Relevant bibliographies by topics / Multiple myeloma; Breast cancer

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Multiple myeloma; Breast cancer'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Multiple myeloma; Breast cancer.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Multiple myeloma; Breast cancer"

1

Gulmez, Ahmet. "Breast cancer after multiple myeloma treatment." Current Problems in Cancer 43, no. 6 (December 2019): 100463. http://dx.doi.org/10.1016/j.currproblcancer.2019.01.004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Savage, David, and T. J. Garrett. "Multiple myeloma masquerading as metastatic breast cancer." Cancer 57, no. 5 (March 1, 1986): 923–24. http://dx.doi.org/10.1002/1097-0142(19860301)57:5<923::aid-cncr2820570507>3.0.co;2-u.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ali, Heba O. E., Zafar Nasir, and Ahmed M. S. M. Marzouk. "Multiple Myeloma Breast Involvement: A Case Report." Case Reports in Radiology 2019 (October 9, 2019): 1–5. http://dx.doi.org/10.1155/2019/2079439.

Full text
Abstract:
Multiple Myeloma involving the breast is very rare and the diagnosis is challenging because the clinical and radiological features of breast multiple myeloma are indistinguishable to other forms of breast disease whether primary or metastatic. In this article the authors report a case presented with breast masses, which were found to be extra osseous Multiple Myeloma. The patient was managed for multiple spinal lesions that were primarily thought to be metastasis from primary breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
4

Al-Said Ali, Ali, Ibtisam Al-Bader, Fatma Al-Ali, Abdel Hamid Elgazzar, and Salah Fayez. "Breast Cancer and Multiple Myeloma at Initial Presentation." Breast Journal 15, no. 1 (January 2009): 103–5. http://dx.doi.org/10.1111/j.1524-4741.2008.00679.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Evens, Andrew M., June M. McKoy, Paul R. Yarnold, Kathyrn McCaffrey, and Charles L. Bennett. "Thalidomide-Associated Thromboembolism in Cancer: Reimbursement for Thalidomide’s “Off-Label” Prescribing under the 2004 Medicare Oral Pharmaceutical Demonstration Project Raises Concerns." Blood 106, no. 11 (November 16, 2005): 2244. http://dx.doi.org/10.1182/blood.v106.11.2244.2244.

Full text
Abstract:
Abstract Purpose: In 1999, one year after its approval by the FDA for erythema nodosum leprosum, thalidomide’s effectiveness as an off-label treatment for multiple myeloma was noted. A 28% rate of thromboembolism with thalidomide-doxorubicin therapy for myeloma was reported in 2001. Thalidomide’s inclusion in the 2004 Medicare Oral Pharmaceutical Demonstration Project as treatment for multiple myeloma represents the only off-label use drug covered. FDA regulations prohibit manufacturer dissemination of comprehensive safety information describing thalidomide-associated thromboembolism (TAT) in the off-label oncology setting. Herein, we reviewed FDA and published information for TAT in the oncology setting. Methods: Adverse event reports contained in FDA databases (n= 190 patients) and 48 prospective clinical trials (n= 2,329 patients) were reviewed for information on thromboembolism occurring among thalidomide-treated cancer patients. Results: TAT occurred after a median of 52 days of therapy (range, 6 to 469 days), with more than half of these events among persons with multiple myeloma. TAT rates of 30% were noted among patients with newly diagnosed multiple myeloma receiving concomitant doxorubicin. Previously treated myeloma patients receiving thalidomide and doxorubicin and newly diagnosed patients on thalidomide, doxorubicin, and low molecular weight heparin had thromboembolism rates of 15% or lower. Conclusions: Revision of FDA regulations to allow dissemination of information describing benefits and toxicities of thalidomide as an off-label cancer treatment is important, particularly for multiple myeloma patients receiving thalidomide under the 2004 Medicare Oral Pharmaceutical Demonstration Project. Cancer drugs covered under the Medicare Replacement Drug Demonstration Project CANCER INDICATION ONCOLOGY DRUG Breast cancer Anastrazole Breast cancer Exemestrane Breast cancer Letrozole Breast cancer Tamoxifen Breast cancer Toremifene Chronic myelogenous leukemia Imatinib mesylate Cutaneous T-cell lymphoma Bexarotene Epithelial ovarian cancer Altretamine GI Stromal Tumor Imatinib mesylate Multiple myeloma Thalidomide Non-small cell lung cancer Gefitinib Non-small cell lung cancer Erlotinib Prophylaxis for ifosfamide-induced hemorrhagic cystitis Mesna
APA, Harvard, Vancouver, ISO, and other styles
6

