Home About us Contact
|
Home About us Contact | ||
|
|
||
Gastrointestinal Epithelium (gastrointestinal + epithelium)
Selected AbstractsPancreatic mucinous lesions: A retrospective analysis with cytohistological correlationDIAGNOSTIC CYTOPATHOLOGY, Issue 11 2006Jing Zhai M.D., Ph.D. Abstract The diagnosis of mucinous pancreatic lesions, which include mucinous noncystic adenocarcinoma, intraductal papillary mucinous neoplasm (IPMN), mucinous cystic neoplasm (MCN), and mucinous metaplasia, is critical, given different clinical management and prognosis. This retrospective study is done to assess the cytological features and pitfalls associated with these entities in cytological samples. A search for pancreatic cytology specimens with histological confirmation of the various pancreatic mucinous lesions was done from 1988 to 2005: 9 mucinous adenocarcinoma, 14 IPMN, 11 MCN, and 3 mucinous metaplasia. The majority (35/37) had been endoscopic ultrasound-guided fine-needle aspirations. The cellularity, background extracellular mucin, epithelial architecture, mucinous nature of the epithelium, cell shape, and nuclear features were evaluated on the cytology material. Of the 22 cytological features evaluated, the presence of three-dimensional clusters, micropapillary structures, and nuclear atypia, which includes nuclear crowding, increased N/C ratio, anisonucleosis, nuclear membrane contour irregularity, clumpy chromatin, and prominent nucleoli, was found to be consistently associated with mucinous adenocarcinoma. There were no statistically significant cytological features, which helped in differentiating IPMN, MCN, and mucinous metaplasia. There was a relatively high false-positive rate in the IPMN group (5/14, 36%). Review of the histological specimen showed severe dysplastic epithelial change in these cases. One false-positive case of mucinous metaplasia (1/3, 33%) showed marked intraepithelial acute inflammation. The cytological diagnosis of mucinous pancreatic lesions remains challenging, except for mucinous noncystic adenocarcinoma. The findings were largely nonspecific in the differentiation between IPMN, MCN, mucinous metaplasia, and incidentally sampled gastrointestinal epithelium. False-positive diagnosis of adenocarcinoma occurs not infrequently in the setting of IPMN with severe dysplastic epithelial change and in lesions with associated acute inflammation, and can be a pitfall in the diagnosis of these lesions. Diagn. Cytopathol. 2006;34: 724,730. © 2006 Wiley-Liss, Inc. [source] Neutrophil gelatinase-associated lipocalin is a marker for dysregulated keratinocyte differentiation in human skinEXPERIMENTAL DERMATOLOGY, Issue 6 2002Lotus Mallbris Abstract: Neutrophil gelatinase-associated lipocalin (NGAL) is a 25-kDa protein initially isolated from the specific granules of human neutrophils. It is a member of the highly heterogeneous lipocalin protein family, which shares a common tertiary structure. Its synthesis is induced in gastrointestinal epithelium in association with inflammation and malignancy. To gain insight into its potential role in other epithelia we have investigated the expression of NGAL in human skin embryonic development, in normal adult skin, and in skin associated with inflammation and neoplastic transformation. In the present study we report that the embryonic expression of NGAL appears to be regulated in a spatio-temporal pattern. It was induced in the interfollicular epidermis at 20,24 weeks of gestational age but thereafter progressively receded towards the hair follicles. In normal adult skin, NGAL was detected solely in association with hair follicles. However, strong induction of NGAL in the epidermis was seen in a variety of skin disorders characterized by dysregulated epithelial differentiation such as psoriasis, pityriasis rubra and squamous cell carcinoma. In these tissues production of NGAL was confined to spatially distinct subpopulations of keratinocytes underlying areas of parakeratosis, whereas skin samples lacking parakeratotic epithelium such as lichen ruber planus, acute contact eczema and basal cell carcinoma were negative for NGAL. Consistent with being a marker for disturbed terminal differentiation, NGAL immunoreactivity showed an inverse pattern when compared with that of the differentiation marker filaggrin. The biologic functions of NGAL in epithelia are not fully known, although an immunomodulatory role in host defense has been proposed. In addition, the transient interfollicular NGAL expression during skin embryogenesis along with the induction of NGAL in adult parakeratotic epidermis suggests it play a role in epithelial differentiation pathways. [source] Metastatic esophageal carcinoma masquerading as inflammatory breast carcinomaINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 3 2007Christy L. Nebesio MD A 50-year-old Caucasian woman with a history of esophageal adenocarcinoma presented with a 3-week history of right breast swelling and progressive erythema. Twenty-two months prior to presentation, she had been diagnosed with adenocarcinoma of the esophagus (T3,N1,M1a) and underwent neoadjuvant chemoradiotherapy followed by surgical resection. On physical examination, the right breast was red, swollen (40% larger