies it currently remains incurable. The interactions between the BM microenvironment and malignant plasma cells have been pivotal to understanding this disease. Previous reports have shown that patients with a haematological malignancy sustain “damage” to their BM, but how much of this is due to the disease and/or the treatment is currently unknown. Furthermore MM plasma cells have been documented to harness the BM microenvironment to their advantage, improving their growth and survival. However, little is known about the functionality of BM mesenchymal stem cells (MSC) in patients with MM disease which form an essential compartment of the BM microenvironment. It was hypothesised that MSC altruistically protect MM cells from therapy and consequently become phenotypically and genetically compromised. To facilitate the study of the effects of chemotherapeutic agents and MM cells on MSC, a non-contact co-culture model was developed that allowed the investigation of functional and genetic damage. In line with previous studies, U266 cells were found to be protected from drug-induced cell death when in co-culture with the stromal cell line HS5. However, the promoting effects of the BM appear to be at the detriment to their own survival. HS5 cells were found to have lower viability, altered morphology and disrupted differentiation when in a non-contact co-culture with U266 cells. Results from this study have revealed that interactions of MSC with MM cells lead to an altruistic protection of MM cells by the BM. This work demonstrates that U266 cells have an improved viability following exposure to chemotherapy when in a non-contact co-culture with MSC/HS5. Furthermore, genotoxic assays also revealed that HS5/MSC interactions with U266 cells protect U266 from the genotoxic effects of melphalan in co-culture, whilst for the first time HS5 morphology was shown to be severely altered following exposure to chemotherapy and when in co-culture with U266 cells. This work has demonstrated, for the first time, the cytotoxic effects of novel agents bortezomib and carfilzomib on HS5 cells when in co-culture with U266 cells. Results from this study also demonstrate that melphalan severely effects the ability of HS5 cells to differentiate in an osteogenic lineage with a further deficiency in differentiation when in co-culture with U266. Adipogenic differentiation of HS5 was unable to take place when in co-culture with MM cells and was again further impaired by chemotherapy. This is the first study to reveal that primary MSC secrete significantly high concentrations of IL-6 compared to the stromal cell line HS5. A further increase in expression of IL-6 was also shown when in co-culture with U266 cells. Increased multi-nucleation was also identified in both HS5 and U266 cells when exposed to either thalidomide, lenalidomide and bortezomib with abnormalities providing possible explanations for the therapy related malignancies and neurotoxicity that is seen in some patients. Genotoxicity to the MSC/HS5 compartment of the co-culture measured by the micronucleus assay was also found to be reduced suggesting that the BM is protected from the DNA damaging effects of some agents when in co-culture with MM cells. Combined work on the functionality and genotoxicity of the interactions between the BM and MM reveal a tropism of MSC and HS5 towards the MM cell line U266. With this research being conducted in a non-contact co-culture, it has indicated that cell-cell contact is not essential to provide protection of both the BM and MM cells against chemotherapy. This research provides further understanding of the MSC and MM interactions’ impact on the functionality of the BM and their protection from genotoxic damage. Elucidating the consequence of cytotoxic and genotoxic damage to MSC via chemotherapy treatment and/or through haematological disease may allow for the development of effective therapies and improve the quality of life for patients with MM.

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Cachia, Elaine. "The involvement of the central nervous system in chemotherapy-induced peripheral neuropathy, and the symptom burden and health-related quality of life in patients with multiple myeloma." Thesis, University of Sheffield, 2013. http://etheses.whiterose.ac.uk/3885/.