YONEYAMA, Kimiyasu, Shigehiro KIKUYAMA, and Renpei OOYAMA. "A CASE OF BREAST CANCER COMPLICATED BY MULTIPLE MYELOMA." Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association) 67, no. 12 (2006): 2796–99. http://dx.doi.org/10.3919/jjsa.67.2796.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Hough, Bruce, Adam Brufsky, and Suzanne Lentzsch. "Metastatic Breast Cancer or Multiple Myeloma? Camouflage by Lytic Lesions." Journal of Oncology 2010 (2010): 1–3. http://dx.doi.org/10.1155/2010/509530.

Full text
Abstract:
We report a case of a female with stage I infiltrating ductal carcinoma who received adjuvant therapy including trastuzumab. One year later she developed lytic lesions and was retreated with trastuzumab that was held after she developed symptomatic heart failure. Lytic lesions were attributed to relapse of breast cancer, and cardiac failure attributed to prior trastuzumab therapy. After complications necessitated multiple hospitalizations, a further workup revealed that the lytic lesions were not metastatic breast cancer but multiple myeloma. Her advanced multiple myeloma was associated with systemic amyloidosis involving gut and heart, which ultimately led to her demise. This report addresses the pitfalls of overlapping symptoms and the question of which patients with suspected metastatic disease should undergo a biopsy.
APA, Harvard, Vancouver, ISO, and other styles
8

Durusu, Mine, M. Kadri Altundağ, Duygu Yazgan Aksoy, Hüseyin Abali, Alev Türker, and Arzu Sungur. "Metastatic Carcinoma of the Breast Mimicking Multiple Myeloma." Tumori Journal 89, no. 1 (January 2003): 106–7. http://dx.doi.org/10.1177/030089160308900124.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Dorantes-Heredia, Rita, Daniel Motola-Kuba, Jose Manuel Ruiz-Morales, Wallace Rafael A. Muñoz-Castañeda, Carolina Vega-Ochoa, and Roberto De la Peña. "Searching for the Culprit: Metastases from a Cancer of Unknown Primary." Case Reports in Oncology 11, no. 2 (August 10, 2018): 541–48. http://dx.doi.org/10.1159/000491600.

Full text
Abstract:
We report a case of metastases from a cancer of unknown primary whose primary site could not be identified during the appropriate pretreatment evaluation. The patient was a 58-year-old woman with a history of passive smoking and with no history of cancer in the family. Her current condition started with asthenia, adynamia, and pallor, followed by palpitations. An abdominopelvic computed tomography (CT) scan was performed, showing multiple osteolytic lesions distributed in all bone structures and axillary adenopathy on the left side. As part of the approach and given the high suspicion of multiple myeloma, tests were performed. The results were negative for multiple myeloma. A PET-CT scan was performed and showed left axillary adenopathy. The breasts and other organs were not affected. Left axillary lymph node resection revealed breast primary metastatic pleomorphic lobular carcinoma. Due to the metastatic disease (caused by the primary breast cancer), it was decided to start chemotherapy.
APA, Harvard, Vancouver, ISO, and other styles
10

Lage, M., D. J. Harrison, B. Barber, and S. Jun. "Burden of hospitalizations associated with skeletal related events in patients with breast cancer or lung cancer and bone metastases or multiple myeloma." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 17083. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.17083.

