Breast Cancer and Flavonoids as Treatment Strategy

Breast cancer is the most prevalent cancer type among women. Despite recent progress in early detection and therapeutic strategies, the rate of mortality is increasing. Anti-estrogens or aromatase inhibitors are preferred to treat the women diagnosed with estrogen-receptor (ER) positive tumors. However, breast tumors usually show intra-tumoral heterogeneity with ER-positive and -negative cells. The advanced breast cancer cells lose the estrogen responsiveness and become aggressive by developing new strategies for rapid proliferation such as mutations in cell cycle machinery. New promising drugs are still being investigating against these types of tumors especially to overcome acquired resistance against chemotherapeutic drugs; however, a successful treatment for metastatic tumors is still unclear. Flavonoids, with various pharmacological activities, are plant or fungus secondary metabolites present in human diet. In plants, beside their role in pigmentation, they may also act as messengers, regulators and cell cycle inhibitors. Therefore, they are being tested in ovarian, cervical as well as breast cancer. Due to the positive correlation between flavonoids-rich diet and lower risk of cancer, flavonoids are referred as chemopreventive agents. The current chapter emphasizes the therapeutic potential of flavonoids and their synthetic analogues as anti-cancer agents in breast cancer providing new insights into the molecular mechanisms

Aging-Related Diseases and Autophagy

Autophagy is fundamental, evolutionary conserved physiological process at molecular level which targets long-lived cytosolic proteins and organelles to be recycled through lysosomal degradation. Diminished autophagic activity caused cellular stress in many organisms following aging, and inhibition of autophagy in model organisms causes degenerative changes and pathologic diseases observed with high incidence ratio generally in older ages. Consequently the delayed senescence or increased longevity in model organisms often stimulate autophagy, and autophagy inhibition compromises anti-aging effects. The cytoprotective function of autophagy is presented in various human diseases such as lung, liver, cardiovascular diseases, neurodegeneration, myopathies, cancer, stroke, infections and metabolic diseases which are found associated with autophagic targets. These pathologies are defined with their age-dependent characteristics, is not fully understood that how autophagy network regulates metabolism and may cause diseases in age-related manner. In this book chapter, we are going to discuss the autophagy and aging relationship in three different parts. In the first section autophagy and aging relationship is going to be presented through explaining responsible signalling network. The autophagy and age-related neurological disorders, genetic basis of age-dependent diseases and the functional role of autophagy is going to be discussed in the second and third part of the chapter

Sea-blue histiocyte syndrome: A case report

In this report we describe a male patient presenting with splenomegaly and multiple nodules within the splenic parenchyma who had associated dyslipidaemia and beta-thalassaemia trait. A splenectomy was performed and histopathologic findings were consistent with the sea-blue histiocyte syndrome. In this case, it is likely that ceroid deposits seen in histopathological specimens might have developed secondarily to dyslipidaemia and increased haematopoietic cell turnover due to associated thalassaemia. Sea-blue histiocyte syndrome should be sought in differential diagnosis of echogenic nodular mass lesions of the spleen especially when there is associated predisposing disease states. Copyright © Hellenic Society of Haematology

Plasmapheresis in the treatment of hyperthyroidism associated with agranulocytosis: A case report

PubMedID: 15493048Plasmapheresis, also known as therapeutic plasma exchange, is used in the treatment of several disorders. Temporary improvement after plasmapheresis in cases with thyrotoxicosis has been reported. A 55-year-old woman presented with agranulocytosis induced by propylthiouracil and clinical signs of heart failure. Three sessions of plasmapheresis were performed. We observed an improvement of thyroid hormone levels and clinical findings as well. Plasmapheresis can be an option when drug treatment of thyrotoxicosis fails. © 2004 Wiley-Liss, Inc

Autocrine Growth Hormone Mediated Curcumin Resistance Overcame by Autophagy Inhibition via Bafilomycin in MDA-MB-231 and T47D Breast Cancer Cells