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Background: Modern treatments extend life expectancy in patients with multiple myeloma (MM) and a high incidence of chemotherapy-induced peripheral neuropathy (CIPN) has evolved. The impact of disease and treatment on health-related quality of life (HRQoL) in MM is poorly characterised. This work aimed to investigate (i) the neuroanatomical functional correlates of pain processing in CIPN and (ii) HRQoL and symptom burden in advanced, intensively-treated myeloma. Methods: First study: twelve neurophysiologically assessed patients with CIPN and 12 healthy volunteers underwent fMRI to determine the brain's haemodynamic response to noxious heat stimuli applied to the extremities. Second study: detailed HRQoL and neuropathy assessments, serum IL-6 and TNF-α levels were measured in 32 patients with MM (median age = 61 yrs, duration of disease = 5.5 yrs) who had previously undergone 3 lines of treatment. Results: First study: Neurophysiological testing in MM patients confirmed peripheral neuropathy in the feet. Significant hypo-activation of the right superior frontal gyrus and hyper-activation in the precuneus were present in response to foot stimulation in the CIPN-myeloma compared to healthy control groups. Significant positive correlation existed between neuropathy score and frontal opercula activation, during foot stimulation in CIPN-myeloma patients. Second study: Thirty-two MM patients (duration of disease = 5.5 yrs) were recruited. Physical functioning was significantly compromised (p < 0.001) and associated with progressive work disability and concerns regarding loss of independence. Fatigue and pain were the predominant symptoms, impacting negatively on physical functioning (p < 0.001). Half of the patients reported neuropathic pain. This sub-group scored lower measures of physical, role and social functioning on EORTC QLQ-C30 and future perspectives from the EORTC MY20 assessments compared to patients without neuropathy. Average pain and pain interference from the BPI-SF were positively correlated (p < 0.05 and p < 0.005, respectively) with serum IL-6 levels. Conclusion: Patients with MM suffer from a high peripheral neuropathy symptomatology burden, leading to a worsening functioning and increased pain. FMRI data indicates that heat-pain stimuli evoke differential activation of distinct cortical regions, suggesting different central pain processing mechanisms in CIPN-myeloma patients. Despite disease control and supportive care, intensively-treated myeloma survivors have significantly compromised HRQoL related to symptom burden.

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Strifler, Susanne [Verfasser], and Stefan [Gutachter] Knop. "Eine späte, dritte Hochdosis-Chemotherapie als wirksame Rezidivbehandlung des fortgeschrittenen multiplen Myeloms / Susanne Strifler ; Gutachter: Stefan Knop." Würzburg : Universität Würzburg, 2018. http://d-nb.info/1159881219/34.

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Книги з теми "Multiple myeloma Chemotherapy"

1

Anderson, Kenneth C., Paul G. Richardson, and Irene M. Ghobrial. Bortezomib in the treatment of multiple myeloma. Basel: Springer, 2010.

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2

Inc, ebrary, ed. Towards individualized therapy for multiple myeloma: A guide for choosing treatment that best fits patients. Singapore: World Scientific Publishing Co., 2009.

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3

Ozon, Lynn. A retrospective analysis of febrile neutropenia in patients with multiple myeloma and lymphoma treated with high-dose chemotherapy and autologous bone marrow transplant in the outpatient setting. c2003, 2003.

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4

Kuypers, Dirk R. J., and Morie A. Gertz. Light-chain deposition disease. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0154_update_001.

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Light-chain deposition disease (LCDD) is characterized by extracellular tissue deposition of non-amyloid monoclonal immunoglobulin light chains (predominantly kappa light chains) in various organs including kidneys, heart, and liver. It is a rare cause of renal insufficiency. In two-thirds of cases it is associated with multiple myeloma, while in the remainder their monoclonal B cell proliferation does not meet the criteria for that diagnosis.Renal involvement occurs almost invariably and dominates the clinical course of the disease: greater than 90% of patients with LCDD have renal functional impairment; acute or rapidly progressive kidney failure usually develops over a period of months. Nephrotic-range proteinuria is present in 40–50% of patients while approximately 20% of patients develop nephrotic syndrome. Arterial hypertension and microscopic haematuria can be present. Extrarenal symptoms are related to affected organs with cardiomyopathy, cachexia, haemorrhages, infections, and MM progression as main causes of death.The diagnosis of LCDD is often delayed and whilst bone marrow examination will often identify associated MM, renal biopsy frequently provides the final diagnostic proof. Abnormal light chains can be detected and quantified by serum or urine protein electrophoresis and immunofixation. Quantification of urine and serum free kappa/lambda light chains has proven a useful screening tool and might also plays a role in therapeutic monitoring.Treatment consists of chemotherapy directed against the monoclonal immunoglobulin-producing plasma cells.