Full text
Abstract:
17083 Background: Patients with bone metastases secondary to cancer often experience skeletal related events (SREs) including pathological fracture, spinal cord compression, hypercalcemia, bone surgery or radiotherapy, or initiation of opioid analgesic use. These SREs result in major morbidity and reduced quality of life. This research examines hospitalizations associated with SREs. Methods: Data for this study were obtained from i3 LabRx Database (05/01/2000 to 03/31/2005). Individuals were included in the analyses if they had at least two diagnoses of breast cancer (based upon an ICD-9 code of 174.xx), lung cancer (162.xx), or multiple myeloma (203.0x) and had at least two diagnoses of bone metastases (198.5x) after the first diagnosis of cancer. In addition, individuals were required to have at least one SRE (based upon a previously published algorithm) on or after their initial diagnosis of bone metastases (their index date). Individuals were required to be continuously insured for at least 6 months prior to, and at least one month post their index date. Data were analyzed until 03/31/2005 or until the end of their continuous coverage, whichever occurred first. Descriptive statistics for each of these cohorts are provided. Results: A total of 1,204 individuals with breast cancer, 1,094 with lung cancer, and 258 with multiple myeloma were included in the study. The vast majority of individuals with breast cancer (96.5%), lung cancer (95.9%), or multiple myeloma (96.8%) were hospitalized. All three patient groups were likely to have SRE-related hospitalizations; multiple myeloma 43.4%, breast cancer 36.2% and lung cancer 35.6%. The average number of days per patient year that patients were hospitalized related to a diagnosis or procedure for a SRE was 6.75 days for patients with lung cancer, 6.56 days for patients with multiple myeloma, and 3.75 days for patients with breast cancer. Conclusion: Hospitalizations related to SREs are common and the number of days per year is substantial. No significant financial relationships to disclose.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Multiple myeloma; Breast cancer"

1

Drake, Mary. "Characterisation of mononuclear cells in peripheral blood stem cell harvests." Thesis, Queen's University Belfast, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287206.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Harrison, Simon James. "Immunotherapy in multiple myeloma." Thesis, University of Glasgow, 2005. http://theses.gla.ac.uk/1054/.

Full text
Abstract:
The BDCA antibodies allowed reliable measurement of dendritic cell (DC) subsets and B cell numbers in the blood of normal subjects, and patients with MM throughout the disease course. The numbers of blood myeloid DC (BmDC) and blood plasmacytoid DC (BpDC) are low throughout the course of the disease, and only improve for a short period of time following autologous HSCT. Thalidomide therapy of patients with relapsed disease was associated with an increase in BmDC1 and BpDC numbers. Monocytes, mobilised at the time of stem cell collection, were used to produce mature DC (matDC) from MM patients and normal donors (ND). The matDC produced from MM patients were of poorer quality as compared to those from ND, despite using combinations of GM/IL-4, GM/IL-13, X4 and MIMIC in the production process. The combinations that contained the X4 maturation cocktail produced the best quality matDC. The DC/T cell system is abnormal in MM patients. Despite this, it is possible to produce antigen loaded mature MoDC from MM patients. When combined with T cell pre-stimulation and IL-2 expansion, these DC are capable of inducing anti-MM cytotoxic T cells, which exhibit considerable anti-MM cytolytic activity. However, the DC from MM patients still display abnormal chemokine receptor expression, which may inhibit their capability to migrate to lymph nodes in-vivo in order to generate these cytotoxic T cell responses. These observations will aid in the optimisation of DC based immune therapies for MM, and suggest that a combined immunotherapy approach using pre-stimulated T cells, MM Ag primed DC and IL-2 may produce better clinical responses in MM patients.
APA, Harvard, Vancouver, ISO, and other styles
3

Dimberg, Lina. "Apoptosis Regulation in Multiple Myeloma." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7099.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Mhadgut, Hemendra M. D., Alay Mansurov, Rabia Zafar, and Koyamangalath Krishnan. "Liver Mass: An Unusual Presentation of Multiple Myeloma." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/asrf/2020/presentations/22.

