Journal articles: 'Multiple myeloma; Breast cancer'

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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.

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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.

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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Campagnaro, Erica, Melissa A. Reimers, Angel Qin, Ajjai S. Alva, Bryan J. Schneider, and Catherine H. Van Poznak. "Use of Bone-Modifying Agents in Myeloma and Bone Metastases: How Recent Dosing Interval Studies Have Affected Our Practice." Journal of Oncology Practice 14, no. 8 (August 2018): 457–64. http://dx.doi.org/10.1200/jop.18.00236.

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The management of bone lesions from advanced solid tumors and multiple myeloma typically includes use of a bone-modifying agent to reduce the risk of skeletal-related events. Recent data demonstrate that when using zoledronic acid to reduce the risk of skeletal-related events in metastatic breast cancer, metastatic prostate cancer, and multiple myeloma, the dosing interval of zoledronic acid may be extended from every 4 weeks to every 12 weeks. The ASCO guidelines on the role of bone-modifying agents in metastatic breast cancer and multiple myeloma address zoledronic acid dosing intervals. Herein, we discuss how new data on dosing of bone-modifying agents influence our clinical practice.

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Witzens-Harig, Mathias, Dirk Hose, Simone Jünger, Christina Pfirschke, Nisit Khandelwal, Anja Seckinger, Heinke Conrad, et al. "Human Multiple Myeloma and Breast Cancer Cells Evade Immune Rejection Through Expression of Carcinoembryonic Antigen-Related Cell Adhesion Molecule 6." Blood 120, no. 21 (November 16, 2012): 2942. http://dx.doi.org/10.1182/blood.v120.21.2942.2942.

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Abstract Abstract 2942 Tumor-specific cytotoxic T cells are common in tumor patients, but ineffectively react against autologous tumor cells. Here, we demonstrate in multiple myeloma and breast cancer that human tumor cells escape recognition by tumor-specific CD8+ T cells through carcinoembryonic antigen-related cell adhesion molecule-6 (CEACAM-6) expression. We demonstrate for the first time CEACAM-6 expression in primary and established myeloma and examined the effects of altered CEACAM expression on cytotoxic T cell activity and cytokine secretion against myeloma and breast cancer cells in vitro —, and in vivo, using a xenotransplant mouse model. Cytotoxic T cells from multiple myeloma patients reacted against myeloma antigens presented by dendritic cells, but not against autologous myeloma cells, which expressed CEACAM6. Gene knockdown or blocking of CEACAM6 on myeloma cells restored CD8+ T-cell reactivity against malignant plasma cells. SiRNA-mediated CEACAM6 knockdown or inhibition by specific mAbs also restored cytokine secretion, cytotoxic activity, and antigen-specific lysis of CEACAM6-positive breast cancer cells. Moreover, CEACAM-6 inhibition was a prerequisite for efficient treatment of xenotransplanted breast tumors by adoptive T cell transfer. CEACAM6 thus plays an important role in inhibiting CD8+ T-cell responses against hematological and epithelial human tumors. Therapeutic targeting of CEACAM6 may be a promising strategy for improving cancer immunotherapy. Disclosures: No relevant conflicts of interest to declare.

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&NA;. "Bisphosphonates reduce tumour-related osteolysis in breast cancer and multiple myeloma." Drugs & Therapy Perspectives 18, no. 7 (July 2002): 17–21. http://dx.doi.org/10.2165/00042310-200218070-00006.

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Talamo, Giampaolo, W. Christopher Ehmann, Nathan G. Dolloff, Jozef Malysz, Joseph J. Drabick, and Witold B. Rybka. "Retrospective analysis of second malignancies in patients with multiple myeloma." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 8090. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.8090.

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8090 Background: Recent data from patients with multiple myeloma (MM) enrolled in randomized clinical trials have shown an increased incidence of second malignancies after treatment with lenalidomide, but the prevalence of second malignancies in the overall MM population is uncertain. Methods: We retrospectively analyzed the medical records of 320 consecutive MM patients followed at the Penn State Hershey Cancer Institute between 2006 and 2010. We excluded from the analysis basocellular and squamocellular carcinomas of the skin. Results: Forty-three patients (13%) were found to have second malignancies, and 5 of them had a third cancer. One pt had 4 cancers. They included cancers of the prostate (8 pts), breast (8), MDS/leukemia (6), colon/rectum (5), melanoma (5), lung (4), uterus (4), bladder (3), kidneys (2), pancreas (2), testicle (1), myeloproliferative disorders (1), and sarcoma (1). Of 50 cancers, 36 (72%) developed before the diagnosis of MM, at a median of 65 months (range, 1-372), and 14 after that, at a median of 37 months (range, 3-104). Lenalidomide was used in 239 (75%) patients, and in 9 of 14 cases of post-MM second malignancies. Conclusions: Second malignancies usually develop before the diagnosis of MM, i.e., MM is the second malignancy for the majority of patients. The use of lenalidomide could not be indicated as a possible carcinogenic factor for the majority of MM patients with second malignancies.

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Coleman, E. A., H. Lynch, C. Enderlin, C. B. Stewart, R. Kennedy, and B. Barlogie. "Determining familial risk of multiple myeloma." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 8111. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.8111.

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8111 Background: The etiology of multiple myeloma (MM) remains unknown although genetic and environmental factors have been implicated. Familial MM has been reported; however, whether this familial tendency is due to genetic factors or environmental exposures or both is not known. Analysis of SEER data showed that Iowa, an agricultural state, had the highest incidence of MM; however, once we adjusted for race, sex, age, and year of diagnosis, the effect of geographic area was small and the main effect was race. This project aims to build a Familial MM Registry of families and investigate the families’ pedigrees and environmental factors to determine the familial risk of MM. The long term goal is to identify myeloma susceptibility loci which ultimately could lead to finding myeloma prone germline mutations. Methods: Patients (n = 67) from the Myeloma Institute for Research and Therapy at the University of Arkansas for Medical Sciences and their family members with MM or a related malignancy (amyloidoses, lymphoma, chronic lymphocytic leukemia, chronic myelogenous leukemia, Waldenstrom's macroglobulinemia, Hairy cell leukemia, acute myelogenous leukemia, acute lymphocytic leukemia, Hodgkin's disease) were interviewed for environmental factors associated with MM and for family history data to complete pedigrees. Pedigrees were analyzed to determine the patterns of inheritance. Results: Data show that 26 patients (39%) have family members with MM (one having five family members with MM) and 34 patients (51%) have family members with related malignancies. Eighteen families (27%) have a putative autosomal dominant mode of genetic transmission of MM. Pancreatic cancer, malignant melanoma, breast cancer and lymphoma may be part of a myeloma syndrome. Pesticide/insecticide exposure, raising cattle or growing cotton were the most prevalent environmental risk factors. Conclusions: The pedigrees suggest the existence of genetic traits affecting MM susceptibility. This work will be part of the efforts to create an international consortium to study familial MM. Research in the area of molecular epidemiology is needed to discover the genetic and environmental determinants of this disease and the reasons for the racial and gender differences. No significant financial relationships to disclose.

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Eden, Joleen Kirsty, Rita Borgen, Rabea Haq, and Richard Dobrashian. "A rare imaging case of bilateral plasmacytoma of the breast." BJR|case reports 6, no. 2 (June 2020): 20190131. http://dx.doi.org/10.1259/bjrcr.20190131.