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Частини книг з теми "Multiple myeloma Chemotherapy"

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Manier, Salomon, Artur Jurczyszyn, and David H. Vesole. "Bridging Chemotherapy: Multiple Myeloma." In The EBMT/EHA CAR-T Cell Handbook, 127–29. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_24.

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AbstractIn the phase 2 KarMMa study, 88% of the patients received bridging therapy with only a 5% response (Munshi et al. 2021). In the CARTITUDE 1 trial, 75% of the patients received bridging therapy, with a reduction in tumour burden observed in 34% of the patients prior to cilta-cel infusion, but no patients achieved a CR or better while on bridging therapy (Madduri et al. 2019). Bridging therapy is recommended for virtually all patients. An exception can be discussed for patients with slowly progressive disease, who may not need to receive bridging therapy after leukapheresis; however, this strategy exposes them to a risk of rapid progression later during the manufacturing period. In the future, with allogeneic CAR-T cells, bridging therapy will likely not be necessary because the time between patient inclusion and CAR-T cell infusion is much reduced.

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Fermand, J. P., Y. Levy, M. Adam, X. Sithy, J. M. Miclea, S. Chevret, J. Gerota, M. Benbunan, M. Seligmann, and J. C. Brouet. "High Dose Chemotherapy and Blood Stem Cell Autologous Graft in Multiple Myeloma." In Advances in haemapheresis, 139–44. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3904-9_17.

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Riordan, Neil H., Thomas E. Ichim, Famela Ramos, Samantha Halligan, Rosalia De Necochea-Campion, Grzegorz W. Basak, Steven F. Josephs, Boris R. Minev, and Ewa Carrier. "Tumor Stem Cells: Therapeutic Implications of a Paradigm Shift in Multiple Myeloma." In Cancer Management in Man: Chemotherapy, Biological Therapy, Hyperthermia and Supporting Measures, 349–62. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9704-0_20.

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Dammacco, Franco, Giuseppe Avvisati, Mario Boccadoro, Vito Michele Lauta, Rita Di Stefano, Alessandro Pileri, and Franco Mandelli. "Maintenance Treatment with Recombinant Interferon Alfa-2b Prolongs Remission and Survival in Patients with Multiple Myeloma Responding to Induction Chemotherapy." In Combination Therapies, 67–72. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3340-5_8.

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Brault, P., E. Gilles, A. Ibrahim, F. Beaujean, S. Jimenz, G. Tertian, M. Hayat, J. H. Bourhis, and J. L. Pico. "First line chemotherapy for patients with multiple myeloma with vad regimen followed by consolidation with high-dose chemoradiotherapy with peripheral stem cells autograft (PSCA): the experience of IGR center." In Cancer Treatment An Update, 885–88. Paris: Springer Paris, 1994. http://dx.doi.org/10.1007/978-2-8178-0765-2_187.

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Baig, Mirza. "Multiple Myeloma." In Practical Radiotherapy and Chemotherapy Planning, 292. Jaypee Brothers Medical Publishers (P) Ltd., 2018. http://dx.doi.org/10.5005/jp/books/13056_40.

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"Chemotherapy, steroids and interferon." In Multiple Myeloma and Related Disorders, 220–40. CRC Press, 2004. http://dx.doi.org/10.1201/b13347-19.

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"Tumours of the haemopoietic system." In Oxford Desk Reference: Oncology, edited by Thankamma Ajithkumar, Ann Barrett, Helen Hatcher, and Sarah Jefferies, 329–92. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198745440.003.0012.

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This chapter covers tumours of the haemopoietic system. Hodgkin lymphoma: clinical features, diagnosis, and staging, treatment of early and advanced stages, management of recurrence, and long-term toxicities and fertility issues are discussed. It outlines current treatment strategies that aim to maintain the high cure rates reached for all stages of the disease with chemotherapy and radiotherapy while further improving outcome and minimizing or preventing therapy-induced complications, such as infertility, cardiopulmonary toxicity, and second malignancies. For non-Hodgkin lymphoma, the clinical features, treatment of low-grade disease, diffuse large B-cell lymphoma, mantle cell lymphoma, cutaneous non-Hodgkin lymphomas, and extranodal involvement are discussed. Diagnosis with molecular profiling is used to define and stratify approaches to treatment for adult acute lymphoblastic leukaemia; adult acute myeloid leukaemia; chronic myeloid leukaemia; chronic lymphocytic leukaemia; hairy cell leukaemia; myelodysplastic syndrome; multiple myeloma; solitary plasmacytoma; monoclonal gammopathy of undetermined significance; smouldering myeloma; Waldenstrom’s macroglobulinaemia; amyloidosis and POEM syndrome; heavy chain disease; and histiocyte disorders.