than the contralateral breast), tender to palpation, and warm to the touch (Fig. 1). No mass was palpable. On the basis of the clinical findings, inflammatory breast carcinoma was suspected. A punch biopsy revealed a poorly differentiated adenocarcinoma with extensive involvement of dermal lymphatics (Fig. 2). The clinical and histologic differential diagnosis included inflammatory breast carcinoma vs. metastatic esophageal adenocarcinoma to the skin of the breast. Figure 1. The affected breast resembled inflammatory breast carcinoma with erythema and prominent edema. The edema resulted in partial inversion of the nipple Figure 2. Within the reticular dermis and dermal lymphatics, there was a poorly differentiated adenocarcinoma. Many of the tumor cells had a signet ring morphology (hematoxylin and eosin, ×200) To resolve this question, immunohistochemical stains for estrogen and progesterone receptors and CDX-2 (BioGenex, San Ramon, CA, USA) were performed. CDX-2 is an intestinal homeobox gene expressed in gastrointestinal epithelium and gastrointestinal tumors. The tumor nuclei were positive for CDX-2 but negative for both steroid receptors (Fig. 3), confirming the diagnosis of metastatic esophageal adenocarcinoma. Figure 3. The tumor cells had strong nuclear immunoreactivity for CDX-2 (CDX-2 immunohistochemical stain, ×400) [source] Adenocarcinoma arising from a mature cystic teratoma of the testisINTERNATIONAL JOURNAL OF UROLOGY, Issue 9 2003TOSHINORI KASAI Abstract A 52-year-old male diagnosed pathologically with metastatic adenocarcinoma of the skin was referred to our department. Physical examination revealed a right scrotal mass the size of child's head and several skin tumors. Right high orchiectomy and resection of skin tumors were performed. Histopathological examination revealed a well-differentiated, mucinous adenocarcinoma originating from the gastrointestinal epithelium in a mature cystic teratoma (dermoid cyst) of the testis and metastatic mucinous adenocarcinoma of the skin. We made a diagnosis of teratoma with malignant transformation (TMT) of the testis. Combination chemotherapy with low-dose cisplatin/5,-deoxy-5-fluorouridine (CDDP/5,-DFUR) was initiated, but the patient died 8 months after orchiectomy. At autopsy, similar mucinous adenocarcinoma of the testis and the skin were observed at the metastatic sites. [source] Regulation of restitution after superficial injury in isolated guinea pig gastric mucosaAPMIS, Issue 4-5 2004ARUN BHOWMIK The immediate response of the gastrointestinal epithelium to superficial (i.e. microscopic) injury is primarily directed towards restoring the disturbed epithelial continuity. Both structural (i.e. cytoskeleton) and humoral (i.e. growth factors and cytokines) involvement in the process has recently been documented. Yet it is unclear whether humoral signaling regulating mucosal recovery after superficial injury is associated with tyrosine phosphorylation, and whether there are other signs of downstream activation of the signaling pathway. To evaluate the effects of exogenous genistein and phorbol-myristate acetate in the assessment of the role of tyrosine receptor-mediated signaling in the immediate repair of gastric mucosa after superficial injury. Guinea pig gastric mucosa was mounted in a Ussing chamber, injured with 1.25 M NaCl, and perfused for 4 h. Simultaneously, potential difference and tissue resistance were recorded. In some sets of experiments the tissue was exposed bilaterally either to genistein in order to inhibit tyrosine receptor-mediated signaling or to 4-phorbol-myristate 13-acetate (PMA) in order to enhance PKC signaling during the 4 h recovery. Phosphotyrosine (PTYR) and protein kinase C (PKC) immunoreactivity were assessed by immunoblotting and by immunohistochemistry. Proliferative activity was determined morphometrically after staining of the tissue for Ki-67 nuclear antigen and expressed as proliferative index (PI). The inhibition of tyrosine kinases with exogenous genistein resulted in a significant decrease of the PTYR and the stimulation of PKC with PMA increased the PTYR. Nevertheless, no change in the PTYR was observed by immunoblotting after superficial injury alone. Several PKC isoenzymes were found in the guinea pig gastric mucosa, including PKC-,, -,, -, and -,. They were unaffected either by the injury or the PMA treatment. The mean PI of tissues subjected to NaCl-injury was higher than that of uninjured control tissues (p<0.05) (n=7). Exposure of tissue to genistein during recovery decreased the PI, while stimulation with PMA increased it (p<0.05 for both) (n=6). Both electrophysiologic and morphologic restitution were sensitive to genistein, but not to PMA. Superficial injury alone does not influence tyrosine phosphorylation to a degree which could be assessed by immunoblotting. Nevertheless, exogenous modulation of tyrosine receptor-mediated signaling results in downstream signaling effects. The injury-associated induction of proliferation is sensitive to modulation of tyrosine phosphorylation and PKC, suggesting that superficial epithelial injury results in endogenous activation of the epithelium, presumably after paracrine stimulation of the neighboring cells. [source] | ||||||||||