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This case reports on secondary extramedullary multiple myeloma within both breasts in the absence of axillary nodal involvement and discusses the difficulty in interpretation with clinical recommendations and learning outcomes. Differentiating plasmacytic lesions in the breast is often difficult as clinical and radiological appearances are known to mimic benignity and high-grade primary breast cancer. Extramedullary presentation can determine progression of the disease and can necessitate cross-sectional imaging. Therefore definitive diagnosis is essential as the clinical management of the patient may be altered.

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Kang, Young Mo, Hong Joo Lee, and Su-Jung Kim. "Metastatic breast cancer with osteolytic skull lesions suspected to be multiple myeloma." Korean Journal of Clinical Oncology 13, no. 2 (December 31, 2017): 152–55. http://dx.doi.org/10.14216/kjco.17024.

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Tomono, Hitoshi, Susumu Fujioka, Kenji Kato, Katue Yoshida, and Yuji Nimura. "Multiple Myeloma Mimicking Bone Metastasis from Breast Cancer: Report of a Case." Surgery Today 28, no. 12 (December 20, 1998): 1304–6. http://dx.doi.org/10.1007/s005950050339.

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Tomono, Hitoshi, Susumu Fujioka, Kenji Kato, Katue Yoshida, and Yuji Nimura. "Multiple myeloma mimicking bone metastasis from breast cancer: Report of a case." Surgery Today 28, no. 12 (December 1998): 1304–6. http://dx.doi.org/10.1007/bf02482821.

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Holecki, Michał, Anna Skorupa, Jan Duława, and Jerzy Chudek. "Hypercalcemia in Patients Treated with Oral Bisphosphonates for Tumor-Induced Osteolysis." Open Access Macedonian Journal of Medical Sciences 1, no. 1 (December 15, 2013): 54–58. http://dx.doi.org/10.3889/oamjms.2013.011.

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Objective: Hypercalcemia as the consequence of an excessive bone resorption is a common complication in patients with cancer. The aim of the study was to analyze the prevalence of hypercalcemia in patients with tumor-induced osteolysis starting therapy with bisphosphonates.Methods: The questionnaire-based survey (data collected during three consecutive examinations within a 3-month period) was conducted among 1,450 patients treated with bisphosphonates for tumor-induced osteolysis.Results: Hypercalcemia was found in 8.7% respondents starting the treatment with bisphosphonates. The most common cause of malignancy-associated hypercalcemia was prostate cancer, multiple myeloma and breast cancer. On the other hand, hypercalcemia was the most prevalent among patients with multiple myeloma, metastatic cancer of an unknown primary origin and bladder cancer. Metastases were reported in 342 patients, while pathological fractures in 37. The normalization of calcium level was obtained in 91.4% of the patients treated with bisphosphonates, mostly clodronate. During the bisphosphonate therapy, pathological fractures occurred in 4.6% of patients and the percentage of the patients reporting bone pain decreased from 79.9% to 30.9%.Conclusion: Multiple myeloma, prostate and breast cancer are the most common causes of hypercalcemia of malignancy in patients with tumor-induced osteolysis starting therapy with bisphosphonates.

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Lontos, Konstantinos, Juraj Adamik, Peng Zhang, Quanhong Sun, David Roodman, Attaya Suvannasankha, and Deborah Lynn Galson. "Semaphorin 4D to suppress bone formation in multiple myeloma." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): 8039. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.8039.

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8039 Background: Myeloma bone disease is characterized by osteoclast activation and long-term osteoblast suppression. We investigated if Semaphorin 4D (Sema4D; CD100) plays a role in these processes. Sema4D has been shown to be a potent osteoblast inhibitor (Negishi-Koga T et al, Nat Med. 2011). A study recently identified that the breast cancer cell line MDA-MB-231 utilizes Sema4D to create osteolysis (Yang Y et al, PLOS One 2016). There have been previous data that Sema4D is increased in the serum of myeloma patients (Terpos et al, Blood 2012) and that co-culturing myeloma cell lines with osteocytes increases the expression of Sema4D mRNA in both (Suvannasankha et al, Blood 2016). We sought to investigate if myeloma cells are using Sema4D to suppress bone formation and if they affect the levels of Sema4D produced by osteoclasts. Methods: We used lentivirus carrying shRNA for Sema4D or control (Scr) to knock down the level of the protein in the 5TGM1 murine myeloma cell line. Knockdown was verified by qPCR and Western Blot. We subsequently co-cultured the 5TGM1 cells with the MC3T3-subclone M4 (MC4) murine stromal cell line for 2 days, removed the myeloma cells and then differentiated the MC4 cells using ascorbic acid and β-glycerolphosphate. At day 5, we analyzed the cells for Runx2 (a critical gene for the differentiation of stromal cells into osteoblasts) expression utilizing qPCR. Also, we performed qPCR in primary osteoclast (OCL) mouse cells differentiating into OCL with RANKL with or without pre-treatment with myeloma-conditioned media for 3 days before the addition of RANKL. Results: When 5TGM1-Scr were co-cultured with MC4 cells the expression of Runx2 on day 5 was decreased (p=0.02). Strikingly, the 5TGM1-shSema4D cells when co-cultured with MC4s did not have the same effect and allowed the upregulation of Runx2 expression on day 5 (p=0.01). Myeloma-conditioned media increased Sema4D expression by OCL throughout the 5 days of differentiation 2 to 3-fold (p=0.01 for day 5). Conclusions: The myeloma cells seem to be utilizing Sema4D both directly and indirectly to inhibit bone formation. Targeted therapy against Sema4D may improve outcomes and fracture-free survival for multiple myeloma patients.

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Key, Timothy J., Elizabeth A. Spencer, and Gillian K. Reeves. "Symposium 1: Overnutrition: consequences and solutions Obesity and cancer risk." Proceedings of the Nutrition Society 69, no. 1 (December 3, 2009): 86–90. http://dx.doi.org/10.1017/s0029665109991698.

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Epidemiological studies have provided convincing evidence that obesity increases the risk for cancers of the oesophagus (adenocarcinoma), colon, pancreas, breast (post-menopausal), endometrium and kidney. The magnitude of the increase in risk varies between cancer sites. For an increase in BMI of 10 kg/m2 relative risks are approximately 2·3 for adenocarcinoma of the oesophagus, 1·5 for colon cancer in men, 1·2 for colon cancer in women, 1·4 for post-menopausal breast cancer, 2·9 for endometrial cancer and >1·5 for kidney cancer, while the size of the effect on cancer of the pancreas is uncertain. There is also evidence that obesity increases the risks for cancers of the gallbladder, malignant melanoma, ovary, thyroid, non-Hodgkin lymphoma, multiple myeloma and leukaemia. Estimates of the percentage of cancers that can be attributed to excess body weight suggest that in the UK and similar countries approximately 5% of all cancers are attributable to overweight and obesity.

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Lipton, A., J. Berenson, R. Knight, Grace Hu, and E. Levy. "Phase 2 trial of Zoledronate vs Pamidronate in multiple myeloma and breast cancer." European Journal of Cancer 35 (September 1999): S360. http://dx.doi.org/10.1016/s0959-8049(99)81875-9.

