Pathology - Research and Practice Journal Impact Factor & Information

Publisher: Elsevier

Journal description

Pathology, Research and Practice provides accessible coverage of the most recent developments across the entire field of pathology: Reviews focus on recent progress in pathology, while Comments look at interesting current problems and at hypotheses for future developments in pathology. Original Papers present novel findings on all aspects of general, anatomic and molecular pathology. Rapid Communications inform readers on preliminary findings that may be relevant for further studies and need to be communicated quickly. Teaching Cases look at new aspects or special diagnostic problems of diseases and at case reports relevant for the pathologist's practice.

Current impact factor: 1.40

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 1.397
2013 Impact Factor 1.562
2012 Impact Factor 1.213
2011 Impact Factor 1.213
2010 Impact Factor 1.258
2009 Impact Factor 1.219
2008 Impact Factor 1.029
2007 Impact Factor 1.08
2006 Impact Factor 0.892
2005 Impact Factor 1.049
2004 Impact Factor 0.681
2003 Impact Factor 0.821
2002 Impact Factor 0.85
2001 Impact Factor 1.163
2000 Impact Factor 0.009
1999 Impact Factor 0.729
1998 Impact Factor 1.068
1997 Impact Factor 0.753

Impact factor over time

Impact factor

Additional details

5-year impact 1.43
Cited half-life 7.90
Immediacy index 0.26
Eigenfactor 0.00
Article influence 0.35
Website Pathology, Research & Practice website
Other titles Pathology, research and practice (Online)
ISSN 0344-0338
OCLC 51232024
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Sarcoma with CIC-DUX4 gene fusion is emerging as the most prevalent subset of Ewing-like undifferentiated small round cell sarcomas with around 50 cases published. We report hereby the case of a 40-year-old male who presented a CIC-DUX4 sarcoma in deep soft tissues in his thigh. He had been diagnosed with neurofibromatosis type 1 at age 19 and over the years underwent resection of multiple neural neoplasms, including two malignant peripheral nerve sheath tumors with classical spindle-cell histopathology. The CIC-DUX4 sarcoma was treated with surgical resection, radiation and chemotherapy, but lung and brain metastases developed and the patient died from the disease 14 months after diagnosis. This is the first case of sarcoma with CIC-DUX4 gene fusion reported in a patient with NF1. Whether this association is coincidental or CIC-DUX4 sarcomas could be related to NF1 remains to be clarified. Study of alternative molecular alterations in EWSR1-negative undifferentiated small round cell sarcomas is clinically relevant, since CIC-DUX4 sarcomas seem to be a very aggressive subset with poor response to the presently used therapeutic regimens.
    Pathology - Research and Practice 09/2015; DOI:10.1016/j.prp.2015.08.003.
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    ABSTRACT: Multistep carcinogenesis involves loss of function of tumor suppressor proteins such as p53 and induction of angiogenesis. Such mechanisms contribute to cutaneous squamous cell carcinoma progression and may be interconnected. We aimed to explore p53 immunoexpression in spectral stages of cutaneous squamous cell carcinoma and correlate expression to both neovascularization and cellular proliferation. We estimated the percentages of immunostained cells for p53 and Ki67 (proliferation marker) in three groups: 23 solar keratoses, 28 superficially invasive squamous cell carcinomas and 28 invasive squamous cell carcinomas. The Chalkley method was used to quantify the microvascular area by neoangiogenesis (CD105) immunomarker in each group. There was no significant difference for rate of p53- and Ki67-positive cells between groups. Significant positive correlation was found between the CD105 microvascular area and the rate of p53 positive cells in superficially invasive squamous cell carcinoma as well as between the rate of p53- and Ki67-positive cells in invasive squamous cell carcinoma. p53 and Ki67 immunoexpression did not increase with cutaneous squamous cell carcinoma progression. Neovascularization in the initial stage of invasion and proliferative activity in the frankly invasive stage were both associated with p53 immunoexpression. Loss of p53 tumor suppressor function through progressive steps may be directly involved in skin carcinogenesis.
    Pathology - Research and Practice 07/2015; DOI:10.1016/j.prp.2015.07.006.