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Derudas, Daniele, and Claudia Concu. "Management of Renal Failure in Multiple Myeloma." In Recent Update on Multiple Myeloma [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105444.

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Multiple myeloma (MM) is a monoclonal plasma cell neoplasia that commonly involves the kidney. Renal impairment is a serious complication during the course of the disease, and it is associated with increased morbidity and mortality. The most frequent mechanism of injury is represented by the precipitation of monoclonal free light chains (FLCs) in the distal tubule of nephron, defining a dramatic condition known as light chain cast nephropathy (LCCN). A prompt and early identification of the cause of renal disease, particularly in case of acute kidney injury (AKI), is mandatory for its effective management, avoiding the development of chronic kidney disease (CKD). In case of LCCN, in order to achieve renal recovery, it is needed, besides preventive measures, urgent intervention based on vigorous rehydration, correction of precipitating factors and effective anti-plasma cell chemotherapy. Currently, the association of the Proteasome Inhibitor Bortezomib with high-dose of Dexamethasone represents the standard association in newly diagnosed patients. The addition of another drug such as Cyclophosphamide or an Immunomodulatory Drugs may improve FLCs reduction but could be toxic. Interesting is the role of the newest therapeutic agents, particularly anti-CD38 Monoclonal Antibodies, whose efficacy and tolerance have been documented in patients without renal impairment. Despite controversial results from randomized studies, recent data suggest that in patients with LCCN and AKI requiring dialysis the association of systemic therapy with an extra-corporeal approach of FLCs removal, may increase renal response recovery rates. In this chapter, it is summarized physio-pathological basis of MM renal impairment, clinical manifestations, diagnostic procedures, and therapeutic management, included autologous stem cell transplantation.

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Heyman, Barbara B. "The Last Years, 1967–1981." In Samuel Barber, 504–53. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190863739.003.0019.

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During the last fifteen years of his life, Barber struggled with depression, alcoholism, and creative blocks. His publisher believed this was due to the reception of Antony and Cleopatra, but Barber’s annual pilgrimages to Europe had begun much earlier, and it was more likely that the forced sale of Capricorn, the home he and Menotti had shared for three decades, contributed to his low morale. The upheaval was equivalent to the dissolution of a marriage. Money from the Metropolitan Opera commission enabled him to build a chalet in Santa Cristina, where he spent most of his time. He did not withdraw from composing but turned to what had been most gratifying: writing vocal music in short forms, choosing biographically pointed texts reflecting a preoccupation with dark and quasi-religious themes. He produced the song cycle Despite and Still, two choral works, and Mutations from Bach for brass. He wrote Chorale for Ascension Day for the Washington National Cathedral and an elaborate work for chorus, vocal solos, and the Philadelphia Orchestra, The Lovers. A commission for the new Alcoa Hall in Pittsburgh resulted in Fadograph of a Yestern Scene, an orchestral piece inspired by a passage in James Joyce’s Finnegans Wake. Barber composed Three Songs, op. 45, and in 1974 wrote a piano piece, Ballade. That commission allowed him to purchase an apartment overlooking Central Park in New York. In the summer of 1978, he began a concerto for oboe and orchestra, but as his health worsened, he realized he would not be able to complete it and titled the single movement Canzonetta for Oboe and String Orchestra. He was diagnosed with multiple myeloma, and in spite of chemotherapy, Barber died on January 23, 1981.

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Тези доповідей конференцій з теми "Multiple myeloma Chemotherapy"

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Kos, M., K. Geibler, K. Ratheiser, I. Pabinger, Ch Korninger, and K. Lechner. "ACQUIRED FACTOR X DEFICIENCY IN MULTIPLE MYELOMA:A COMPLETE RESPONSE TO CHEMOTHERAPY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643292.