Full text
Abstract:
Multiple myeloma is characterized by proliferation of plasma cells in the bone marrow, producing monoclonal immunoglobulin. It accounts for 17% of hematologic malignancies in the US. Diagnosis is often suspected in the setting of bone lytic lesions, anemia, hypercalcemia or renal failure. Rarely, multiple myeloma can present with soft tissue involvement which can be difficult to diagnose. Below we present one such presentation. Our patient is a 53-year-old who was initially diagnosed with multiple myeloma six years back when he presented to hospital with back and right leg pain. On admission he was found to have multiple lytic lesions involving the appendicular and axial skeleton. On further workup, bone marrow biopsy showed 30% plasma cells with IgG kappa monoclonal protein elevation. Patient was diagnosed with ISS stage II multiple myeloma. He was treated with standard regimen with Velcade, Revlimid and dexamethasone with excellent response. Patient was evaluated for stem cell transplant however did not qualify for it due to social challenges. Patient was continued on maintenance therapy with Velcade and Revlimid for 8 cycles prior to clinical relapse with lytic lesions in the C-spine. At this point patient was switched to different therapeutic regimen with pomalidomide, carfilzomib and dexamethasone and had excellent response for 35 cycles on this regimen. Patient had interruption in treatment for 3 months due to other medical comorbidities. A repeat bone marrow biopsy which was done in November of 2019 revealed extensive bone marrow involvement with 70% plasma cells concerning for relapse. Patient was started on single agent daratumumab in December 2019 however had a difficult course interrupted by right-sided abdominal pain, persistent nausea and decreased appetite requiring hospital admission. Further workup revealed a 2.7 cm lesion in the liver as well as a 4.9 x 7.3 cm T11 left paraspinal soft tissue mass. Biopsy of the liver lesion revealed sheets of kappa restricted abnormal plasma cells concerning for progression of disease. Given the involvement of the visceral organ and the extent of his disease, it was decided to switch patient's treatment from single agent daratumumab to a multi agent chemotherapy regimen with dexamethasone, cyclophosphamide, etoposide and cisplatin. Patient received his 1st cycle inpatient and had marked symptomatic improvement and was discharged home. His M-protein spike reduced from 3.9 to 1.8 g/dl post once cycle of treatment. Soft tissue involvement by multiple myeloma is rare event. Though malignant plasma cells may diffusely infiltrate the liver parenchyma, the nodular spread is unique. In review by Talamo et al, out of 2,584 patients with MM, only 11 had liver plasmacytomas. This phenomenon is driven by lack of expression of adhesion molecules, increased heparanase-1 expression and loss of chemokine receptors on myeloma cells. Such alterations in cell architecture lead to more aggressive disease behavior. At present time treatment for this unique patient population does not differ from other MM cases. It is important for clinicians to recognize the possibility of such event.
APA, Harvard, Vancouver, ISO, and other styles
5

Cook, Gordon. "Immune regulation in multiple myeloma : the host-tumour conflict." Thesis, University of Glasgow, 2000. http://theses.gla.ac.uk/6140/.

Full text
Abstract:
The data presented in this thesis demonstrates that the malignant plasma cells of multiple myeloma are capable of suppressing the activation of T lymphocytes. The myeloma cells prevent activation of T cells from healthy donors by allo-antigen, mitogen and IL-2, mediated by the production of soluble, immuno-suppressive factor. This factor was responsible for inducing cell cycle arrest and failure of the T cells to progress into the autocrine IL-2 autocrine pathway, which is of critical importance in the activation of T cells. To further investigate this interaction an in vitro model system was developed to examine the key stages of T cell activation and homeostasis. Myeloma cells constitutively expressed high levels of TGF-1 mRNA transcripts as detected by RT-PCR which were translated into latent protein and secreted as detected by immunohistochemistry and ELSIA, respectively. The reversal of the immuno-suppression induced by the myeloma cells using the specific TGF-1 antagonist, Latency Associated Peptide, confirmed that TGF-1 is a major factor in myeloma-associated suppression of T lymphocyte activation. It was demonstrated that the myeloma cells prevent the T cells, upon activation, from up-regulating the surface expression of the -chain of the IL-2R thus preventing the formation of the high-affinity receptor. The reduced expression of IL-2R resulted from altered transcription of the -chain gene in response to re-stimulation of primary T cells with IL-2. When signalling events in primary T cells responding to re-stimulation with Il-2 was examined, myeloma cells inhibited the phosphorylation of both STAT3 and STAT5. However, using a novel IL-2-dependnet T cell line (IDBL), which does not require the expression of the high affinity IL-2R for its responses to IL-2, it was shown that these cells are insensitive to the myeloma-derived TGF-, in terms of DNA synthesis and proliferation, despite demonstrating failure of phosphorylation of STAT5. It was demonstrated that phosphorylation of STAT3 was unchanged when IDBL cells were co-cultured with myeloma cell lines.
APA, Harvard, Vancouver, ISO, and other styles
6

Okumura, Setsuko. "Feasibility of breast-conserving therapy for macroscopically multiple breast cancer." Kyoto University, 2004. http://hdl.handle.net/2433/147559.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Faiman, Beth Marie. "Peripheral Neuropathy and Diarrhea Symptoms in Multiple Myeloma." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1417619492.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Machin, Reinaldo Franqui. "Destabilizing NEK2 overcomes resistance to proteasome inhibition in multiple myeloma." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6104.