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Bloomfield, D. J. "Should bisphosphonates be part of the standard therapy of patients with multiple myeloma or bone metastases from other cancers? An evidence-based review." Journal of Clinical Oncology 16, no. 3 (March 1998): 1218–25. http://dx.doi.org/10.1200/jco.1998.16.3.1218.

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PURPOSE To review objectively the evidence for the use of bisphosphonates for the reduction of skeletal events or the management of pain due to multiple myeloma or bone metastases from other types of cancer. METHODS MEDLINE was searched from 1976 onwards using the MeSH terms "exp diphosphonates/," "exp bone neoplasms/," "exp multiple myeloma/," and "bone metastases" as text words. Bibliographies of reports on these topics and major medical and scientific journals were searched. Experts in the field were approached. The question was defined and the evidence stratified in a hierarchical manner according to classification of study design. There were sufficient studies to enable the use of randomized trials only to address the questions. Effectiveness was defined and the evidence reviewed in a systematic manner. RESULTS AND CONCLUSION Eighteen randomized trials were identified. No meta-analyses are available. There is level I evidence (defined as an appropriately conducted randomized clinical trial with a statistically significant result) for the use of bisphosphonates to reduce both skeletal events and pain in multiple myeloma and in breast cancer patients with metastatic bone disease. There is also level I evidence for their use as part of a pain management program for bone metastases from carcinoma of the breast, lung, and prostate, and for symptomatic myeloma. The bisphosphonates appear to be well tolerated.

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Hu, Mimi I., Ana O. Hoff, Bela Toth, K. Altundag, Marcella Johnson, Carla Warneke, Ajay Nooka, et al. "Osteonecrosis of the Jaw or Maxilla after Intravenous Bisphosphonates for Multiple Myeloma and Breast Cancer: Long-Term Follow-Up Shows a Slow Rate of Healing." Blood 108, no. 11 (November 16, 2006): 5121. http://dx.doi.org/10.1182/blood.v108.11.5121.5121.

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Abstract Osteonecrosis of the jaw or maxilla (ONJM) is a rare but clinically significant disorder recently reviewed in a large retrospective study by our group (Hoff et al, 27th ASBMR Meeting 2005, Presentation #1218). A subset of the ONJM patients with breast cancer or myeloma was followed at the University of Texas M.D. Anderson Cancer Center (UTMDACC) dental clinic. This analysis describes the natural history of ONJM in this subset. Thirteen of 29 ONJM patients treated with intravenous bisphosphonates (IVBP) at UTMDACC and 1 ONJM patient treated elsewhere were evaluated in the dental clinic for more than 6 months (myeloma, n=7; breast cancer, n=7). Measurement of the maximum length of exposed bone was documented at each visit. Each patient received a standard regimen of conservative dental care with debridement only when indicated. All patients received zoledronic acid (mean cumulative dose 80mg; range 24–152mg) and 10 patients also received pamidronate (mean cumulative dose 1665mg; range 90–2700mg). This subset was followed for a median duration of 18.2 months (range: 7.1–67.3 months). The mean length of exposed bone at initial evaluation was 11 mm (range: 2–29 mm). The lesion from baseline to the most recent clinic visit progressed in 7 patients (50%), remained stable in 2 (14%), regressed in 2 (14%), and resolved in 3 (21%). Persistent ONJ was seen if IVBP was stopped (n=8), decreased in frequency (n=1), or continued at the same dose/frequency (n=2) (Graphs 1, 2). Complete resolution occurred in 3 multiple myeloma patients; IVBP was decreased in one and discontinued in 2 of the resolved cases (heavy lines on Graph 1). Our experience shows that ONJM is a disorder with slow resolution in most patients, lasting as long as 5 years. In the oncologic setting where there is clear benefit of bisphosphonate therapy, studies to optimize the dosing regimen may be needed. Graph 1. Myeloma (n=7) Graph 1. Myeloma (n=7) Graph 2. Breast Cancer (n=7) Graph 2. Breast Cancer (n=7)

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Snegovoy, A. V., V. B. Larionova, and I. B. Kononenko. "Differences in interactions with the bone microenvironment between solid tumors and multiple myeloma: pathogenetic aspects. Possibilities and effectiveness of osteomodifying agents in multiple myeloma." Oncohematology 16, no. 1 (April 14, 2021): 64–72. http://dx.doi.org/10.17650/1818-8346-2021-16-1-64-72.

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Bone metastasis is one of the most common manifestations of advanced malignant process. Many tumors, especially breast, prostate and lung cancer, multiple myeloma, are characterized by a high incidence of bone damage (up to 7080 %) and clinical complications. Intense pain, hypercalcemia, spinal cord compression, pathological fractures, the need for radiation and surgical treatment (combined in the name «skeletal system related events») can occur even with single metastases. In the treatment of patients with bone metastases, a multidisciplinary approach is used; however, the basis is specific antitumor therapy and osteomodifying agents. They affect bone remodeling and microenvironment.

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Beltran, Brady, Luis Riva, Daniel del Carpio, Ivan Fernandez, Luis Vera, Rocio Reategui, Fernando Hurtado de Mendoza, Jorge Castillo, and Antonio A. Carrasco-Yalan. "Osteonecrosis of the Jaw Related to Bisphosphonates Therapy in Multiple Myeloma and Metastatic Prostate Cancer Patients. A Latin American Report: An Adverse Event To Look For!!." Blood 110, no. 11 (November 16, 2007): 5162. http://dx.doi.org/10.1182/blood.v110.11.5162.5162.

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Abstract Background: Association between osteonecrosis of the jaw (ONJ) and aminobisphosphonate treatment in patients (pts.) with multiple myeloma, breast cancer and prostate cancer has been increasingly reported in the literature. Risk factors for this complication include presence of infection, recent dental extraction and any oral surgical procedure with bone exposure. Patients and Methods: All patients with myeloma multiple or prostate cancer diagnosis treated at two institutions from Lima with either IV zoledronic acid or pamidronate from 2005–2007 were evaluated using outpatient records. Patients with ONJ were identified and their characteristics were compared to all patients receiving bisphosphonate therapy. Results: One hundred eighty three patients were evaluated. One hundred three had metastatic prostate cancer, and eighty myeloma multiple. All patients with myeloma multiple received pamidronate and all patients with prostate cancer received zoledronic acid. Six patients developed ONJ (3.2%). Five pts. were male and one female; a median age of 62 (range 50–74) and 5 had metastatic prostate cancer and 1 myeloma multiple. Zoledronic acid and pamidronate were involved in 5 and 1 cases respectively. The median number of bisphosphonate infusions prior to the development of ONJ was 16 (range 12–20). No patient had dental extraction or oral surgical procedure before ONJ. Bone exposition occurred in four cases. Treatment was antibiotics in all cases and surgery in two. Conclusions: ONJ is a serious complication of bisphosphonate therapy and it affected a significant proportion of our Latino american patients.

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Suvannasankha, Attaya, Colin Crean, Isaac Carrera Ochoa, G. David Roodman, and John Chirgwin. "PTHrP May Contribute to Cachexia Accompanying Multiple Myeloma Bone Disease." Blood 132, Supplement 1 (November 29, 2018): 4450. http://dx.doi.org/10.1182/blood-2018-99-115680.