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A 64 year old women without any previous history of bleeding diathesis presented with bone pain and gastrointestinal bleeding. An isolated severe factor X deficiency (factor X activity 0.5%, factor X antigen less than 12.5%) was found. No inhibitor that inactivated factor X in vitro or interfered with factor X assay could be demonstrated. Substitution therapy with a prothrombin complex preparation containing factor X (PPSB Biotest) was given. Factor X recovery in the first 2 days was lower than expected (below 20%) and half life of factor X was shortened (150 minutes). Subsequently, a diagnosis of multiple myeloma (light chain myeloma, type kappa) was made. Amyloidosis was excluded by electronmicroscopic examination of rectum biopsies. Chemotherapy according to the M2 protocol (Case et al) was initiated. Factor X recovery improved dramatically within 2 weeks and there was a continuous increase of factor X activity and antigen during chemotherapy. After 6 courses a complete haematological remission (less than 5% plasma cells in the bone marrow, disappearance of light chains) was obtained and factor X activity and antigen returned to normal.Isolated factor X deficiency is a wellknown complication of amyloidosis. To our knowledge, this is the first case of factor X deficiency in multiple myeloma without amyloidosis. The complete normalization of factor X after successful chemotherapy indicates that plasma cell proliferation may have been the cause of the factor X deficiency. Binding of factor X to plasma cells containing light chains could be a possible explanation, and we are currently examining this hypothesis.

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Zhang, Xingding, Lin Qi, and Lin Yang. "Abstract 680: HMGB1 regulates autophagy and apoptosis to promote chemotherapy resistance in multiple myeloma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-680.

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Siddiqui, Mohammad F., Sridhar Badireddi, Elias Anaissie, Bart Barlogie, and Federick C. Hiller. "Effect Of High Dose Chemotherapy And Autologous Stem Cell Transplantation On Pulmonary Function In Multiple Myeloma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3036.

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Gopan, Gayatri, Geetha Narayanan, Sreejith G. Nair, Prakash Purushothaman, Rona Joseph, Rekha A. Nair, and Jagathnath Krishna. "Outcome of Treatment in Elderly Myeloma—A Single-Centre Experience." In Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735368.

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Abstract Introduction Multiple myeloma (MM) accounts for approximately 1% of all cancers and 10% of all hematologic malignancies. In our institution, we see around 200 patients with myeloma every year. We present our experience with multiple myeloma in the patients aged more than 60 years. Objectives This is a retrospective study of 300 newly diagnosed multiple myeloma patients above 60 years of age treated in the Department of Medical Oncology, Regional Cancer Center, Thiruvananthapuram, Kerala, India, during the period between 2014 and 2017. The medical records of the patients were studied and following data were collected: demographic and clinical details, diagnostic and staging workup, primary treatment, response assessment, relapse, and survival. Survival was estimated using the Kaplan–Meier method. Results A total of 300 patients were included in the study. The median age was 66 years with a male-to-female ratio of 1.4:1. The common clinical presentations were backache (134), fatigue (49), lower respiratory infection (20), and paraparesis (14). Monoclonal protein was immunoglobulin (Ig)-G in 199 patients (66.6%), IgA in 52 patients (17.4%), IgM in 2 patients, and IgD in 1 patient. Light-chain disease was seen in 42 patients (14%). One hundred and sixty patients (53.5%) had ISS stage III. Only 285 patients received treatment, of which 203 (67.8%) received bortezomib-based regimen, - bortezomib and dexamethasone (BD; 33.4%); bortezomib, lenalidomide, and dexamethasone (BLD; 19.7%); bortezomib, cyclophosphamide, and dexamethasone (VCD; 8.7%); bortezomib, thalidomide, and dexamethasone (BTD; 2.3%); and bortezomib, melphalan, and prednisolone (3.7%). Nonbortezomib-based regimens used were melphalan and prednisolone (MP) alone or with thalidomide or lenalidomide (15%), lenalidomide and dexamethasone (LD; 10.4%), and thalidomide and dexamethasone (TD; 2%). Response assessment was done as per IMWG guidelines. Fifty-seven (26.3%) patients achieved complete response (CR), 94 (43.3%) achieved very good partial response (VGPR), 19 (8.8%) attained partial response (PR), 15 (5.6%) had stable disease, and 46 (15.4%) developed progressive disease. With bortezomib-based regimens, 119 patients (58.3%) achieved CR/VGPR, and with non-bortezomib based regimens, 42 patients (51.2%) achieved CR/VGPR. One hundred and forty-three patients (47.8%) received maintenance therapy of which 79 received maintenance with bortezomib, 49 with lenalidomide, and 15 with thalidomide. The average duration of maintenance was 24 months. Second-line chemotherapy regimens were used in 37 patients. Agents used were MP, LD, TD, and VCD. With second-line treatment, 15 patients achieved VGPR, 10 patients achieved partial response, and 25 patients developed progressive disease. Third-line chemotherapy regimens were used in 22 patients and the regimens used were pomalidomide and dexamethasone, MP, TD, LD, vincristine, doxorubicin, and dexamethasone and carfilzomib and dexamethasone. At a median follow-up of 34 months, the 2-year overall survival (OS) was 68%. The median progression-free survival was 21 months. The 2-year OS for patients receiving initial bortezomib-based regimen was 67.8% and non-bortezomib based regimen was 68% which was similar. Conclusion In this study, CR/VGPR rates and 2-year OS in patients treated with bortezomib and non-bortezomib based regimens were not statistically significant.