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    ABSTRACT: Recently, there are several studies about cancer stem cells (CSC), indicating that they are the cells that initiate the tumor, provide progression, metastasis and responsible for the aggressive tumor behavior. The purpose of this study is to investigate the expressions of CD24, CD44, their different combinations, ALDH1 and CD133 in invasive ductal carcinoma. Their relationships with clinicopathologic parameters, such as tumor grade, lymphovascular invasion, tumor size, axillary lymph node involvement, stage, hormone receptors, HER2 expression, basal like tumors, triple negative status and prognosis were also investigated. Tissue microarray method was used to investigate ımmunohistochemical CD24, CD44, ALDH1 and CD133 expressions in 105 invasive ductal carcinoma cases. CD133 expression was significantly associated with tumor size (p=0.023) and stage (p=0.009). CD133 expression was decreased in tumors with larger tumor size, higher stage and lymphovascular invasion. CD133 expression was positively correlated with CD44 (r=0.212, p=0.032) and CD44(+)/CD24(+) (r=0.202, p=0.040) expressions. CD44, CD24 and ALDH1 expressions showed no significant relationship and correlation with clinicopathologic features. There was a significant relationship (p=0.048) between CD44(+)/CD24(-/low) phenotype and basal like tumors. EGFR expression was positively correlated with CD44(+)/CD24(-/low) phenotype (r=0.211, p=0.036). Basal like tumors are enriched for CSCs with CD44(+)/CD24(-/low) phenotype. CD133 can detect a different population of CSC in breast carcinoma. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 06/2015; DOI:10.1016/j.prp.2015.05.011
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    ABSTRACT: The aim of this study was to explore the difference in high mobility group A1 (HMGA1) expression and isocitrate dehydrogenase (IDH) 1 R132H point mutation in initial and recurrent glioblastoma multiforme (GBM), and to further identify whether the expression of HMGA1 has a role in the malignant progression of GBM. Paired initial and recurrent GBM specimens from the same patient were evaluated using immunohistochemical analysis. The association between HMGA1 expression and progression-free survival time (PFST) was analyzed. Three patients were confirmed with IDH-1 R132H mutations in both initial and recurrent groups (3/25, 12%). There was a significant difference in HMGA1 expression between initial and recurrent GBM (P=0.002), and patients with tumors expressing HMGA1 at higher level had a significantly shorter PFST (7.3 months versus 11.1months; P=0.044). Our study indicates that recurrent GBM express HMGA1 at a higher level and that HMGA1 overexpressoin is associated with shorter PFST in patients with GBM. These findings suggest that HMGA1 potentially plays an important role in the treatment of GBM. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 05/2015; 211(8). DOI:10.1016/j.prp.2015.05.004
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    ABSTRACT: KRAS mutation status has predictive significance in EGFR-antibody treatment of colorectal adenocarcinoma. The aim of the study was the evaluation of KRAS mutation status in correlation to KRAS copy numbers and ploidy status. Colorectal adenocarcinomas (n=52) were assembled into a TMA and analyzed by FISH. Probes for centromeres 4 and 10 were applied as surrogate markers for the ploidy status. In addition, a dual color FISH probe set for the centromere of chromosome 12 and the KRAS gene was applied to the TMA to analyze numerical alterations and KRAS gene copy numbers. Further we analyzed DNA sequence profiles of KRAS codons 12 and 13 to assess the allele status of the mutation within the tumor samples. KRAS mutation was confirmed in 24 cases, while 28 cases showed a wild-type KRAS status. The majority of cases showed diploid FISH signals for chromosomes 4 and 10. Near triploid FISH signals were observed in only 2 cases, 12 cases were hypodiploid, and 8 cases were hyperdiploid. In 6 cases, trisomy 12 could be ascertained. In total, aneuploidy could be detected in 28 cases, including cases with trisomy 12 and hyposomy 10. Tumors with aneuploid chromosomal content had a worse prognosis compared to euploid tumors, however, without reaching statistical significance (p=0.231). Hypodiploid carcinomas carried the worst prognosis. Specifically, monosomy 10 was significantly associated with reduced survival (p=0.039). Increased FISH signals of KRAS did not correlate significantly with relapse (p=0.916). FISH analysis can be used as a surrogate marker for the ploidy status. Loss of chromosome 10 may serve as a potential adverse prognostic marker being indicative for tumor progression. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 05/2015; 211(9). DOI:10.1016/j.prp.2015.05.008