Curcumin, a plant derived natural compound, has anti-oxidant, anti-proliferative and apoptotic effect on various cancer cells such as prostate, colon and breast cancer. Autocrine growth hormone (GH) expression induced breast cancer invasion-metastasis has been reported in vivo and in vitro cancer models. Autophagy is a vesicule-mediated clearance mechanism and one of the handicap against drug-induced apoptotic cell death. In this study, our aim was to investigate the molecular machinery of curcumin induced apoptotic cell death under autophagy inhibition conditions in autocrine GH expressing MDA-MB-231 and T47D breast cancer cells. Although autocrine GH induced curcumin resistance, this effect was slightly prevented by time-dependent curcumin treatment in MDA-MB-231 and T47D breast cancer cells. In addition, curcumin induced autophagy vacuole formation was determined by acridine orange staining in MDA-MB-231 and T47D wt/GH+ breast cancer cells. Moreover, curcumin triggered autophagy through upregulating Beclin-1, Atg3, Atg12 expressions and LC3 cleavage in each cell line. Concomitantly, BiP, IRE1α and Calreticulin expressions were upregulated following 3 h curcumin exposure in MDA-MB-231 wt and GH+ cells. According to MTT cell viability assay, autocrine GH-mediated curcumin resistance was overcome by bafilomycin and curcumin co-treatment in MDA-MB-231 and T47D GH+ cells. Moreover, curcumin and bafilomycin co-treatment induced cell cycle arrest at G1 phase in MDA-MB-231 GH+ cells, G2/M arrest in T47D GH+ breast cancer cells. In conclusion, autocrine GH-triggered curcumin resistance was overcome by autophagy inhibition condition by bafilomycin treatment in a dose-dependent manner in MDA-MB-231 and T47D GH+ breast cancer cells

Craniofacial Fibrous Dysplasia Involvements of Mccune-Albright Syn-drome: A Review with an Additional Case

Background: McCune-Albright Syndrome (MAS) is a genetic disorder with a triad of endocrine diseases, cafe-au-lait macules and fibrous dysplasias. Craniofacial fibrous dysplasia is a term that is used to describe the fibrous dysplasia, which was localized at the craniofacial skeleton and is common in MAS patients. Objective: The objective of this review is to determine the involvement frequency of cranial and facial bones in patients with MAS and CFD. Methods: Articles in PubMed was searched with the following details "(mccune[Title/Abstract] OR albright[Title/Abstract]) OR ("craniofacial fibrous dysplasia"[MeSH Terms] OR ("craniofacial"[All Fields] AND "fibrous"[All Fields] AND "dysplasia"[All Fields]) OR "craniofacial fibrous dysplasia"[All Fields])". The articles in which the authors did not state the involved bones or did not add any radiographic images were excluded from the study. Results: 26 cases in 25 articles met the inclusion criteria. Among the 26 cases and our case, sphenoid and frontal bones were involved in 17 cases, parietal and occipital bones were involved in 15 cases, mandible and ethmoid bone were involved in 14 cases, maxilla-zygoma-temporal and palate was involved in 13, 11, 6 and 3 cases, respectively. Palate was involved in cases where maxilla was also involved. Our case was the only case that was evaluated with CBCT. Conclusion: Routine follow-ups are important since new CFDs can occur in different cranial or facial bones. 2D imaging techniques may not be able to demonstrate early CFDs; thus, an advanced imaging technique should be used after MAS diagnosis

Tuberculosis leading to reversible myelofibrosis: A case report

Myelofibrosis also known as myeloid metaplasia and agnogenic myeloid metaplasia is characterized by the replacement of bone marrow with fibrous tissue or scarring. The disorder is mostly idiopathic or secondary that accounts for about 10% of all cases. The association of mycobacterial diseases and haematologic abnormalities is well known. Tuberculosis can cause different types of alterations of normal bone marrow including fibrosis. Conceivable mechanisms for the development of bone marrow fibrosis in tuberculosis include abnormal production or signalling of cytokines like transforming growth factor-ß, platelet derived growth factor and fibroblast growth factor. We describe a 57-year-old man with bone marrow fibrosis. Antituberculosis treatment was initiated after obtaining a positive smear of pleural fluid. An improvement of both clinical status and haematologic disturbances was observed. Tuberculosis should be considered in the differential diagnosis of myelofibrosis especially in endemic regions and empiric antituberculosis treatment can be acceptable in some occasions

Radiological evaluation of the periosteal reactions in the jaws: a retrospective CBCT study

Objectives The objective of this study is to evaluate the relationship between the radiological features of periosteal reactions (PR) and histopathological features of the lesions