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Siddiqui, Mohammad F., Sridhar Badireddi, Eilias Annaisie, Bart Barlogie, and Frederick C. Hiller. "Effect Of High Dose Chemotherapy And Autologous Stem Cell Transplantation On Obstructive Lung Disease In Multiple Myeloma." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4474.

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Simijonović, Dušica, Marko Antonijević, Edina Avdović, Zorica Petrović, and Zoran Marković. "INHIBITORY EFFECT OF COUMARIN BENZOYLHYDRAZONES ON MCL-1 PROTEIN." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.442s.

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The protein that controls cell differentiation in acute myeloid leukemia is MCL-1. High-level of this protein causes the carcinogenesis. In this paper inhibitory effect of two coumarin benzoylhydrazones,(E)-2-hydroxy-N’-(1-(2-oxo-2H-chromen-3-yl)ethylidene)benzohydrazide (A) and (E)-4-hydroxy-N’-(1-(2-oxo-2H-chromen-3-yl)ethylidene)benzohydrazide (B) against MCL-1 protein was investigated. For this purpose, a molecular docking simulations were used. The obtained results showed that compound A showed better activity than compound B. Also, the docking simulations against MCL-1 protein were performed for melphalan or (2S)-2-amino- 3-{4-[bis(2-chloroethyl)amino]phenyl}propanoic acid and two 4-chlorocoumarin benzoylhydrazone derivatives, N′-[(E)-(4-chloro-2-oxo-2H-chromen-3-yl)- methylidene]benzohydrazide (4a) and N′-[(E)-(4-chloro-2-oxo-2H-chromen-3-yl)- methylidene]-4-hydroxybenzohydrazide (4b). In this study, melphalan as a chemotherapy drug commonly used in treating multiple myeloma and compounds 4a and 4b as structurally similar compounds with A and B were used as reference compounds. It was shown that these reference compounds exhibited similar activity as compound B. In addition, the potential toxicology of compounds A and B, as well as reference compounds was determined by the ProTox-II webserver. The results revealed that compounds A and B are 3 to 5 times lower toxic than reference compounds.

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Silva, Ariosto S., Alexander Anderson, Robert Gillies, and Robert Gatenby. "Abstract 21: Understanding the progression and chemotherapy resistance of Multiple Myeloma in the bone marrow through evolutionary computational models and in vitro experiments." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-21.

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Shires, Karen, and Kirsty Wienand. "Abstract B18: MAGEC1 and BAGE2 mRNA expression can be used to monitor chemotherapy treatment responses in multiple myeloma patients and pre-empt clinical relapse." In Abstracts: AACR International Conference: New Frontiers in Cancer Research; January 18-22, 2017; Cape Town, South Africa. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.newfront17-b18.