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Abstract Background: Cachexia, an energy-wasting disorder of adipose and skeletal muscles, occurs commonly in advanced cancers and is a serious problem that interferes with response to treatment and affects quality of life. Treatment or cachexia is yet available. Chemotherapy and radiation may further worsen cachexia. Cachexia in cancer bone metastasis was described in breast and prostate cancers where cancer cells induce osteolysis and systemic muscle wasting, with PTHrP secreted by tumor cells as a driver of the process. PTHrP increases RANKL-induced osteolysis and stimulates browning of white fat, which in turn, induces skeletal muscle wasting via unknown secreted factor(s). Since MM cells express PTHrP, we asked whether PTHrP drives white to brown fat conversion in MM. Methods: First, we established an ex vivo organ co-culture assay (EVOCA) of neonatal mouse bone and cancer cells to study this conversion, using solid tumor osteolytic cell lines; PC3 prostate cancer cells and MDA231 breast cancer cells. GFP-expressing tumor cells engrafted onto the mouse calvariae causing lytic lesions within 7-14 days of culture. Bone (mouse) and tumor (human) gene expression was analyzed by RT-PCR using species-specific PCR primers, compared to RPL32 loading control. Tumor burden was measured by human RPL32. Mean gene changes between conditions were compared using paired t-tests. Tumor PTHrP and bone TRAP levels increased in tumor/bone co-culture compared to tumor alone and bone alone. Bone thermogenic genes UCP1 and DiO2 were increased in PC3 and MDA231 co-culture compared to bone alone (5.3 and 4.1 folds), respectively (p=0.05, and 0.04), supporting white to brown fat conversion. We then applied the EVOCA for MM studies. Results: EVOCA of MM cell lines 8226 and JJN3 caused similar histologic lytic lesions and TRAP induction of bones, similar to the PC3 and MDA231 findings. Both cell lines significantly induced bone UCP1 and DiO2, compared to bone alone. UCP1 and DiO2 induction by 8226 was 5.4 and 3.2 folds, respectively (p=0.02, and 0.04), while induction of bone UCP1 and DiO2 by JJN3 was 3.8 and 2.8 folds, respectively (p=0.05, and 0.03). Bone treated with recombinant PTHrP (positive control) strongly induced UCP1 and DiO2 (7.2 and 4.6 folds). EVOCA of MM cell lines were treated with available anti-myeloma agents and bisphosphonate. Bortezomib and lenalidomide dramatically decreased tumor growth and TRAP induction. Zoledronic strongly inhibited TRAP induction and marginally inhibited tumor growth. However, these agents had marginal effects on tumor-induced UCP1 and DiO2 upregulation. PTHrP neutralizing antibody partially blocked UCP1 and DiO2 induction by MM cells and had no effects on MM cell growth. To further evaluate for a direct contribution of PTHrP on fat browning, preadipocyte cell lines 3T3-L1 were differentiated into fat-laden adipocytes and treated with recombinant PTHrP, conditioned media (CM) from 8226 culture, CM from EVOCA of bone alone and CM from bone+8226 cells for 24 hours. UCP1 and DiO2 were upregulated by both PTHrP and CM of bone+8226 cells, compared to untreated 3T3-L1 cells, and 3T3-L1 treated with CM from bone alone. The UCP1 and DiO2 upregulation by CM of bone+8226 cells was modestly blocked by PTHrP neutralizing antibody. Conclusion: MM cells colonized to bones activate osteolysis, changes of fat genes compatible with fat browning; characterics of cachexia. Cachexia in MM may be attributed to other factors in addition to PTHrP. The backbone anti-myeloma drugs, Lenalidomide and Bortezomib, and the antiresorptive Zoledronic acid have limited effect on tumor-induced fat browning. Bone+MM coculture allows concurrent assessment of tumor, bone and fat changes, and can be applied to studies of novel agents to combat cachexia in myeloma. Disclosures Suvannasankha: Glaxo Smith Klein: Research Funding; Janssen: Research Funding; Celgene: Honoraria; Amgen: Research Funding.

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Huang, Xiangao, Maurizio Di Liberto, David Chiron, Ruben Niesvizky, Anna C. Schinzel, William C. Hahn, and Selina Chen-Kiang. "Sensitizing shRNA Screen for Molecular Targets in CDK4/CDK6-Based Combination Therapy in Multiple Myeloma." Blood 124, no. 21 (December 6, 2014): 3440. http://dx.doi.org/10.1182/blood.v124.21.3440.3440.

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Abstract CDK4 and CDK6 are rarely mutated but are overexpressed or hyperactivated at a very high frequency in human cancers. By inhibiting CDK4/CDK6 with an exceptionally selective and reversible inhibitor, palbociclib (PD 0332991), we have developed a novel strategy to reprogram cancer cells for cytotoxic killing through induction of prolonged early G1 arrest (pG1). We have demonstrated that pG1 sensitizes cancer cells expressing Rb, the substrate of CDK4 and CDK6, to cytotoxic killing by forcing an imbalance in gene expression because only genes scheduled for early G1 are expressed. This sensitization is exacerbated after palbociclib withdrawal due to incomplete restoration of gene expression despite S phase synchronization (pG1-S). This study aims to identify genes that mediate pG1-S sensitization to two clinically-relevant agents for myeloma, the proteasome inhibitors carfilzomib and bortezomib, in model cell lines by a sensitizing pool genome-wide shRNA screen, and by validating the hits in a clinical trial of palbociclib in combination with bortezomib and dexamethasone. We ranked the hits based on the enrichment of target shRNAs, and representation in replica of each cell lines and among different human myeloma cell lines (HMCLs) as well as functional analyses. In myeloma cells, cell cycle control by palbociclib was intact in all hits, demonstrating that CDK4 and CDK6 are indispensable for myeloma replication. Among the top ranking 20 candidates, we found that NEDD4L was essential for proteasome inhibitor killing, FTH1 modulated the threshold of killing by diverse agents especially in pG1-S, and IL10RAappeared to be required for pG1-S sensitization to proteasome inhibitors. Moreover, RNA-sequencing analysis of primary myeloma cells from a phase II clinical trial targeting CDK4/CDK6 with palbociclib in combination with bortezomib in myeloma revealed that a higher level of FTH1 expression in myeloma cells in vivo correlated with sensitivity to this therapy, suggesting a role for FTH1 in differential sensitivity to this CDK4/CDK6-based therapy in myeloma. Selective inhibition of CDK4/CDK6 with palbociclib, or another specific inhibitor such as LY2835219 or LEE011, in combination therapy has now achieved unprecedented clinical efficacy in diverse human cancers. Most notably, palbociclib more than doubled the progression free survival of metastatic breast cancer patients when it was combined with letrozole, and has been designated a “breakthrough therapy” by the FDA for breast cancer. Our work provides the first insight into genes that mediate cell cycle sensitization to cytotoxic killing through selective CDK4/CDK6 inhibition. It provides an exciting potential for further investigation in a clinical context, such as the ongoing phase I clinical trial combining palbociclib with the immunomodulatory drug lenalidomide in patients with relapsed/refractory myeloma. Disclosures Huang: Celgene: Research Funding. Off Label Use: PD 0332991 (palbociclib) is a specific CDK4/CDK6 inhibitor used to stop the cell cycle.. Niesvizky:Onyx: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Millennium: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Celgene: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau. Chen-Kiang:Celgene: Consultancy, Research Funding.