Full text
Abstract:
Multiple Myeloma (MM) is an incurable plasma cell malignancy and, although novel treatment regimes in the past decade have improved patient outcome, long-term treatment leads to relapse and refractory disease. The centrosomal kinase NEK2 is found overexpressed in MM and promotes chromosomal instability, drug resistance and increased proliferation. Although much research shows NEK2 having a detrimental effect in cancer, much of its mechanisms of overexpression and drug resistance has not been studied in detail. In this work we expand our understanding of NEK2 in MM. Using Tandem Affinity Purification coupled with Mass Spectrometry, we show that NEK2 directly interacts with the de-ubiquitinase USP7. We confirm this interaction in cell lines of MM and lung cancer. Since USP7 has been shown to have important cancer-promoting roles we tested if USP7 was necessary for NEK2-driven bortezomib resistance. We found that USP7 shRNA was sufficient to sensitize the bortezomib resistant NEK2 overexpressing cells to bortezomib. Surprisingly, we found that USP7 inhibition with shRNA or by treatment with the small molecule USP7 inhibitor P5091 led to depletion of NEK2 protein in every cell line tested. Previous research shows USP7’s main function is a de-ubiquitinase and, since NEK2 is a target of the ubiquitin-proteasome system, we hypothesized USP7 may be de-ubiquitinating NEK2. Through western blots and immunoprecipitations, we show the NEK2-USP7 interaction promotes the de-ubiquitination and subsequent stabilization of NEK2, presenting USP7 as the first discovered de-ubiquitinating enzyme of NEK2. To understand how NEK2 promotes drug resistance in cancer we studied a previously published list of NEK2-regulated genes and, using the UCSC genome browser (Track Name:GM12878+TNFa RELA) ChIP-seq data, we found approximately half of these genes have the NF-κB transcription factor p65 bound throughout the gene sequence. We also produced a signaling score using an average of 11 known targets of NF-κB and patients with high NEK2 showed a significantly increased score of NF-κB signaling. Additionally, through western blots and immunofluorescence, we found that patients with high NEK2 protein levels consisitently had activation higher signal of p65 protein and phosphorylated p65 at Serine 536, indicative of increased activity. We then causally show NEK2 activates canonical NF-κB by performing western blots and a dual-luciferase reporter assay on control and NEK2 overexpressing cells. Using AKT and PP1α inhibitors, we found that NEK2 drives NF-κB by phosphorylating and inactivating PP1α, leading to hyperactive AKT. Using this model of NEK2-NF-κB activation, we aimed at targeting NEK2 directly with the small molecule drugs INH1 (depletes NEK2 protein) and P5091 (inhibits USP7 activity) in empty vector control cells, NEK2 overexpressing cells or cells with an acquired drug resistance phenotype. Our results show that both INH1 and P5091 can overcome bortezomib resistance in cell lines and in vivo. Another aspect of MM disease we targeted in this work was bone disease. Bone disease in MM is common and causes bone pain and fractures but a much is still regarding what drives these lesions. We found that NEK2 expression in patients correlates with a presence of bone lesions, based on FDG-PET scan and MRI. Using our previously published list of NEK2 regulated genes, we found Heparanase (HPSE) is directly correlated to NEK2 expression. HPSE is an extracellular protein shown to promote differentiation of the bone destroying cell, osteoclast. Using western blots, RT-qPCR and ELISA, we found NEK2 increases HPSE expression and extracellular release. HPSE was also on the list of genes upregulated by NEK2 found to have p65 bound to the gene, thus we tested if NEK2 was driving HPSE through the NF-κB. Accordingly, we found NEK2 drives HPSE through the NF-κB pathway and, consistent with our previous results, in a USP7-dependent manner. Using bone marrow macrophages and conditioned media from empty vector control or NEK2 overexpressing cells, we found NEK2 promtoes increased differentiation of osteoclasts and inhibition of HPSE blocked this effect, strongly suggesting HPSE is the mediator of this effects. Importantly these findings were recapitulated in vivo. Empty vector or NEK2 overexpressing cells were injected through the tail vein to allow dissemination to the bone marrow. microCT and Xray revealed mice injected with NEK2 overexpressing cells showed reduced bone density, compared to empty vector cells. Additionally, H&E and TRAP staining confirmed our in vitro results by showing higher osteoclast levels in bone sections of mice injected with NEK2 overexpressing cells. Lastly, we show a novel role for the ATPase TRIP13 as a cofactor for USP7 de-ubiquitinating activity. TRIP13 is overexpressed in cancer, has been shown to be an oncogene and promotes drug resistance. By systematically targeting TRIP13 overexpressing cells with drugs that inhibit different pathways we found TRIP13 drug resistance is diminished by inhibiting USP7. We found that TRIP13 binds with USP7 and by western blots and immunoprecipitations we show it is necessary for the de-ubiquitination of NEK2. Furthermore, we also found TRIP13 shows a hyperactive USP7 phenotype, shuttling PTEN out of the nucleus and stabilizing MDM2, in a USP7 dependent manner. In summary, this work shows the de-ubiquitinase USP7, coupled with the ATPase TRIP13 stabilizes NEK2 by de-ubiquitination, this leads to accumulation of NEK2 and activation of the canonical NF-κB pathway through PP1α/AKT, which promotes drug resistance and activates HPSE, increasing osteoclast differentiation and bone destruction.
APA, Harvard, Vancouver, ISO, and other styles
9