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    ABSTRACT: Little is known about the squamous morular component (SMC) in colorectal neoplasms because of its rarity. The aim of the present study is to elucidate the morphological, immunohistochemical and genetic characteristics of SMCs in colorectal adenomas. Five colorectal adenomas having SMCs were resected from five patients endoscopically. On immunohistochemical examination (four cases), all SMCs were positive for cytokeratin 5/6 in their cytoplasm and positive for β-catenin in their cytoplasm and nuclei. A nuclear positivity of p63 was detected in one SMC. All SMCs were negative for p53, chromogranin A, synaptophysin and NCAM. There was no Ki-67 expression in any of the SMCs. We detected none of mutations of β-catenin, KRAS and BRAF by microdissection and polymerase chain reaction-direct sequence in any of the four examined SMCs. SMCs are a rare but problematic finding in colorectal adenomas. Using immunohistochemistry for β-catenin, cytokeratin 5/6, Ki-67, p53, chromogranin A, synaptophysin and NCAM can facilitate the diagnosis of these peculiar cell nests. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 05/2015; DOI:10.1016/j.prp.2015.05.002
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    ABSTRACT: We characterize invasive urothelial carcinoma (UC) exhibiting urothelial basal cell immunohistochemical markers. Consecutive invasive UCs were immunostained with CK20 and urothelial basal cell markers, cytokeratin 5 (CK5)/CD44. Immunostaining for CK5 and CD44 was scored as follows: positive for staining of more than 25% thickness of the epithelial nest or epithelium and low for lesser immunoreactivity. Invasive urothelial carcinoma (UC) exhibiting positive CK5/CD44 staining was designated as basal-like UC (BUC). In this study, of 251 invasive UC (pT1 in 57% and pT2-4 in 43%), BUC accounted for 40% of cases (accounting for most pT2-4 UC) and often presented as non-papillary UC without previous history of UC. In addition, BUC exhibited uniform nuclei with lesser degree of atypia than non BUC and decreased or negative cytokeratin 20 reactivity. Nested and microcystic variants of UC immunohistochemically stained as BUCs. Invasive non-BUCs were often papillary with marked cytologic atypia and pleomorphism, and accounted for most pT1 UC. The rates of perivesical invasion, lymph node and distant metastases were higher for BUC than non-BUC. All nine cases with absent/minimal residual in situ UC in 102 radical cystectomy specimens were from invasive non-BUC. BUC is distinguished from non-BUC due to this aggressive behavior, distinct immunohistochemical profile, and predominant non-papillary architecture. Our findings are consistent with recent studies identifying a subtype of muscle-invasive UC with molecular expression of basal cell and luminal cell molecular profiles. Our study further supports categorizing invasive UCs into these subtypes with different biological behaviors, possibly contributing to better therapeutic strategies. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 05/2015; 211(8). DOI:10.1016/j.prp.2015.05.005
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    ABSTRACT: The increased risk of malignancy in the post-renal transplant population has been well documented. Renal carcinoma is more common in this population, usually arising in native kidneys. Rarely, tumors arise in the transplanted kidney. Our case series reports four cases of malignancy in allograft kidneys, one of which is a first reported case of translocation RCC in a transplanted kidney. The renal transplantation database (1584 patients) at St. Michael's Hospital was reviewed for malignancies arising in allograft kidneys: reports and pathology slides were reviewed. Four cases of malignancies arising in the allograft kidney were identified among our kidney transplant population. One patient developed a high grade urothelial carcinoma in the donor kidney post BK virus infection. The other 3 cases were renal cell carcinomas: one clear cell renal cell carcinoma, one translocation renal cell carcinoma, and one papillary renal cell carcinoma. The translocation renal cell cancer had confirmed TFE3 protein over-expression by immunohistochemistry. Molecular testing of the tumors in all 4 cases identified two separate genetic profiles, favored to represent tumors arising from donor tissues along with infiltrating recipient lymphocytes. Previous reports suggested that epithelial malignancies in allograft kidneys are rare. We identified 4 such tumors in 1584 transplant patients. Further, we identified the first reported case of translocation RCC in an allograft kidney. While the rate of malignancy in allograft kidneys is low, screening of the donor kidneys by ultrasound and/or urine cytology may be of use in detecting these lesions. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 04/2015; 211(8). DOI:10.1016/j.prp.2015.04.009