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Rosenbloom, Barry E., Neal J. Weinreb, Ari Zimran, Katherine A. Kacena, Joel Charrow, and Elizabeth Ward. "Gaucher disease and cancer incidence: a study from the Gaucher Registry." Blood 105, no. 12 (June 15, 2005): 4569–72. http://dx.doi.org/10.1182/blood-2004-12-4672.

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Abstract Patients with Gaucher disease (GD) are alleged to be at an increased risk of malignant disorders, possibly due to potential chronic stimulation of the immune system and lymphoproliferation associated with storage of glucocerebroside in tissue macrophages. Because previous reports of increased risk of malignancy in GD may have been affected by small patient numbers and ascertainment bias, 2742 patients with GD from the International Gaucher Registry were studied. The number of cancers identified among patients in the registry was compared with that expected in the US population of similar attained age and sex. The majority of patients were young or middle-aged adults at the time of last follow-up, with only 14% older than age 60. There were 10 patients with multiple myeloma, yielding an estimated relative risk of 5.9 (95% confidence interval [95% CI]: 2.8, 10.8). The relative risk of cancer overall was 0.79 (95% CI: 0.67, 0.94), and the subgroups for cancers of the breast, prostate, colon and rectum, lung, and hematologic malignancies other than myeloma did not yield statistically significant higher risks. This study suggests that, in general, patients with Gaucher disease are not at highly increased risk of cancer, at least during early and middle age. However, there appears to be a significantly higher risk of multiple myeloma of which physicians should be aware when caring for these patients. (Blood. 2005;105:4569-4572)

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Oronza A. Botrugno, Silvia Bianchessi, Desirée Zambroni, Michela Frenquelli, Daniela Belloni, Lucia Bongiovanni, Stefania Girlanda, et al. "ATR addiction in multiple myeloma: synthetic lethal approaches exploiting established therapies." Haematologica 105, no. 10 (November 14, 2019): 2440–47. http://dx.doi.org/10.3324/haematol.2018.215210.

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Therapeutic strategies designed to tinker with cancer cell DNA damage response have led to the widespread use of PARP inhibitors for BRCA1/2-mutated cancers. In the haematological cancer multiple myeloma, we sought to identify analogous synthetic lethality mechanisms that could be leveraged upon established cancer treatments. The combination of ATR inhibition using the compound VX-970 with a drug eliciting interstrand cross-links, melphalan, was tested in in vitro, ex vivo, and most notably in vivo models. Cell proliferation, induction of apoptosis, tumor growth and animal survival were assessed. The combination of ATM inhibition with a drug triggering double strand breaks, doxorucibin, was also probed. We found that ATR inhibition is strongly synergistic with melphalan, even in resistant cells. The combination was dramatically effective in targeting myeloma primary patient cells and cell lines reducing cell proliferation and inducing apoptosis. The combination therapy significantly reduced tumor burden and prolonged survival in animal models. Conversely, ATM inhibition only marginally impacted on myeloma cell survival, even in combination with doxorucibin at high doses. These results indicate that myeloma cells extensively rely on ATR, but not on ATM, for DNA repair. Our findings posit that adding an ATR inhibitor such as VX-970 to established therapeutic regimens may provide a remarkably broad benefit to myeloma patients.

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Raaijmakers, Marc H. G. P., Elke P. L. M. de Grouw, Leonie H. H. Heuver, Bert A. van der Reijden, Joop H. Jansen, George Scheffer, Rik J. Scheper, Theo J. M. de Witte, and Reinier A. P. Raymakers. "Impaired breast cancer resistance protein mediated drug transport in plasma cells in multiple myeloma." Leukemia Research 29, no. 12 (December 2005): 1455–58. http://dx.doi.org/10.1016/j.leukres.2005.04.013.

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Nastro, E., C. Musolino, A. Allegra, G. Oteri, M. Cicciù, A. Alonci, E. Quartarone, C. Alati, and F. S. De Ponte. "Bisphosphonate-Associated Osteonecrosis of the Jaw in Patients with Multiple Myeloma and Breast Cancer." Acta Haematologica 117, no. 3 (December 12, 2006): 181–87. http://dx.doi.org/10.1159/000097876.

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Chang, Stephanie T., Adam S. Tenforde, Christopher D. Grimsrud, Felice S. O'Ryan, Joel R. Gonzalez, David M. Baer, Malini Chandra, and Joan C. Lo. "Atypical femur fractures among breast cancer and multiple myeloma patients receiving intravenous bisphosphonate therapy." Bone 51, no. 3 (September 2012): 524–27. http://dx.doi.org/10.1016/j.bone.2012.05.010.

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Vennepureddy, A., V. Motilal Nehru, Y. Liu, F. Mohammad, and J. P. Atallah. "Synchronous Diagnosis of Multiple Myeloma, Breast Cancer, and Monoclonal B-Cell Lymphocytosis on Initial Presentation." Case Reports in Oncological Medicine 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/7953745.

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The cooccurrence of more than one oncologic illness in a patient can present a diagnostic challenge. Here we report an unusual case of concomitant existence of multiple myeloma, breast cancer, and monoclonal B-cell lymphocytosis on initial presentation. The challenge was to accurately diagnose each disease and stage in order to maximize the therapeutic regimen to achieve cure/remission. Successful management of the patient and increased life expectancy can be achieved by multidisciplinary management and patient-oriented approach in multiple primary malignant synchronous tumors.

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Qaisar, Abdul Matin, Ghazanfar Ali Sirhindi, and Shamayal Mandokhel. "CANCER TYPES;." Professional Medical Journal 21, no. 01 (December 4, 2018): 116–22. http://dx.doi.org/10.29309/tpmj/2014.21.01.1901.

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Introduction: This study attempts to highlight the relation of various types ofcancers to abnormalities in liver and renal function tests. Objectives: Correlation of derangedrenal and liver function tests to different types of cancers in industrial workers who are exposed toindustrial chemicals and carcinogens. Patients and Methods: This non-interventional studyincluded 100 hundred confirmed cases of cancer were selected and studied from July 2011 toDecember 2011. The study was conducted at Fatima Memorial Hospital/College of Medicine &Dentistry, Lahore . Results: Out of these 100 patients, 21 had CA lung, 19 had lymphoma, 14 hadsarcoma, 13 had CA breast, 6 had CA prostate, 4 had CA liver, 3 had CA colon, 3 had CA ovary, 3had CA testis, 2 had leukemia, 2 had multiple myeloma, 2 had CA gall bladder, 2 had CA stomach,1 had CA esophagus, 1had CA tongue, 1had CA parotid, 1 had CA rectum, 1 had CA cervix and 1had CA larynx. Among lymphoma, non-Hodgkin lymphoma was more than Hodgkin lymphoma(out of 19 patients, 13 had non-Hodgkin and 6 had Hodgkin lymphoma). Out of 14 patients ofsarcomas, 5 had Ewing sarcoma, 4 had chondrosarcoma, 3 had fibrosarcoma and 2 hadliposarcoma. Similarly the serum bilirubin levels in liver cancer, ovarian cancer, multiplemyeloma, stomach and gall bladder cancer were 1.50±0.31, 1.17±0.10, 1.46±0.15 and1.40±0.50 mg% were 32.38±18.81, 37.73±4.35, 34.43±4.35, 45.00±46.17, 31.33±44.70,65.25±31.14, 33.67±80.90, 99.00±73.08, 50.00±98.49, 33.50±75.0, 36.50±85.0 and49.0±11.0 μ/l respectively which were statistically significantly higher (p<0.05) then controlindividuals. respectively which were significantly higher (p<0.05) than the control individualsSimilarly the ALT levels in lung cancer, lymphoma, sarcoma, breast cancer , prostate cancer, livercancer, leukemia, ovarian cancer, cancer of colon, multiple myeloma, cancer of testis andstomach. The mean serum creatinine levels in lung cancer, liver cancer and cancer of colon were0.89±0.05, 0.90±0.16 mg% respectively which were significantly higher than the controlindividuals (p<0.05). Conclusions: The renal and liver function tests should be frequentlymonitored in cancer patients from industrial back grounds.