Zabalo, Joaquin. "A Mathematical Model Describing the Early Development of Multiple Myeloma." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/366.

Full text
Abstract:
Multiple myeloma is a malignant bone marrow plasma cell tumor which is responsible for approximately 12,000 deaths per year in the United States and two percent of all cancer deaths. It is recognized clinically by the presence of more than ten percent bone marrow plasma cells, the detection of a monoclonal protein (M-protein), anemia, hypercalcemia, renal insufficiency, and lytic bone lesions. The disease is usually preceded by a premalignant tumor called monoclonal gammopathy of undetermined significance (MGUS), which is present in one percent of adults over the age of fifty, three percent over the age of seventy and ten percent of those in the tenth decade. MGUS is also recognized by the detection of M-protein, but with less than ten percent bone marrow plasma cells and without the other features exhibited by myeloma. The majority of MGUS patients remain stable for long periods without ever developing myeloma. Only a small percentage of patients with MGUS eventually develop multiple myeloma. However, the reason for this is not yet known. Once the myeloma stage is reached, a sequence of well-understood mutational evets eventually lead to the escape of the tumor from the control of the immune system. We propose a mathematical model of tumor-immune system interactions at the onset of the disease in an effort to better understand the early events that take place and their influence on the outcome of the disease. The model is calibrated with parameter values obtained from available data and we study the resulting dynamics. Next, we study how the behavior of the system is affected as parameters are varied. Finally, we interpret the results and draw some conclusions.
APA, Harvard, Vancouver, ISO, and other styles
10

Kendrick, Felicity. "Modelling immunoglobulin metabolism and its effect on prognostic utility in multiple myeloma." Thesis, University of Warwick, 2018. http://wrap.warwick.ac.uk/104030/.

Full text
Abstract:
Multiple myeloma is a cancer of plasma cells. In multiple myeloma, a clone of plasma cells in the bone marrow secretes a unique, monoclonal immunoglobulin (Ig), whose biological properties depend on its type and structure. The monoclonal Ig offers a convenient opportunity for clinicians to monitor the response of the tumour to therapy via the secreted protein, which is readily quantified in a blood sample. Responses to treatment are assigned based on the percentage reduction in monoclonal Ig; however, response criteria do not take into account the different metabolic half-lives of the proteins. 70% of multiple myeloma patients have either monoclonal IgA- or monoclonal IgG-producing clones. IgA and IgG have metabolic half-lives of 6 days and 23 days, at normal concentrations, respectively. The large difference in their metabolic half-lives suggests that they would respond at different rates during therapy. The elimination rate of IgG is concentration-dependent due to saturable recycling by a receptor. This could further impact upon its response during therapy, with the possibility that IgG is eliminated from the body at different rates at the beginning of therapy, when its concentration is high, and at the end of therapy, when its concentration has decreased. In this thesis compartmental models of IgG metabolism from the literature are analysed and parameter values are estimated from available data. A model of IgA metabolism is sourced in the literature. These models are used to predict the responses of monoclonal IgA and IgG during therapy. The simulations are able to replicate typical monoclonal IgA and IgG responses seen in a clinical trial of patients with relapsed and refractory multiple myeloma. Importantly, the plasma cell clone is not directly accessible to measurement and therefore not available to validate model-based predictions. However, monoclonal Ig responses are not evaluated by their ability to predict the tumour burden, but by the strength of their association with patient survival. In this thesis, a prediction is made of how the different metabolic properties of IgA and IgG may influence their association with survival outcomes. Evidence for this effect is then evaluated in data from a clinical trial using the methods of survival analysis.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Multiple myeloma; Breast cancer"

