Histology and histopathology Vol.30, nº5 (2015)
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- PublicationOpen AccessHuman resident CD34+ stromal cells/telocytes have progenitor capacity and are a source of αSMA+ cells during repair(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Díaz-Flores, L.; Gutiérrez, R.; García, M.P.; González, M.; Sáez, F.J.; Aparicio, F.; Díaz-Flores Jr., L.; Madrid Cuevas, Juan FranciscoWe studied the progenitor capacity of human resident CD34+ stromal cells/telocytes (SC/TCs) in the enteric wall affected by inflammatory/repair processes (appendicitis, diverticulitis of large bowel and Crohn’s disease of the terminal ileum) at different stages of evolution (inflammatory, proliferative and remodelling). In these conditions, CD34+ SC/TCs are activated, showing changes, which include the following overlapping events: 1) separation from adjacent structures (e.g., from vascular walls) and location in oedematous spaces, 2) morphological modifications (in cell shape and size) with presence of transitional cell forms between quiescent and activated CD34+ SC/TCs, 3) rapid proliferation and 4) loss of CD34 expression and gain of αSMA expression. These events mainly occur in the inflammatory and proliferative stages. During the loss of CD34 expression, the following findings are observed: a) irregular cell labelling intensity for anti-CD34, b) co-localization of CD34 and actin, c) concurrent irregular labelling intensity for αSMA and d) αSMA expression in all stromal cells, with total loss of CD34 expression. While CD34 expression was conserved, a high proliferative capacity (Ki-67 expression) was observed and vice versa. In the segments of the ileum affected by Crohn’s disease, the stromal cells around fissures were αSMA+ and, in the transitional zones with normal enteric wall, activated CD34+ SC/TCs were observed. In conclusion, human resident CD34+ SC/TCs in the enteric wall have progenitor capacity and are activated with or without differentiation into αSMA+ stromal cells during inflammatory/repair processes.
- PublicationOpen AccessLymphoid hyperplasia and lymphoma in KSHV K1 transgenic mice(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Berkova, Zuzana; Wang, Shu; Sehgal, Lalit; Pate, Keyur Pravinchandra; Prakash, Om; Samaniego, FelipeGrowing evidence supports the involvement of human herpervirus 8, Kaposi’s sarcoma associated herpesvirus (KSHV), in the pathology of primary effusion lymphoma, multicentric Castleman’s disease, and Kaposi’s sarcoma, but the exact mechanism of KSHV contribution to the oncogenic process remains elusive. We studied transgenic mice expressing the ORF K1 of KSHV, whose position in the KSHV genome corresponds to known lymphoproliferative genes of other herpesviruses. K1 protein was previously shown to contain a constitutively active ITAM domain, involved in activation of Akt and pro-survival signaling, and to inhibit Fas-mediated apoptosis by interfering with binding of FasL. All this pointed to a possible role of K1 in the pathogenesis of KSHV-associated cancers. K1 transgenic mice (80-90%) developed lymphoid hyperplasia and splenomegaly at 8 and 10 months of age, 25% had confirmed diagnosis of lymphoma, and 50% developed abdominal and/or hepatic tumors by 18 months of age. Histological examination showed loss of splenic architecture and increased cellularity. Lymph nodes showed disrupted architecture with effaced follicles and other pathological changes, including signs of angiofollicular lymphoid hyperplasia. One of the livers showed signs of angiosarcoma. In summary, our histology results revealed pathological changes in K1 transgenic mice similar to lymphoma, Castleman’s disease, and angiosarcoma, suggesting that K1 may contribute to the development of KSHV-associated cancers.