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Rand, Kristin A., Chi Song, Amie E. Hwang, Carol A. Huff, Leon Bernal-Mizrachi, Michael H. Tomasson, Sikander Ailawadhi, et al. "Genetic Susceptibility Markers of Multiple Myeloma in African-Americans." Blood 124, no. 21 (December 6, 2014): 2030. http://dx.doi.org/10.1182/blood.v124.21.2030.2030.

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Abstract Multiple myeloma (MM) is 2-3 times more common among African-Americans compared to non-Hispanic whites. The 2-3-fold increased risk among family members of cases suggests a genetic contribution to risk. Genome-wide association studies (GWAS) in populations of European ancestry have identified seven novel risk loci at 2p23.3 (rs6746082), 3q26.2 (rs10936599), 3p22.1 (rs1052501), 6p21.32 (rs2285803), 7p15.3 (rs4487645), 17p11.2 (rs4273077) and 22q13.1 (rs877529) (Broderick, et al. Nat Genet, 2011, Chubb, et al. Nat Genet, 2013), three of which were replicated in another European series (Martino et al., Br J Haematol, 2012). Here we examined the index signals and conducted fine-mapping for each locus in a case-control study of 1,049 multiple myeloma cases and 7,084 controls of African ancestry to identify better markers of risk and novel independent loci in seven previously reported regions in this high risk population. Incident cases were recruited from 10 clinical centers and SEER cancer registries from 2011 to 2013 and genotyped using the Illumina HumanCore GWAS array. Control data were obtained from previous genome-wide studies of breast and prostate cancer, genotyped using the Illumina 1M-Duo in 4425 male controls from the African Ancestry Prostate Cancer Consortium (consisting of 14 independent studies) and 2632 female controls from a breast cancer GWAS of African-American women (consisting of 9 independent studies). Imputation to 1000 Genomes (March 2012 release) was conducted for regions around six of the previously identified single nucleotide polymorphisms [SNPs] (the HLA region harboring rs2285803 is still being imputed, results will be presented). A case-control analysis of SNPs/indels >1% frequency within 250 kb of each index variant was conducted using unconditional multivariable logistic regression adjusting for age, sex and five leading principal components. Region-specific alpha levels were determined through permutation tests. The minimum alpha level across the six regions was α=0.002. All previously reported risk variants were common in African-Americans (minor allele frequency [MAF] >0.05). For five of the six SNPs, we had ≥94% power to detect the same effect observed in non-Hispanic whites, and 64% power for the less common variant rs10936599 (MAF=0.07). We observed directionally consistent effects (odds ratio [OR]>1) for the six risk variants tested, with three replicating at p≤0.05 (7p15.3, p=1.4x10-7; 17p11.2, p=0.05; 22q13.1, p=0.02). For three of the six regions, we observed better markers of risk in African-Americans that were correlated with the index SNP in Europeans (7p15.3, rs56333627, p=1.5x10-5, r2=0.89; 17p11.2, rs34562254, p=2.9x10-3, r2=0.90; 22q13.1, rs2092410, p=1.1x10-4 r2=.71). The missense variant identified in the 17p11.2 region (rs34562254, Pro251Leu) is located in TNFRSF13B, which encodes the protein TACI, a B cell surface receptor which plays a role in B cell maturation, apoptosis and antibody production by inducing activation of transcription factors including NFAT and NFκβ. In addition, there is evidence suggesting that TACI is involved in MM pathogenesis. Our results demonstrate that many of the risk loci for MM found in European ancestry populations are also risk loci in men and women of African ancestry and that by fine-mapping, we are able to identify variants that better capture risk in populations of African ancestry. Disclosures Terebelo: Celgene Corp: Membership on an entity's Board of Directors or advisory committees. Lonial:Millennium: The Takeda Oncology Company: Consultancy, Research Funding; Celgene: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; Bristol-Myers Squibb: Consultancy, Research Funding; Onyx Pharmaceuticals: Consultancy, Research Funding.

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Dreyfus, Brian, Joshua Mitchell, Daniel Lenihan, and Melissa Laurie. "CARDIOVASCULAR EVENTS ARE VERY FREQUENT IN LUNG CANCER AND MULTIPLE MYELOMA WHEN COMPARED TO BREAST CANCER SURVIVORS." Journal of the American College of Cardiology 75, no. 11 (March 2020): 10. http://dx.doi.org/10.1016/s0735-1097(20)30637-9.

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Echart, C., M. Distaso, I. Vlodavsky, C. Mitsiades, K. C. Anderson, P. G. Richardson, and M. Iacobelli. "Effects of defibrotide on tumour adhesion and invasion in multiple myeloma, breast cancer and renal cell cancer." Journal of Clinical Oncology 26, no. 15_suppl (May 20, 2008): 8600. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.8600.

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Body, J. J., R. Bartl, P. Burckhardt, P. D. Delmas, I. J. Diel, H. Fleisch, J. A. Kanis, et al. "Current use of bisphosphonates in oncology. International Bone and Cancer Study Group." Journal of Clinical Oncology 16, no. 12 (December 1998): 3890–99. http://dx.doi.org/10.1200/jco.1998.16.12.3890.

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PURPOSE The purpose of this article is to review the recent data on bisphosphonate use in oncology and to provide some guidelines on the indications for their use in cancer patients. DESIGN The group consensus reached by experts on the rationale for the use of bisphosphonates in cancer patients and their current indications for the treatment of tumor-induced hypercalcemia and metastatic bone pain in advanced disease and for the prevention of the complications of multiple myeloma and of metastatic bone disease are reviewed. RESULTS Bisphosphonates are potent inhibitors of tumor-induced osteoclast-mediated bone resorption. They now constitute the standard treatment for cancer hypercalcemia, for which we recommend a dose of 1,500 mg of clodronate or 90 mg of pamidronate; the latter compound is more potent and has a longer lasting effect. Intravenous bisphosphonates exert clinically relevant analgesic effects in patients with metastatic bone pain. Regular pamidronate infusions can also achieve a partial objective response by conventional International Union Against Cancer criteria and enhance the objective response rate to chemotherapy. In breast cancer, the prolonged administration of oral clodronate 1,600 mg daily reduces the frequency of morbid skeletal events by more than one fourth, whereas monthly pamidronate infusions of 90 mg for only 1 year in addition to chemotherapy reduce by more than one third the frequency of all skeletal-related events. The use of bisphosphonates to prevent bone metastases remains experimental. Last, bisphosphonates in addition to chemotherapy are superior to chemotherapy alone in patients with stages II and III multiple myeloma and can reduce the skeletal morbidity rate by approximately one half. CONCLUSION Bisphosphonate use is a major therapeutic advance in the management of the skeletal morbidity caused by metastatic breast cancer or multiple myeloma, although many questions remain unanswered, notably regarding the optimal selection of patients and the duration of treatment.