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    ABSTRACT: Blue nevus, a pigmented skin lesion, affects the dermal melanocytes that are rich in melanin. Its occurrence on skin has been well described in literature. Less commonly, involvement of mucosal surfaces especially genitourinary tract has also been noticed. Here we present a rare case of a blue nevus involving the rectum. So far there has been only one prior description of the blue nevus involving the gastrointestinal mucosa. Differentiation of this lesion from melanoma is the key. Simple excision of the blue nevus with a biopsy forceps during the colonoscopy is an effective management. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 04/2015; 211(8). DOI:10.1016/j.prp.2015.04.007
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    ABSTRACT: Gastrokine 1 (GKN1) is a stomach-specific protein important in the replenishment of the surface lumen epithelial cell layer and in maintaining mucosal integrity. A role in cell proliferation and differentiation has also been hypothesized. Despite these findings, the function(s) as well as the cellular localization of GKN1 in the cellular machinery are currently not clarified. The investigation of subcellular localization of GKN1 in gastric cancer cells can provide insights into its potential cellular roles. Subcellular fractions of gastric cancer cells (AGS) transfected with full-length GKN1 (flGKN1) or incubated with recombinant GKN1 (rGKN1) lacking the first 20 amino acids at N-terminal were analyzed by Western blot and confocal microscopy and compared with those from normal gastric tissue. Wild type GKN1 (wtGKN1) and flGKN1 were revealed in the cytoplasm and in the membrane fractions of gastric cells, whereas rGKN1 was revealed in the cytoplasmic fractions, but a high amount was detected in the membrane pellet of the AGS lysate. The cellular distribution of GKN1 was also confirmed by confocal microscopy. The purified protein was also used to highlight its possible association with actin through confocal microscopy, pelleting assay, and size-exclusion chromatography. GKN1 co-localizes with actin in normal gastric tissue, but no direct interaction was observed between the two proteins in vitro. Most likely, GKN1 indirectly participates in actin stabilization since its overexpression in gastric cancer cells strongly increases the expression of tight and adherens junction proteins. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 04/2015; 211(8). DOI:10.1016/j.prp.2015.04.008
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    ABSTRACT: Primary or metastatic melanocytic tumors in the sellar region are rare and can pose a diagnostic challenge. Here we describe a case of a 74-year-old man who underwent radiological investigations for a transient episode of blurred vision. Based on the clinical and endocrinological findings and MRI results, the patient was assumed to have a clinically non-functioning pituitary macroadenoma, which was followed-up over a 2-year period. He did not have any endocrine symptoms or progressive visual deterioration, and no history of past malignancy, including melanoma. Endocrinological investigation was unremarkable; blood hormone levels were within the normal ranges except for low serum total testosterone and bioavailable testosterone levels without symptoms of hypogonadism. The longitudinal MRI follow-up demonstrated a gradual increase in the size of the tumor over the course of 11 months. For this reason, the patient underwent surgery. Pathologic examination including histology, immunohistochemistry and electron microscopy achieved the correct diagnosis of melanocytic tumor of the sellar region morphologic examination is essential in the diagnosis of melanocytic tumors. Hmb-45 is an important diagnostic biomarker in melanocytic lesions. The use and exploration of miRNA, Ki67 and osteopontin are important in understanding the genesis, progression, and prognosis in treatment of patients with melanocytic tumors. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 04/2015; 211(9). DOI:10.1016/j.prp.2015.04.005
