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Advances in genomics, bioinformatics and the creation of model organisms have identified many genes associated with polycystic kidney diseases. Historically, these genes were not necessarily associated with ciliopathies, but it appeared that many connections can be made between the cystic kidney disease and function of the primary cilium. Indeed, the proteins encoded by these genes are localized to the cilium itself, to the basal body or are known to regulate the expression and localization of ciliary proteins. The goal of this article is to describe the multiple cellular processes that may lead to the development of renal cysts if they are deregulated. These include changes in proliferation rate, cell polarity or signaling pathways involved in embryonic kidney development. To highlight the role of the primary cilium in cystogenesis, I will discuss several studies investigating the function of ciliary genes and cilia in the kidneys of different model organisms.
Bronchogenic cysts represent a rare form of cystic malformation of the respiratory tract. Primarily located in the mediastinum if occurring early in gestation as opposed to the thoracic cavity if arising later in development. However, they can arise from any site along the foregut. They exhibit a variety of clinical and radiologic presentations, representing a diagnostic challenge, especially in areas with endemic hydatid disease. Endoscopic drainage has emerged as a diagnostic and potentially therapeutic option but has been complicated by reports of infection. Surgical excision remains the standard of care allowing for symptomatic resolution and definitive diagnosis via pathologic examination; minimally invasive approaches such as robotic and thoracoscopic approaches aiding treatment. Following complete resection, prognosis is excellent with essentially no recurrence.
Orthokeratinized odontogenic cysts are keratinizing jaw cysts and due their association with impacted teeth and keratinaceous content, they resemble odontogenic keratocysts but differ in regards to biological behaviour, being less aggressive. To unravel the nature of OOCs, as they resemble epidermoid cysts histologically and due to their developmental resemblances to OKCs, this study was conducted.
Spinal arachnoid cysts (SAC) are intradural lesions, which may provoke a compression of the spinal cord and roots. Endoscopic techniques are increasingly used to minimize the surgical access and the postoperative scar tissue. Shunts may also represent an option. The aim of this paper is to illustrate the technique of endoscopic-assisted fenestration and positioning of a cysto-peritoneal diversion in a thoracic SAC using a flexible endoscope and to perform a systematic literature review on this subject.
The authors have reviewed the clinical and histopathologic features of nine cases of lacrimal ductal cysts. Six of these were proven histologically, and three were diagnosed clinically. All presented as masses, three with pain, five with tenderness and two with acute expansion due to hemorrhage in one case and following crying and deep sea diving in the other. Six were treated surgically and three are being followed clinically. The six lesions examined histologically were all ductal cysts with evidence of scarring and inflammation. The differential diagnosis and management are outlined.
Background and aims. Odontogenic cysts and tumors have a wide spectrum of clinical characteristics that lead to the different management strategies. Since definite diagnosis is difficult in some cases, it has been suggested that CD56 may be a candidate marker for definitive diagnosis of some odontogenic tumors. The present study was designed to examine CD56 expression in lesions with histopathological similarities. Materials and methods. In this cross-sectional, analytical study the subjects were 22 ameloblastomas, 13 dentigerous cysts, 10 keratocystic odontogenic tumors (KCOT), 4 adenomatoid odontogenic tumors (AOT), 3 orthokeratinized odonto-genic cysts, 3 calcifying odontogenic cysts (COC) and one glandular odontogenic cyst (GOC). All the samples were examined for CD56 immunoreactivity. Data were analyzed using chi-square test. Results. Twenty cases (91%) of ameloblastomas, 3 (75%) AOT, 4 (40%) KCOT and one case of GOC were positive for CD56. None of the dentigerous cysts, COC and orthokeratinized odontogenic cysts was CD56-positive. There was a significant difference in the CD56 expression between ameloblastoma and dentigerous cyst, as well as COC. Also, KCOT showed significantly higher expression than orthokeratinized odontogenic cyst. Conclusion. In this study CD56 expression was limited to the odontogenic tumors and more aggressive cystic lesions. This marker can be a useful aid for distinguishing cysts and tumors from similar lesions.
High-risk human papillomavirus (HPV) DNA has been reported to be present in branchial cleft cysts, but further information is required to clarify the role of HPV infection in branchial cleft cysts. The presence of HPV, the viral load and the physical statuses in samples from six patients with branchial cleft cysts were investigated using the polymerase chain reaction (PCR), quantitative PCR, in situ hybridization (ISH) using HPV DNA probes and p16INK4a immunohistochemical analysis. High-risk type HPV-16 DNA was identified in four of the six branchial cleft cysts analyzed. Of the HPV-positive branchial cleft cysts, three exhibited mixed-type integration of HPV. HPV DNA was distributed among the basal-to-granular layers of the cystic wall in ISH analysis, and p16INK4a was weakly expressed in the nuclei and cytoplasm of the same layers in patients with integration. ISH revealed that one patient with episomal-type infection exhibited HPV DNA in the cyst wall and did not express p16INK4a. Two patients without evidence of HPV infection exhibited weak p16INK4a expression in the superficial cyst-lining cells of branchial cleft cysts. These results indicate that infection with high-risk HPV types may be common in branchial cleft cysts. In addition, p16INK4a is not a reliable surrogate marker for HPV infection in branchial cleft cysts.