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Mastroianni, Antonio, Rossella Panella, and Daniele Morelli. "Differential diagnosis between bone relapse of breast cancer and lambda light chain multiple myeloma: role of the clinical biochemist." Tumori Journal 105, no. 6 (February 24, 2019): NP17—NP19. http://dx.doi.org/10.1177/0300891619832521.

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Purpose: The integration of expertise between oncologist and clinical biochemist for the monitoring and diagnosis of plasma cell dyscrasia is crucial. In some cases, medical laboratory scientists can provide an original contribution using the appropriate techniques to arrive at a diagnosis. Methods: We report a case of 67-year-old woman who was admitted to our hospital for bone pain. Imaging studies showed multiple diffuse bone lytic lesions, and a laboratory screen revealed anemia and altered creatinemia; serum capillary zone electrophoresis confirmed a monoclonal peak in the γ-zone that had been known since 2011, typed as immunoglobulin G kappa by immunosubtraction electrophoresis. The patient had undergone surgery for breast cancer in 2013, and based on her clinical history, the oncologist suspected the presence of bone metastases from the breast cancer and opted for relative therapy. Immunosubtraction, however, showed a very small reduction in lambda free light chains in the beta zone, but it was difficult to establish if was a monoclonal component, and consequently additional tests were performed. Discussion: A monoclonal component composed of only lambda free light chains was evidenced. This result in association with multiple diffuse bone lytic lesions observed led us to suspect multiple myeloma and not bone metastases from the breast cancer. Based on these observations, we encouraged the oncologist to conduct an osteomedullary biopsy, allowing us to make a diagnosis of low-grade stage II lambda light chain multiple myeloma. Conclusion: In this report, we show how the expertise of the clinical biochemist was instrumental in solving this case.

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Renoir, Jack-Michel, Céline Bouclier, Amélie Seguin, Véronique Marsaud, and Brigitte Sola. "Antioestrogen-mediated cell cycle arrest and apoptosis induction in breast cancer and multiple myeloma cells." Journal of Molecular Endocrinology 40, no. 3 (January 14, 2008): 101–12. http://dx.doi.org/10.1677/jme-07-0143.

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Antioestrogens (AEs) are synthetic molecules that block proliferation and induce apoptosis in breast cancer (BC) cells, principally by competing with oestradiol for binding to oestrogen receptors. Their antiproliferative activity and their pro-apoptotic capacity are well documented and a small number of molecules of this class are currently used clinically for the treatment of BC. AEs also inhibit cell cycle progression and/or induce apoptosis in multiple myeloma (MM) cells. Encouraging preliminary results have been obtained with patients and on xenografts with MM, providing a rational basis for the clinical use of AEs. This review focuses on antioestrogen-mediated signalling for blocking targets involved in the cell cycle, survival and apoptosis in both BC and MM cells. Improvement in our understanding of the mechanisms underlying the relationships between these compounds and their targets should lead to more beneficial therapeutic strategies.

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Lei, Meng, Huayun Feng, Enhe Bai, Hui Zhou, Jia Wang, Yanru Qin, Haoyang Zhang, et al. "Discovery of a novel dipeptidyl boronic acid proteasome inhibitor for the treatment of multiple myeloma and triple-negative breast cancer." Organic & Biomolecular Chemistry 17, no. 3 (2019): 683–91. http://dx.doi.org/10.1039/c8ob02668h.

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Yu, Hui-I., Hui-Ching Shen, Shu-Hsin Chen, Yun-Ping Lim, Hsiang-Hsun Chuang, Tsai-Sung Tai, Fang-Ping Kung, Chieh-Hsiang Lu, Chia-Yi Hou, and Ying-Ray Lee. "Autophagy Modulation in Human Thyroid Cancer Cells following Aloperine Treatment." International Journal of Molecular Sciences 20, no. 21 (October 25, 2019): 5315. http://dx.doi.org/10.3390/ijms20215315.

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Aloperine, an alkaloid isolated from Sophora alopecuroides, exhibits multiple pharmacological activities including anti-inflammatory, antioxidant, antiallergic, antinociceptive, antipathogenic, and antitumor effects. Furthermore, it exerts protective effects against renal and neuronal injuries. Several studies have reported antitumor effects of aloperine against various human cancers, including multiple myeloma; colon, breast, and prostate cancers; and osteosarcoma. Cell cycle arrest, apoptosis induction, and tumorigenesis suppression have been demonstrated following aloperine treatment. In a previous study, we demonstrated antitumor effects of aloperine on human thyroid cancer cells through anti-tumorigenesis and caspase-dependent apoptosis induction via the Akt signaling pathway. In the present study, we demonstrated the modulation of the autophagy mechanism following the incubation of multidrug-resistant papillary and anaplastic human thyroid cancer cells with aloperine; we also illustrate the underlying mechanisms, including AMPK, Erk, JNK, p38, and Akt signaling pathways. Further investigation revealed the involvement of the Akt signaling pathway in aloperine-modulated autophagy in human thyroid cancer cells. These results indicate a previously unappreciated function of aloperine in autophagy modulation in human thyroid cancer cells.

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Turner, Joel G., Jana L. Gump, Chunchun Zhang, James M. Cook, Douglas Marchion, Lori Hazlehurst, Pamela Munster, Michael J. Schell, William S. Dalton, and Daniel M. Sullivan. "ABCG2 expression, function, and promoter methylation in human multiple myeloma." Blood 108, no. 12 (December 1, 2006): 3881–89. http://dx.doi.org/10.1182/blood-2005-10-009084.

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AbstractWe investigated the role of the breast cancer resistance protein (BCRP/ABCG2) in drug resistance in multiple myeloma (MM). Human MM cell lines, and MM patient plasma cells isolated from bone marrow, were evaluated for ABCG2 mRNA expression by quantitative polymerase chain reaction (PCR) and ABCG2 protein, by Western blot analysis, immunofluorescence microscopy, and flow cytometry. ABCG2 function was determined by measuring topotecan and doxorubicin efflux using flow cytometry, in the presence and absence of the specific ABCG2 inhibitor, tryprostatin A. The methylation of the ABCG2 promoter was determined using bisulfite sequencing. We found that ABCG2 expression in myeloma cell lines increased after exposure to topotecan and doxorubicin, and was greater in logphase cells when compared with quiescent cells. Myeloma patients treated with topotecan had an increase in ABCG2 mRNA and protein expression after treatment with topotecan, and at relapse. Expression of ABCG2 is regulated, at least in part, by promoter methylation both in cell lines and in patient plasma cells. Demethylation of the promoter increased ABCG2 mRNA and protein expression. These findings suggest that ABCG2 is expressed and functional in human myeloma cells, regulated by promoter methylation, affected by cell density, up-regulated in response to chemotherapy, and may contribute to intrinsic drug resistance.

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Rugani, Petra, Christian Walter, Barbara Kirnbauer, Stephan Acham, Yvonne Begus-Nahrman, and Norbert Jakse. "Prevalence of Medication-Related Osteonecrosis of the Jaw in Patients with Breast Cancer, Prostate Cancer, and Multiple Myeloma." Dentistry Journal 4, no. 4 (September 27, 2016): 32. http://dx.doi.org/10.3390/dj4040032.