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    ABSTRACT: Kidney sarcomas are rare, representing only 1% of malignant renal tumors. We herein report the case of a 70-year-old woman that was admitted for an episode of confusion in relation to hypertensive encephalopathy. Imaging investigations revealed a large mass in the right kidney with extension to the renal hilum. The patient underwent right open radical nephrectomy. The histopathologic study disclosed a 15-cm, myxoid and cellular, pleomorphic tumor with elongated, curvilinear, thin-walled vessels, and focal necrosis that involved the upper and middle segments of the kidney. Immunohistochemically, the tumor cells showed strong positivity for vimentin, bcl2 protein (nuclear staining pattern), CD34, CD99, and alpha-methylacyl coenzyme A racemase. The tumor was diagnosed as myxofibrosarcoma (MFS) grade 2 according to the FNCLCC system. To the best of our knowledge, this is the first report of an MFS arising from the kidney. Thus, MFS is an uncommon soft tissue tumor that can exceptionally arise from the kidney. The differential diagnosis with other myxoid tumors is of vital importance because it includes lesions with subtle differences and extremely variable biological behavior. Radical surgery is the treatment of choice. Long-term follow-up is recommended because of the tumor's capability for local recurrence and distant metastasis. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 04/2015; 211(8). DOI:10.1016/j.prp.2015.04.004
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    ABSTRACT: Infiltrating angiolipoma and osteolipoma of the hand are rare. A 40-year-old man presented with slowly enlarging swelling of his right hand for two and half years without functional deficit but it became painful with slight limitation of movement for the past few months. Plain radiograph showed a large soft tissue swelling with specks of calcifications. Ultrasonography and magnetic resonance imaging revealed an infiltrative mass in the right palm deep to the flexor tendons. As biopsy suggested infiltrative angiolipoma of skeletal muscle, debulking of the tumor was performed. The tumor showed coexistence of all four mesenchymal elements, fat, blood vessel, smooth muscle and bone in various combinations in the form of angiolipomatous, osteolipomatous, ossified intramuscular hemangiomatous, myolipomatous and angiomyolipomatous patterns throughout the entire tumor. Small meningothelial-like whorls of spindle cells were focally seen, some showed intramembranous ossification forming small woven bony spicules in their centers. There were no atypical cells or lipoblasts. Staining for CDK4, MDM2, p16, HMB45 and Melan A was negative. The diagnosis was "infiltrating hybrid mesenchymal tumor of skeletal muscle showing lipomatous, hemangiomatous, leiomyomatous and osseous features". The fairly even admixture of the various components supports the neoplastic participation of each individual element. Hybrid mesenchymal tumor most probably originates from multipotent neoplastic cells showing multidirectional differentiation. Copyright © 2015 Elsevier GmbH. All rights reserved.
    Pathology - Research and Practice 03/2015; 211(6). DOI:10.1016/j.prp.2015.02.007
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    ABSTRACT: The aim of the present study was to determine the chemokine RANTES (regulated on activation, normal T-cell expressed, and secreted) levels in plasma and atherosclerotic plaques and to assess their diagnostic efficacy in the evaluation of vulnerable plaques. The rabbit models of vulnerable atherosclerotic plaque (VAP) were established by high fat diet and pharmaceutical triggering. The serum RANTES levels of VAP group (91.97 ± 8.51 ng/ml) were significantly higher than that of AS (atherosclerosis) group (50.03 ± 2.92 ng/ml). Consistently, the mRNA and protein of RANTES in vulnerable atherosclerotic plaques were also obviously up-regulated compared to AS group (P < 0.01). Moreover, corrected plaque area and vulnerability index of VAP group proved to be significantly higher than AS group. The correlation coefficient between RANTES and plaque vulnerability indicated that RANTES, especially plaque RANTES, was positively correlated with VAP. In addition, increased expression of Nuclear factor kappa B p65 (NF-κB p65) was observed in VAP group compared to AS group (P < 0.05), which partly accounted for the increased RANTES levels. In conclusion, positive associations between RANTES and plaque vulnerability suggest that higher RANTES levels may be associated with atherosclerosis and high-risk plaques. Our study highlights the utility of both serum and plaque RANTES levels as indicators of plaque vulnerability in the field of preventive cardiology.