Adrenal disorders are common in ferrets, but there are few studies on cystic lesions of the adrenal gland. The present study describes pathological and immunohistochemical features of adrenal cysts in eleven ferrets and discusses their histogenesis. In nine of eleven cases examined, which included seven, one, and one right, left, and bilateral cases, respectively, cysts were in the adrenal cortex and lined with epithelial cells. These epithelial cells contained an Alcian blue-negative/PAS-positive material and were positive for cytokeratin (CK) 7. The staining pattern was similar to that of biliary epithelial cells in the ferret. In five of the cases, there were small ducts adjacent to the cysts that were positive for CK7 and CK20 and negative for CK19. Based on the anatomical proximity between the right adrenal and liver, the immunohistochemical features of the small duct cells were comparable to those of hepatic oval cells. These results indicate the possibility that these adrenocortical cysts in the ferret originated from the biliary system. In the other two cases, the cysts lacked an epithelial cell lining, and there were dilated lymphoid vessels around the cysts. These cysts were assumed to have developed in the adrenal medulla, because the cyst wall was positive for glial fibrillary acidic protein and there were adrenal medullary cells positive for synaptophysin in the cyst wall. Therefore, the medullary cysts may have been associated with dilated vasculatures.
The spermatogonial stem cell (SSC) compartment is maintained by self-renewal of stem cells as well as fragmentation of differentiating spermatogonia through abscission of intercellular bridges in a random and stochastic manner. The molecular mechanisms that regulate this reversible developmental lineage remain to be elucidated. Here, we show that histone H3K27 demethylase, JMJD3 (KDM6B), regulates the fragmentation of spermatogonial cysts. Down-regulation of Jmjd3 in SSCs promotes an increase in undifferentiated spermatogonia but does not affect their differentiation. Germ cell-specific Jmjd3 null male mice have larger testes and sire offspring for a longer period compared to controls, likely secondary to increased and prolonged maintenance of the spermatogonial compartment. Moreover, JMJD3 deficiency induces frequent fragmentation of spermatogonial cysts by abscission of intercellular bridges. These results suggest that JMJD3 controls the spermatogonial compartment through the regulation of fragmentation of spermatogonial cysts and this mechanism may be involved in maintenance of diverse stem cell niches.
Ovarian endometrial cysts cause some kinds of ovarian cancer, and iron is considered as one factor of carcinogenesis. In contrast, hypoxia is associated with progression, angiogenesis, metastasis, and resistance to therapy in cancer. We investigated hypoxia-induced perturbation of iron homeostasis in terms of labile iron, iron deposition, and iron regulatory protein (IRP) in ovarian endometrial cysts. Iron deposition, expression of IRPs, and a protein marker of hypoxia in human ovarian endometrial cysts were analyzed histologically. The concentration of free iron and the pO2 level of the cyst fluid of human ovarian cysts (n = 9) were measured. The expression of IRP2 under hypoxia was investigated in vitro by using Ishikawa cells as a model of endometrial cells. Iron deposition and the expression of IRP2 and Carbonic anhydrase 9 (CA9) were strong in endometrial stromal cells in the human ovarian endometrial cysts. The average concentration of free iron in the cyst fluid was 8.1 ± 2.9 mg/L, and the pO2 was 22.4 ± 5.2 mmHg. A cell-based study using Ishikawa cells revealed that IRP2 expression was decreased by an overload of Fe(II) under normoxia but remained unchanged under hypoxia even in the presence of excess Fe(II). An increase in the expression of IRP2 caused upregulation of intracellular iron as a result of the response to iron deficiency, whereas the protein was degraded under iron-rich conditions. We found that iron-rich regions existed in ovarian endometrial cysts concomitantly with the high level of IRP2 expression, which should generally be decomposed upon an overload of iron. We revealed that an insufficient level of oxygen in the cysts is the main factor for the unusual stabilization of IRP2 against iron-mediated degradation, which provides aberrant uptake of iron in ovarian endometrial stromal cells and can potentially lead to carcinogenesis.
Of 52 patients (39 women and 13 men; mean age, 65 years) with idiopathic macular cysts or holes, 17 had bilateral involvement. During a mean follow-up period of 28 months, 50% of the macular cysts progressed to holes. Eight of nine eyes with cysts and visual acuities of 6/15 (20/50) or worse at the initial examination developed holes. No holes developed in eyes that had not had cysts at the initial examination. This demonstrated the importance of examining the fellow eye when making a prognosis. Posterior vitreous detachment was present in all the eyes with macular holes and absent in all the eyes with macular cysts at the initial examination. Whenever a cyst progressed to a hole, posterior vitreous detachment also developed. Twenty-five patients had systemic hypertension, 31 had undergone a hysterectomy, taken systemic estrogen, or both, three had adult-onset diabetes mellitus, and 12 smoked cigarettes.