1

Dancing with cancer: A healing through visualization. Dallas, Tex: Noteman Press, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Wagner, John R. Thirty and terminal: Cancer survival. Seattle, WA: Infinity Pub., 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hayat, M. A. Methods of Cancer Diagnosis, Therapy, and Prognosis: Ovarian Cancer, Renal Cancer, Urogenitary tract Cancer, Urinary Bladder Cancer, Cervical Uterine Cancer, Skin Cancer, Leukemia, Multiple Myeloma and Sarcoma. Dordrecht: Springer Science+Business Media B.V., 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

GOVERNMENT, US. An Act to Amend the Public Health Service Act to Provide for Research, Information, and Education with Respect to Blood Cancer. [Washington, D.C: U.S. G.P.O., 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Gearin-Tosh, Michael. Living proof: A medical mutiny. New York: Scribner, 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Gearin-Tosh, Michael. Living proof: A medical mutiny. New York: Scribner, 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Foote, MaryAnn, G. Molineux, and Tara Arvedson. Twenty years of G-CSF: Clinical and nonclinical discoveries. Basel: Springer, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Peter, Gale Robert, Juttner Christopher, and Henon P. R, eds. Blood stem cell transplants. Cambridge, [U.K.]: Cambridge University Press, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Gasparetto, Christina, and Dharshan Sivaraj. Understanding Multiple Myeloma. Jones & Bartlett Learning, LLC, 2017.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Jerome E., Ph.d. Tanner. Myeloma (The Biology of Cancer). Chelsea House Publications, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Multiple myeloma; Breast cancer"

1

Workman, Paul. "Reflections and Outlook on Targeting HSP90, HSP70 and HSF1 in Cancer: A Personal Perspective." In Advances in Experimental Medicine and Biology, 163–79. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-40204-4_11.

Full text
Abstract:
Abstract This personal perspective focuses on small-molecule inhibitors of proteostasis networks in cancer—specifically the discovery and development of chemical probes and drugs acting on the molecular chaperones HSP90 and HSP70, and on the HSF1 stress pathway. Emphasis is on progress made and lessons learned and a future outlook is provided. Highly potent, selective HSP90 inhibitors have proved invaluable in exploring the role of this molecular chaperone family in biology and disease pathology. Clinical activity was observed, especially in non small cell lung cancer and HER2 positive breast cancer. Optimal use of HSP90 inhibitors in oncology will likely require development of creative combination strategies. HSP70 family members have proved technically harder to drug. However, recent progress has been made towards useful chemical tool compounds and these may signpost future clinical drug candidates. The HSF1 stress pathway is strongly validated as a target for cancer therapy. HSF1 itself is a ligandless transcription factor that is extremely challenging to drug directly. HSF1 pathway inhibitors have been identified mostly by phenotypic screening, including a series of bisamides from which a clinical candidate has been identified for treatment of ovarian cancer, multiple myeloma and potentially other cancers.
APA, Harvard, Vancouver, ISO, and other styles
2

Gullo, Charles A. "Multiple Myeloma." In Encyclopedia of Cancer, 2401–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3898.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Gullo, Charles A. "Multiple Myeloma." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_3898-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Gullo, Charles A. "Multiple Myeloma." In Encyclopedia of Cancer, 2948–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_3898.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wadhwa, Shilpi, David Y. Johnson, and Frank E. Johnson. "Multiple Myeloma." In Patient Surveillance After Cancer Treatment, 487–88. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60327-969-7_98.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Dicato, Mario A. "Multiple Myeloma." In Side Effects of Medical Cancer Therapy, 277–84. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70253-7_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Bianchi, Giada, and Kenneth C. Anderson. "Multiple Myeloma." In Targeted Therapy in Translational Cancer Research, 145–56. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118468678.ch14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Dicato, Mario A. "Multiple Myeloma." In Side Effects of Medical Cancer Therapy, 459–64. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-787-7_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Bianchi, Giada, and Kenneth C. Anderson. "Multiple Myeloma." In The American Cancer Society's Oncology in Practice, 463–83. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781118592168.ch33.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Mina, Roberto, and Antonio Palumbo. "Multiple Myeloma." In Management of Hematological Cancer in Older People, 203–18. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2837-3_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Multiple myeloma; Breast cancer"