    Pathology - Research and Practice 12/2014; 210(12). DOI:10.1016/j.prp.2014.03.012
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    ABSTRACT: Inflammatory myofibroblastic tumor is an uncommon tumor regarded as “intermediate malignancy”. We present the clinical, pathological and molecular features of a mesenteric inflammatory myofibroblastic tumor in a 9-month-old male infant. The patient was referred to Anna Meyer Children Hospital of Florence, Italy, for an asymptomatic abdominal mass measuring about 7 cm. The lesion was radically excised, and the postoperative course was uneventful. Histologically, the tumor was composed of spindle cells immunopositive for vimentin and desmin admixed with an inflammatory infiltrate. Rearrangement of ALK gene was demonstrated by FISH and immunohistochemistry (cytoplasmic, perinuclear and punctate immunocoloration). The peculiar punctate ALK immunocoloration suggested a possible unusual ALK gene rearrangement involving the CLTC gene.
    Pathology - Research and Practice 12/2014; 210(12). DOI:10.1016/j.prp.2014.03.011
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    ABSTRACT: Temsirolimus acts as a mammalian target of rapamycin (mTOR)-dependent autophagic inhibitor. In order to clarify its effects and mechanisms on human salivary adenoid cystic carcinoma (ACC), we examined that whether temsirolimus induced autophagy as the mTOR inhibitor in ACC, both in vitro and in vivo. In this study, MTT assay showed that the inhibition effect of temsirolimus assumed an obvious dose-response relationship on ACC-M cells, and the 50% inhibitory concentration (IC50) approached 20 μmol/l; numerous autophagosomes were observed by the transmission electron microscopy (TEM) in temsirolimus treatment groups; what's more, expression of LC3 and Beclin1 was significantly up-regulated by temsirolimus. More importantly, the xenograft model provided further evidence of temsirolimus-induced autophagy in vivo, by inhibiting mTOR activation as well as up-regulation the expression of Beclin1. These results suggest that temsirolimus could act as an mTOR inhibitor to induce autophagy in adenoid cystic carcinoma both in vitro and in vivo.
    Pathology - Research and Practice 11/2014; 210(11). DOI:10.1016/j.prp.2014.03.008
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    ABSTRACT: Background and aims: TRAF2- and NCK-interacting kinase (TNIK) is a member of the germinal center kinase family and a transcription factor 4 (TCF4) interactor is recruited to promoters of Wnt target genes via phosphorylation of the TCF/β-catenin complex. The aim of this study was to evaluate the TNIK, the active form of TNIK (p-TNIK), and β-catenin expression in hepatocellular carcinoma (HCC), and to identify the prognostic significance of p-TNIK. Methods: We assessed the expression status of TNIK, p-TNIK, and β-catenin by using immunohistochemical analysis of 302 HCCs in 8 tissue microarray blocks, and we evaluated their clinicopathologic features and survival rates based on their p-TNIK expression. Results: Of 302 HCCs, 92.7% stained positive for TNIK in the cytoplasm. Nuclear expression of p-TNIK was identified in 7.9% HCCs. Aberrant cytoplasmic expression of β-catenin was identified in 77.2% and nuclear expression in 3.3%. p-TNIK nuclear staining was positively correlated to β-catenin nuclear expression (P=0.036). Cytoplasmic and nuclear expression of p-TNIK was more frequently observed in high Edmondson-Steiner (ES) nuclear grade groups (P=0.030). Nuclear p-TNIK expression was also associated with pathological M1 stage (pM1 stage) patients (P<0.0001). Aberrant cytoplasmic expression of β-catenin was more frequently identified in larger tumors (P=0.014). Univariate (DFS, P=0.049; OS, 0.037) and multivariate analysis (DFS, P=0.006; OS, P=0.003) confirmed the independent prognostic significance of nuclear p-TNIK expression. Conclusion: This is the first time that nuclear p-TNIK expression was studied in HCC, and p-TNIK nuclear expression was associated with poor prognosis and is a candidate prognostic marker for HCC.
    Pathology - Research and Practice 10/2014; 210(10). DOI:10.1016/j.prp.2013.10.007