- PublicationOpen AccessAssessment of murine brain tissue shrinkage caused by different histological fixatives using magnetic resonance and computed tomography imaging(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Wehrl, Hans F.; Bezrukov, Ilja; Wiehr, Stefan; Lehnhoff, Mareike; Fuchs, Kerstin; Mannheim, Julia G.; Quintanilla-Martine, Leticia; Kohlhofer, Ursula; Kneilling, Manfred; Pichler, Bernd J.; Sauter, Alexander W.Especially for neuroscience and the development of new biomarkers, a direct correlation between in vivo imaging and histology is essential. However, this comparison is hampered by deformation and shrinkage of tissue samples caused by fixation, dehydration and paraffin embedding. We used magnetic resonance (MR) imaging and computed tomography (CT) imaging to analyze the degree of shrinkage on murine brains for various fixatives. After in vivo imaging using 7 T MRI, animals were sacrificed and the brains were dissected and immediately placed in different fixatives, respectively: zinc-based fixative, neutral buffered formalin (NBF), paraformaldehyde (PFA), Bouin-Holland fixative and paraformaldehyde-lysine-periodate (PLP). The degree of shrinkage based on mouse brain volumes, radiodensity in Hounsfield units (HU), as well as non-linear deformations were obtained. The highest degree of shrinkage was observed for PLP (68.1%, P<0.001), followed by PFA (60.2%, P<0.001) and NBF (58.6%, P<0.001). The zinc-based fixative revealed a low shrinkage with only 33.5% (P<0.001). Compared to NBF, the zinc-based fixative shows a slightly higher degree of deformations, but is still more homogenous than PFA. Tissue shrinkage can be monitored non-invasively with CT and MR. Zinc-based fixative causes the smallest degree of brain shrinkage and only small deformations and is therefore recommended for in vivo ex vivo comparison studies.
- PublicationOpen AccessSIP1 predicts progression and poor prognosis in pharyngeal squamous cell carcinoma(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Jouppila-Mättö, Anna; Mannermaa, Arto; Sironen, Reijo; Kosma, Veli-Matti; Soini, Ylermi; Pukkila, MattiObjectives: The epithelial-mesenchymal transition (EMT) is a crucial process in tumorigenesis that enables tumor cells to invade and metastasize. The transcription factors SIP1, SLUG, ZEB1, SNAI1, and TWIST are fundamental in regulating EMT. We investigated the relationships between several clinicopathological variables, prognosis, and SIP1, SLUG, or ZEB1 in a retrospective pharyngeal squamous cell carcinoma (PSCC) cohort. Study Design: Immunohistochemistry was used to evaluate the expression of SIP1, SLUG, and ZEB1 in 108 tumor samples from a retrospective cohort of patients with PSCC. Results: Tumors with positive epithelial SIP1 immunostaining were more advanced (SIII-IV, p=0.02) and had more lymph node metastases (p=0.04) than SIP1-negative tumors. Tumors with positive stromal staining of SIP1 relapsed more often than SIP1-negative tumors (p=0.007). Negative SIP1 immunoreactivity correlated significantly with better disease-specific survival (DSS) and better overall survival (OS) (p=0.012 and p=0.003 for epithelial reactivity, p=0.018 and p=0.003 for stromal reactivity, respectively). Lack of epithelial SIP1 expression remained an independent and favorable prognostic factor in a Cox proportional hazards model (p=0.046), together with high Karnofsky performance status score and low T class (p<0.001 for both). Co-expression of SNAI1, TWIST, and SIP1 in tumor epithelium predicted even shorter DSS than SIP1 expression alone (p<0.001) in the present study cohort. Conclusions: SIP1 is related to cancer progression and appears to be an independent prognostic factor in PSCC.
- PublicationOpen AccessMast cells or not? - CD117 positive cells in esophageal leiomyoma(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Ye, Ju Xiang; Liu, Yan; Qin, Yun; Ma, Xiao Long; Zhong, Hao Hao; Zhang, Yan; Shi, Xue YingThe presence of CD117 positive cells in esophageal leiomyoma may lead to a misdiagnosis of GIST. We reviewed 46 esophageal tumors which were smooth muscle tumors or GIST. Based on morphology, immunohistochemistry and mutation analysis, there were 44 (95.6%) leiomyomas, 1 (2.2%) leiomyosarcoma, and 1 (2.2%) GIST. Variable numbers of CD117 positive cells were seen in all leiomyomas. Tryptase immunostaining identified mast cells in 93.2% (41/44) of leiomyomas, and the number of mast cells per tumor decreased significantly from tumors of the upper esophagus to the esophageal-gastric junction (p<0.01). Immunofluorescence study further confirmed the presence of two types of CD117 positive spindle cells which included spindle-shaped mast cells and DOG-1- positive interstitial cells of Cajal. This is the first study to systemically review mast cells in esophageal leiomyomas and tumors which may be included in the differential diagnosis. We demonstrate that both spindled mast cells and hyperplastic interstitial cells of Cajal are present within esophageal leiomyomas. The immunoreactivity of these cells with CD117 may suggest a diagnosis of GIST, but the presence of mast cells itself supports a diagnosis of esophageal leiomyoma.
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