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Zhan, Fenghuang, Fang Xiao, Maurizio Zangari, Hongwei Xu, Benjamin Mughal, and Guido J. Tricot. "Targeting NEK2 Kinase In Drug-Resistant Multiple Myeloma with Small Molecule Inhibitors." Blood 116, no. 21 (November 19, 2010): 788. http://dx.doi.org/10.1182/blood.v116.21.788.788.

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Abstract Abstract 788 Background: Treatment failure in malignant diseases, including multiple myeloma (MM), is due to drug resistance of a minor population of cancer cells, already present de novo. Gene expression profiling (GEP) data can be obtained repeatedly during different phases of treatment. Thus, it is possible to monitor newly acquired genetic changes in the drug-resistant MM clone. Materials and Methods: Nineteen primary MM patients enrolled in protocol 25009, provided 59 samples, obtained at baseline, pre-1st, pre-2nd, post-2nd stem cell transplant, and in consolidation. GEP was performed using Affymetrix U133Plus2 chips. In addition, a total of 2552 samples with GEP and clinical data, obtained from published studies, were analyzed. We induced NEK2 over-expression and knockdown using a lentiviral delivery system. A NEK2 inhibitor, NI-2, was identified by screening a kinase inhibitor library including 160 compounds and was used for our in vitro and in vivo studies. Results: By comparing serial GEP samples at baseline versus after treatment or at rapid relapse, we defined 56 genes associated with drug resistance. Ten of the top 20 genes belong to the well established chromosomal instability (CIN) signature. The mean expression levels of CIN genes define a high-risk score present in 10% of newly diagnosed MM patients, which is associated with shorter durations of response, event-free (EFS) (HR = 4.8; P < 0.001), and overall survival (OS)(HR = 5.2; P < 0.001). NEK2 is a serine-threonine kinase and a CIN gene. It was the most significant of the 56 genes related to drug resistance. We found that high expression of NEK2 was associated with a shorter EFS and OS in multiple other cancers, such as breast, lung, AML, mesothelioma, glioma and mantle cell lymphoma. As expected, NEK2 over-expression induced CIN in MM cells evidenced by array-CGH. Over-expressing NEK2 in multiple cancer cell lines resulted in enhanced cell proliferation and increased drug resistance, whereas knockdown of NEK2 by sh RNA induced cancer cell death and growth inhibition. NI-2, a NEK2 kinase inhibitor, significantly suppressed NEK2 activity and induced cancer cell apoptosis, most pronounced in cancer cells with induced NEK2 over-expression. Our in vivo studies in the 5TGM1 C57BL/KaLwRij myeloma mouse model confirm that NI-2 treatment indeed overcomes drug resistance and extends mouse survival also drug-resistant 5GM1 cells were infused (P < 0.01). NI-2 showed a synergistic killing effect on MM cells when combined with bortezomib. Conclusion: We conclude that NEK2 is an important indicator of drug resistance, and therefore, of poor prognosis in MM and many other cancers. It represents a logical target to overcome drug resistance. In combination with other chemotherapies, it may result in the curing of previously incurable neoplasias, including MM. Our future work will aim at modifying NEK2 inhibitors to optimize activity and decrease toxicity of NEK2 kinase inhibitors in collaboration with our medicinal chemistry colleagues. Disclosures: No relevant conflicts of interest to declare.

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Liu, Jinsha, Priyanka Pandya, and Sepideh Afshar. "Therapeutic Advances in Oncology." International Journal of Molecular Sciences 22, no. 4 (February 18, 2021): 2008. http://dx.doi.org/10.3390/ijms22042008.

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Around 77 new oncology drugs were approved by the FDA in the past five years; however, most cancers remain untreated. Small molecules and antibodies are dominant therapeutic modalities in oncology. Antibody-drug conjugates, bispecific antibodies, peptides, cell, and gene-therapies are emerging to address the unmet patient need. Advancement in the discovery and development platforms, identification of novel targets, and emergence of new technologies have greatly expanded the treatment options for patients. Here, we provide an overview of various therapeutic modalities and the current treatment options in oncology, and an in-depth discussion of the therapeutics in the preclinical stage for the treatment of breast cancer, lung cancer, and multiple myeloma.

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Guo, Ying, An Thuy Ngo-Huang, and Jack B. Fu. "Perspectives on Spinal Precautions in Patients Who Have Cancer and Spinal Metastasis." Physical Therapy 100, no. 3 (February 10, 2020): 554–63. http://dx.doi.org/10.1093/ptj/pzz178.

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Abstract Bones are the third most common site for cancer metastases, and the axial skeleton is the most frequent skeletal location. In a postmortem study, bone metastases were reported in 70% of breast and prostate cancer patients. Bone metastases from breast, lung, prostate, thyroid, and kidney cancers account for 80% of all bone metastases. Bone lesions exist in 60% of newly diagnosed multiple myeloma patients. With increasing numbers of people who have survived cancer, many patients with cancer and axial skeletal bony metastases will be seen by physical and occupational therapists. Guidelines are lacking on how to perform physical examinations and provide exercise programs for these patients without compromising the diseased spine. In this article, we discuss the available evidence for similar spinal conditions, the biomechanics of spinal load, and changes associated with posture and weight load. We provide recommendations on how to assess a patient’s strength, how to strengthen without compromising the diseased spine, and how to teach patients to use correct body mechanics during mobility and activities of daily living.

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., Dwiwahyonokusuma, I. Gede Eka Wiratnaya, Gede Agung Krisna Yudha, and I. Gede Mahardika Putra. "Increased tumor marker ca-125 in multiple myeloma: a case report." International Journal of Research in Medical Sciences 8, no. 9 (August 26, 2020): 3355. http://dx.doi.org/10.18203/2320-6012.ijrms20203692.

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Multiple myeloma (MM) is a malignant B-cell lymphoproliferative disorder of the marrow, with plasma cells predominating. It is unlikely to encounter rising level of any tumor marker in MM patient. We present a case of 46-year-old female came to the orthopaedic clinic with chief complains of pain on her right arm, left shoulder and right hip after 5 months. The results of the bone survey of these patients showed multiple lytic lesions with a punched-out appearance in calvaria. The expansive lytic mass was seen with cortical destruction in one third proximal metaphysis to diaphysis of humerus with periosteal reaction and surrounding soft tissue mass. The basic metabolic panel (BMP) result of these patient is hipocellular with decrease of erythroid, myeloid, and megakaryocytes activity and there are 30% plasma cells with positive myeloma cells. Therefore, the patient was diagnosed with MM. The laboratory result of these patient also showed elevation of carbohydrate antigen 125 (CA-125) marker to 56 and 92 (normal range is <35). The patient reported herein showed clear signs and symptoms of MM accompanied by elevated level of CA-125 and CA-15.3 tumor markers. Elevated CA-125 values most often are associated with epithelial ovarian cancer, although levels also can be increased in other malignancies such as endometrial, fallopian tube, breast, lung, esophageal, gastric, hepatic, and pancreatic. However, there were no clear mechanism of how a malignant B-cell lymphoproliferative disorder of the marrow stimulates the production of tumor marker such as CA-125.

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

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