Pineal cysts (PCs) are a benign lesion of the pineal gland that have been known to the medical community for a long time. With a prevalence rate of approximately 1% in the general population, PC is often a reason for medical counseling. The natural course of PC morphology has not been well described. In this study, we present a longitudinal magnetic resonance imaging (MRI) study of patients with PCs, with special focus on those who showed an increase or decrease in PC size.
Objective Obesity is one of the risk factors for pancreatic cancer and a prognostic factor for acute-chronic pancreatitis. Aim To explore the relationship and association between obesity and pancreatic cysts over a 25-year period in African American patients. Methods We reviewed the medical records of 207 patients diagnosed with pancreatic cysts via radiology and pathology data from January 1988 to December 2012. A control group was selected from a separate group of healthy patients without a history of pancreatic disease. The patients were evaluated in five groups according to the last 20 years of diagnosis in five-year intervals. Results Most patients with pancreatic cyst (73%) were overweight (defined as a body mass index (BMI) ≥ 25), and 53% had a history of chronic pancreatitis compared to patients in the control group. There was a significant difference between the two groups; 79% of patients group were overweight (BMI ≥ 25) vs. 66% in control group (p = 0.02). The incidence of obese and overweight patients was significant (85%) during the 2008 to 2012 interval for the test group (p = 0.009). Conclusion Given the increasing proportion of obese pancreatic cyst patients in recent decades compared to the proportion noted in the 1990s, obesity plays a large role in the formation of pancreatic cysts.
Thymic epithelial cells (TECs), derived from polarized two-dimensional (2D) oriented endodermal cells, are distinguished from other epithelial cells by their unique three-dimensional (3D) phenotype. However, some polarized epithelial cells remain present in the normal thymus, forming thymic cysts at the cortico-medullary junction. Here, we analyse the dynamics, origin and phenotype of such thymic cysts. In time-course experiments, we show a reverse correlation between thymic cyst expansion and the presence of thymocytes, suggesting a default pathway for the development of TECs in the absence of thymocytes. By transplanting isolated TEC populations into E15 fetal thymic lobes, we provide evidence that medullary thymic epithelial cells (mTECs), rather than cortical thymic epithelial cells (cTECs) contribute to the formation of thymic cysts. Finally, thymi of reporter mice reveal that the cysts originate from epithelia committed to a thymic fate, as indicated by the expression of Foxn1. The 2D-phenotype of cyst-lining TECs is not caused by a downregulation of Foxn1 expression, since a significant proportion of these cells in the embryonic and adult thymus continues to express Foxn1 at the protein level.
Intraductal papillary mucinous neoplasms (IPMNs) and mucinous cystic neoplasms (MCNs) are non-invasive neoplasms that are often observed in association with invasive pancreatic cancers, but their origins and evolutionary relationships are poorly understood. In this study, we analyze 148 samples from IPMNs, MCNs, and small associated invasive carcinomas from 18 patients using whole exome or targeted sequencing. Using evolutionary analyses, we establish that both IPMNs and MCNs are direct precursors to pancreatic cancer. Mutations in SMAD4 and TGFBR2 are frequently restricted to invasive carcinoma, while RNF43 alterations are largely in non-invasive lesions. Genomic analyses suggest an average window of over three years between the development of high-grade dysplasia and pancreatic cancer. Taken together, these data establish non-invasive IPMNs and MCNs as origins of invasive pancreatic cancer, identifying potential drivers of invasion, highlighting the complex clonal dynamics prior to malignant transformation, and providing opportunities for early detection and intervention.
The aim of this study was to systematically review scientific literature in orderto describe the characteristics and prognosis of malignant entities developing from odontogenic cysts. A search in Pubmed (MEDLINE) and Cochrane databases was conducted. The inclusion criteria were articles published in English related to the malignisation of odontogenic cysts in humans. The exclusion criteria were articles that do not specify the type of odontogenic cyst, malignisation of parakeratinised keratocysts, the presence of an ameloblastic carcinoma and metastasis from distant primary tumours. The selected articles were classified according to Strength of Recommendation Taxonomy criteria. Statistical analysis of the data was carried out using statistical package software SPSS version 22.0. From the 1,237 articles initially obtained, the authors included 3 case series and 45 case reports in the end. Descriptive analysis showed that men have a disposition for malignisation from odontogenic cysts and they frequently appear at the posterior mandible, with pain and swelling being the most frequent signs and symptoms. Follicular cysts were the entities that underwent the most malignant changes with well differentiated squamous cell carcinomas being the most prevalent type of malignancy. The real prognosis of this malignancy is not known because of the heterogeneity of available studies. Key words:Odontogenic cysts, squamous cell carcinoma, neoplastic cell transformation, oral cancer.
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