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Devi, Pinki, Ganapathi Bhat, and Harish S. Ahuja. "To Predict Success of Postapheresis Yield and Post–Autologous Transplant Engraftment Based on Preapheresis Peripheral Blood CD34+ Cell Counts: An Indian Scenario–Based Study." In Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735370.

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Abstract Introduction The use of hematopoietic stem cells for autologous and allogeneic transplantation has increased in the recent past significantly, due to introduction of newer chemotherapeutic drugs, immunological techniques, and better stem cell technology. Among the bone marrow and peripheral blood stem cells, collection of the latter being more convenient to the patient and associated with faster granulocyte and platelet engraftment has been known as preferred method for mobilization. Peripheral blood stem cells can be extracted from the autologous or allogeneic donor. Mobilization of the stem cells for autologous stem cell transplant is traditionally done using growth factors alone or in combination with chemotherapy, with or without an additional mobilizing agent. A significant number of hematological malignancy patients are poor mobilizers, (i.e., they are unable to achieve the minimal target cell dose during their first round of mobilization).Therefore, a prediction for a successful stem cell mobilization ideally should be made before initiating any apheresis procedure to spare those with a low rate of success from the risks associated with apheresis procedure. Preapheresis CD34 cell count can predict postapheresis yield and hence, can help to reduce the collection sessions. Reduction of apheresis sessions decreases the discomfort, inconvenience, time, and monetary expenses. Objectives This study was aimed to analyze preapheresis and postapheresis CD34+ cell counts. Materials and Methods Patients of any age and gender with diagnosis of hematological malignancies admitted for autologous stem cell transplantation for hematological malignancies (including Hodgkin lymphoma, non-Hodgkin lymphoma, and multiple myeloma) and germ cell tumors in our institute from July 2008 to July 2016 were included in the study. The post-GCSF CBC, preapheresis CBC, CD34+ cell counts, and postapheresis CBC, CD34+ cell counts, mononuclear cell counts to predict the outcome of amount of yield. The effect on engraftment will be measured according to the defining criteria of achieving a sustained peripheral blood neutrophil count of >500 × 106/L (Wolff 2002) and a platelet count of more than >20 × 109/L (Teltschik et al. 2016) independent of platelet transfusion for at least 7 days. Collection of stem cells was done using apheresis machine (COBE SPECTRA). Complete peripheral blood counts using automated analyzers. Peripheral blood CD34 + cell counts and postapheresis CD34+ cell count using BD FACS CANTO II flow cytometer. To calculate postapheresis yield, the related CD34 count measured by flow cytometer was multiplied by the apheresis product volume and divided by the recipient’s body weight (kg). Number of CD34+ cells collected = (CD34 cell concentration in final product) × (final product volume). Results A total of 100 patients who underwent a total of 320 apheresis sessions were included in the study. There were 78 males and 22 females. We also found a significant correlation between preapheresis CD34 + cell count and postapheresis CD34 percentage on days 1, 2, and 3 of the apheresis sessions. In our study, to obtain more than 1.31 × 106 cells (median = 1.04, range: 0.15–4.70), an absolute count of pre apheresis CD34 + cells ≥14 cells would be necessary. A target of CD34 + cells ≥ 2 × 106/kg was obtained in majority of patients if a concentration of ≥25 CD34 + cells was present in postapheresis collection. Conclusion Compiling our results with the previous published data, we conclude that there is a strong correlation between preapheresis absolute CD34 + cell counts and postapheresis CD34 + cell count. Our study also suggests that the minimum absolute cell count of >10 cells/μL is required, to achieve a target of >2–5 × 106 cells for postapheresis yield.

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Звіти організацій з теми "Multiple myeloma Chemotherapy"

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Li, Zonghong, Xuewei Yin, Hongyan Xiao, Chunyi Lyu, Yuping Si, Zhenzhen Wang, Xueyan Dong, Yueli Liu, and Ruirong Xu. Efficacy and safety of bendamustine combined with chemotherapy for relapsed/refractory multiple myeloma A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0038.

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