1

Mishima, Yuji, Yasuhito Terui, and Kiyohiko Hatake. "Abstract A015: Intrapatient heterogeneity of multiple myeloma is evenly distributed in multiple myeloma lesions." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a015.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Thibaud, Santiago, Aaron Etra, Ryan Subaran, Zachry Soens, Scott Newman, Rong Chen, Ajai Chari, et al. "Abstract 868: Heritable cancer mutations in multiple myeloma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-868.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Corradini, Andrea, Martin Hansen, and Toma Savic. "Measuring the Frailty Index of Multiple Myeloma Cancer Patients." In 10th EAI International Conference on Pervasive Computing Technologies for Healthcare. ACM, 2016. http://dx.doi.org/10.4108/eai.16-5-2016.2263785.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Tompkins, Van S., Zhimin Gu, Hongwei Xu, Guido Tricot, Fenghuang Zhan, and Siegfried Janz. "Abstract B38: Targeting FOXM1 in multiple myeloma." In Abstracts: AACR Precision Medicine Series: Synthetic Lethal Approaches to Cancer Vulnerabilities - May 17-20, 2013; Bellevue, WA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.pms-b38.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Matsui, William. "Abstract PL3-2: Translating multiple myeloma stem cells." In Abstracts: AACR International Conference on Translational Cancer Medicine--; Mar 21–24, 2010; Amsterdam, The Netherlands. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcme10-pl3-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Andreotti, Gabriella, Veronique Benhaim-Luzon, Paul Brennan, Silvia de Sanjose, Laura Costas Caudet, Adele Seniori Costantini, Perluigi Cocco, et al. "Abstract B115: A pooled analysis of smoking and alcohol drinking and risk of multiple myeloma in the International Multiple Myeloma Consortium." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-b115.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Duma, Narjust, Miguel Gonzalez Velez, Jesus Vera-Aguilera, Richardo Parrondo, Veronica Mariotti, Jonas Paludo, Yucai Wang, Ronald Go, and Alex Adjei. "Abstract A27: Diversity in multiple myeloma clinical trials." In Abstracts: Tenth AACR Conference on The Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; September 25-28, 2017; Atlanta, GA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7755.disp17-a27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Anderson, Kenneth. "Abstract IA13: Novel therapeutic targets in multiple myeloma." In Abstracts: AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.tcm17-ia13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Kumar, Shaji. "Abstract CN03-03: Therapeutic interventions to prevent progression of MGUS to multiple myeloma." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-cn03-03.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Guillerey, Camille, Lucas Ferrari de Andrade, Slavica Vuckovic, David Ritchie, Marta Chesi, Leif Bergsagel, Geoffrey R. Hill, Ludovic Martinet, and Mark J. Smyth. "Abstract B155: Anti-CD137 mAb therapy of multiple myeloma." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b155.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Multiple myeloma; Breast cancer"

1

Li, Tianfang. Multiple Aperture Radiation Therapy (MART) to Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada456141.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Shou, Zhenyu. Multiple Aperture Radiation Therapy (MART) for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada432996.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ott, Jurg. Statistical Genetics Methods for Localizing Multiple Breast Cancer Genes. Fort Belvoir, VA: Defense Technical Information Center, September 1996. http://dx.doi.org/10.21236/ada326461.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ott, Jurg. Statistical Genetic Methods for Localizing Multiple Breast Cancer Genes. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada301699.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ott, Jurg. Statistical Genetics Methods for Localizing Multiple Breast Cancer Genes. Fort Belvoir, VA: Defense Technical Information Center, September 1997. http://dx.doi.org/10.21236/ada337861.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Lauring, Josh. Multiple Cooperating Oncogenes Drive Recurrent Breast Cancer-Associated Chromosomal Amplifications: Creation of Isogenic Human Cell Line Models. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada612716.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lauring, Josh. Multiple Cooperating Oncogenes Drive Recurrent Breast Cancer-Associated Chromosomal Amplifications: Creation of Isogenic Human Cell Line Models. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada583983.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Multiple myeloma; Breast cancer' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography