Stable ARMADILLO REPEAT KINESIN 2 in light inhibits hypocotyl elongation and facilitates light-induced cortical microtubule reorientation in Arabidopsis.

Hypocotyls undergo different morphogenesis in light and dark conditions, with cortical microtubules being reoriented in response to light to coordinate cell growth status. Kinesins are microtubule-based motor proteins that are mostly responsible for transporting organelles and vesicles, although some can also regulate microtubule organization; however, it is currently not known whether they are involved in microtubule reorientation and hypocotyl elongation. In this study, we found that ARMADILLO REPEAT KINESIN 2 (ARK2) negatively regulated the hypocotyl elongation of Arabidopsis. The hypocotyl cells of plants with the ark2 null allele were longer than those of the wild type and had relatively more transversely arranged cortical microtubules. In addition, ARK2 co-localized with cortical microtubules and facilitated the light-induced reorientation of the cortical microtubule arrays. Interestingly, the ARK2 protein is stable in the light and degraded through the 26S proteasome pathway in the dark. Furthermore, we determined that ARK2 could interact with the E3 ubiquitin ligase CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), which contributed to down-regulation of ARK2 in darkness that might benefit hypocotyl growth in the dark.

ARK2 stabilizes the plus-end of microtubules and promotes microtubule bundling in Arabidopsis.

Microtubule dynamics and organization are important for plant cell morphogenesis and development. The microtubule-based motor protein kinesins are mainly responsible for the transport of some organelles and vesicles, although several have also been shown to regulate microtubule organization. The ARMADILLO REPEAT KINESIN (ARK) family is a plant-specific motor protein subfamily that consists of three members (ARK1, ARK2, and ARK3) in Arabidopsis thaliana. ARK2 has been shown to participate in root epidermal cell morphogenesis. However, whether and how ARK2 associates with microtubules needs further elucidation. Here, we demonstrated that ARK2 co-localizes with microtubules and facilitates microtubule bundling in vitro and in vivo. Pharmacological assays and microtubule dynamics analyses indicated that ARK2 stabilizes cortical microtubules. Live-cell imaging revealed that ARK2 moves along cortical microtubules in a processive mode and localizes both at the plus-end and the sidewall of microtubules. ARK2 therefore tracks and stabilizes the growing plus-ends of microtubules, which facilitates the formation of parallel microtubule bundles.

[Effect of baicalin on inflammatory response and TLR4/NF-κB signaling pathway of human brain microvascular endothelial cell after hypoxia-reoxygenation injury].

In this study, the oxygen-glucose deprivation(OGD) model in the human brain microvascular endothelial cell(HBMEC) was used to simulate the ischemic neuronal damage and observe the inflammatory response, explore the possible mechanisms for treating cerebral ischemia/reperfusion and improving memory impairment from the view point of inhibiting inflammatory response, which is of great reference significance for related Chinese medicine treatment of ischemic diseases. HBMECs were given with drugs at the same time of OGD injury, and reoxygenated for 2 h after 4 h treatment. Cell supernatant was then collected, and the inflammatory factors in cell supernatant were detected. Immunofluorescence assay was used to detect HBMECs morphology and expression of p-nuclear factor kappa-light-chain-enhancer of activated B(p-NF-κB); Western blot was used to detect expression changes of Toll like receptor 4(TLR4), myeloid differentiation primary response 88(MYD88) and p-NF-κB. The results showed that, after OGD modeling, the levels of interleukin 6(IL-6), IL-1α, IL-1ß and tumor necrosis factor-α(TNF-α) were significantly increased; baicalin protected HBMEC, inhibited intranuclear transcription of p-NF-κB, significantly decreased HBMEC release of inflammatory factors caused by OGD injury, and inhibited the expression of TLR4, MYD88, and p-NF-κB. The studies suggested that baicalin had obvious protective effect on HBMECs damaged by OGD, and could inhibit inflammatory response. Its protection mechanism may be related to inhibiting TLR4 signaling pathways.

Rab-H1b is essential for trafficking of cellulose synthase and for hypocotyl growth in Arabidopsis thaliana.

Cell-wall deposition of cellulose microfibrils is essential for plant growth and development. In plant cells, cellulose synthesis is accomplished by cellulose synthase complexes located in the plasma membrane. Trafficking of the complex between endomembrane compartments and the plasma membrane is vital for cellulose biosynthesis; however, the mechanism for this process is not well understood. We here report that, in Arabidopsis thaliana, Rab-H1b, a Golgi-localized small GTPase, participates in the trafficking of CELLULOSE SYNTHASE 6 (CESA6) to the plasma membrane. Loss of Rab-H1b function resulted in altered distribution and motility of CESA6 in the plasma membrane and reduced cellulose content. Seedlings with this defect exhibited short, fragile etiolated hypocotyls. Exocytosis of CESA6 was impaired in rab-h1b cells, and endocytosis in mutant cells was significantly reduced as well. We further observed accumulation of vesicles around an abnormal Golgi apparatus having an increased number of cisternae in rab-h1b cells, suggesting a defect in cisternal homeostasis caused by Rab-H1b loss function. Our findings link Rab GTPases to cellulose biosynthesis, during hypocotyl growth, and suggest Rab-H1b is crucial for modulating the trafficking of cellulose synthase complexes between endomembrane compartments and the plasma membrane and for maintaining Golgi organization and morphology.

Expression and clinical implications of HAb18G/CD147 in hepatocellular carcinoma.

AIM: HAb18G/CD147 is an important factor in invasion and metastasis of hepatocellular carcinoma (HCC). However, the clinical implications of HAb18G/CD147 expression in HCC are still unclear. In this study, we clarify the clinical significance of HAb18G/CD147. We characterize the association between HAb18G/CD147 expression and presentation of fibrosis or chronic hepatitis B, as well as its effect on HCC development. METHODS: The expression of HAb18G/CD147 in human hepatocarcinoma cell lines was analyzed by reverse transcription polymerase chain reaction and western blotting. Tumor tissues were obtained from HCC patients who underwent surgical resection between 2002 and 2006. All patients who had received previous therapy were excluded. HCC tissues were analyzed by immunohistochemistry using anti-HAb18G/CD147. RESULTS: HAb18G/CD147 was widely expressed in Hep-G2, SMCC-7721 and BEL7402 cell lines, but not expressed in L-02, a human normal hepatic cell line. HAb18G/CD147 was mainly localized to the membrane of tumor cells in 74.0% (37/50) HCC patients. We found that higher HAb18G/CD147 expression and poor tumor differentiation were correlated with patient survival (P = 0.026 and P = 0.014, respectively). Furthermore, the distribution of HAb18G/CD147 was similar to that of hepatitis B virus (HBV) infection, but negatively related to hepatic cirrhosis. CONCLUSION: HAb18G/CD147 has shown its potentials in HCC development and patient survival. Moreover, it may also cooperate with chronic HBV infection and cirrhosis during HCC development. Its functions in the two factors may be different. Therefore, HAb18G/CD147 may be a marker for poor prognosis in HCC patients and could be a useful therapeutic target for interfering with or reversing HCC progression.

Proteomics analysis of coronary atherosclerotic heart disease with different Traditional Chinese Medicine syndrome types before and after percutaneous coronary intervention.

OBJECTIVE: To investigate the underlying protein molecular mechanisms of "Qi stagnation and blood stasis syndrome" (QS) and "Qi deficiency and blood stasis syndrome" (QD), as two subtypes of coronary artery disease (CAD) in Traditional Chinese Medicine (TCM), following percutaneous coronary intervention (PCI). METHODS: In this study, a total of 227 CAD patients with QS and 211 CAD patients with QD were enrolled; all participants underwent PCI. Label-free quantification proteomics were employed to analyze the changes in serum in two subtypes of CAD patients before and 6 months after PCI, aiming to elucidate the intervention mechanism of PCI in treating CAD characterized by two different TCM syndromes. RESULTS: Biochemical analysis revealed significant changes in tumor necrosis factor-α, high density lipoprotein cholesterol, blood stasis clinical symptoms observation, and Gensini levels in both patient groups post-PCI; Proteomic analysis identified 79 and 95 differentially expressed proteins in the QS and QD patient groups, respectively, compared to their control groups. complement C8 alpha chain, complement factor H, apolipoprotein H, apolipoprotein B, plasminogen, carbonic anhydrase 2, and complement factor I were altered in both comparison groups. Furthermore, enrichment analysis demonstrated that cell adhesion and connectivity-related processes underwent changes in QS patients post-PCI, whereas lipid metabolism-related pathways, including the peroxisome proliferator-activated receptor signaling pathway and extracellular matrix receptor interaction, underwent changes in the QD group. The protein-protein interaction network analysis further enriched 52 node proteins, including apolipoprotein B, lipoprotein (a), complement C5, apolipoprotein A4, complement C8 alpha chain, complement C8 beta chain, complement C8 gamma chain, apolipoprotein H, apolipoprotein A-Ⅱ, albumin, complement C4-B, apolipoprotein C3, among others. The functional network of these proteins is posited to contribute to the pathophysiology of CAD characterized by TCM syndromes. CONCLUSION: The current quantitative proteomic study has preliminarily identified biomarkers of CAD in different TCM subtypes treated with PCI, potentially laying the groundwork for understanding the protein profiles associated with the treatment of various TCM subtypes of CAD.

The role of PTPN13 in invasion and metastasis of lung squamous cell carcinoma.

OBJECTIVES: PTPN13 is a new candidate tumor-suppressing gene. To investigate the PTPN13 expression and its potential function in the invasion and metastasis of lung squamous cell carcinoma (LSCC), we performed this study in 91 primary LSCC tissues and the adjacent non-cancerous tissues. METHODS: The mRNA expression of PTPN13 and FAK was quantitated by reverse transcription polymerase chain reaction. The protein expression of PTPN13, focal adhesion kinase (FAK) and phosphorylated FAK (P-FAK) was evaluated using immunohistochemical staining and western blotting. The association among PTPN13 expression, FAK expression and the clinicopathological parameters were analyzed. RESULTS: PTPN13 expression was down-regulated in LSCC, and was negatively correlated with the cancer grade and stage. FAK mRNA, as well as FAK protein level was elevated in LSCC tissues. P-FAK level, also found increased, had no association with FAK mRNA and FAK protein expression, but had a negative correlation with the PTPN13 expression. P-FAK level had a significant positive correlation with the TNM classification. CONCLUSION: The over-expression of FAK and increased FAK phosphorylation plays an important role in the invasion and metastasis of LSCC.

Clinical impact of HAb18G/CD147 expression in esophageal squamous cell carcinoma.

BACKGROUND: HAb18G/CD147 expression has been associated with many tumor invasion molecules, which play important roles in recurrence and poor differentiation of esophageal squamous cell carcinoma (ESCC). However, the clinical implications of HAb18G/CD147 in ESCC are still unclear. AIMS: In this study, we clarified the clinical significance of HAb18G/CD147 and characterized the association between HAb18G/CD147 and tumor invasion in ESCC cases. METHODS: Tumor tissues were obtained from 86 ESCC patients who underwent surgical resection between 2002 and 2005. All patients that had received previous therapy were excluded. ESCC tissues were analyzed by IHC using anti HAb18G/CD147 antibody. The expression of HAb18G/CD147 mRNA in esophageal cancer cell lines was analyzed by RT-PCR. RESULTS: HAb18G/CD147 was uniformly expressed in EC109 and EC871214 cell lines, but negatively expressed in EPC2, esophageal normal squamous cell line. HAb18G/CD147 mainly localized to the membrane of tumor cells in 84.9% of ESCC patients (64 out of 86 cases). Furthermore, we also found that higher HAb18G/CD147 expression levels significantly correlated with lymph node metastasis, depth of tumor invasion and differentiation (P < 0.05). But the expression levels of HAb18G/CD147 in lymph node metastatic tissues were almost equal to that in the primary tumor tissues. Furthermore, lymph node metastasis and expression of HAB18G/CD147 were independent prognostic indicators in ESCC. CONCLUSIONS: The expression of HAb18G/CD147 might be involved in the progression and survival of ESCC. Therefore, HAb18G/CD147 could be a clinical marker for the poor prognosis in ESCC patients and may also be a potentially therapeutic target to improve the progression of ESCC.

Detection of IgM and IgG Antibodies to Human Parvovirus B19 in Sera of Patients with Thymoma-Associated Myasthenia Gravis.

Much uncertainty still exists about the viral etiology of myasthenia gravis (MG). To address this, we explored the relationship between human parvovirus B19 (PVB19) infection and MG by investigating the presence of PVB19-specific antibodies in serum. A total of 131 patients with MG (including 47 with thymoma-associated MG, 14 with hyperplasia-associated MG, and 70 with unknown thymic lesions) and 172 healthy volunteers were enrolled in this study. Enzyme linked immunosorbent assay was conducted to detect virus-specific antibodies in cell-free serum. The data were analyzed using Pearson chi-square (χ2) and Fisher's exact tests. In the 131 patients with MG, there was no significant difference between male (53.41 ± 14.65 years) and female (50.19 ± 15.28 years) groups regarding mean age (p > 0.05). Among all MG subgroups, the largest age group comprised participants aged 30-60 years. We found that the frequency of detecting immunoglobulin G (IgG) antibodies against PVB19 VP1 and VP2 was significantly higher among patients with MG (68.70%) than in healthy controls (41.86%) (p < 0.001). In particular, the positive rate for anti-PVB19 IgG in patients with thymoma-associated MG (35/47, 74.47%) was significantly higher than that in healthy participants (72/172, 41.86%; p < 0.001). The findings of this study indicate that PVB19 infection may play a role in the etiopathogenesis of MG, particularly in patients with thymoma-associated MG. The study protocol was registered at ClinicalTrials.gov with the identifier ChiCTR-1900023338.

RICH2, a potential tumor suppressor in hepatocellular carcinoma.

Rho GTPase-activating proteins (RhoGAPs) are implicated in the development and progression of hepatocellular carcinoma (HCC). We tested the idea that RICH2 is a tumor suppressor in HCC. Consistent with this, RICH2 was downregulated in HCC and HCC cell lines and RICH2 expression negatively correlated with the tumor size, TNM stage and metastasis in HCC. RICH2, in a Cdc42 dependent manner, regulated the formation of filopodia in HCC and stable overexpression of RICH2 significantly inhibited the clone formation, proliferation and invasion of HCC cells in vitro. Gene set enrichment analysis (GSEA) showed that the expression of RICH 2 positively correlated with the expression of WNT5a, that exert antagonistic effect on canonical WNT signalling whereas RICH2 expression inversely correlated with the expression of ß-catenin (CTNNB1), that is involved in the proliferation and invasion HCC. These findings concurred with co-immunoprecipation of RICH2 with endogenous Cdc42, Rac1, and ß-catenin. Finally, RICH2 overexpression suppressed tumor growth in vivo. The findings support the idea that RICH2 might act as a tumor suppressor in HCC.

Downregulation of microRNA-1 in esophageal squamous cell carcinoma correlates with an advanced clinical stage and its overexpression inhibits cell migration and invasion.

Esophageal squamous cell carcinoma (ESCC) is one of most common and fatal forms of cancer worldwide. Recent studies have suggested that an aberrant microRNA (miRNA or miR) expression signature exists in ESCC. In the present study, in order to determine the involvement of miRNA in the development and progression of ESCC, the expression profiles of miRNA in 8 paired ESCC tissues and corresponding normal esophageal tissues were analyzed by miRNA microarray. A total of 43 differentially expressed miRNAs, including 27 downregulated and 16 upregulated miRNAs were found in the ESCC tissue samples. Among these miRNAs, we found that miR-1 was significantly downregulated. Subsequently, the expression of miR-1 was validated in 64 pairs of primary ESCC samples by RT-qPCR. The expression level of miR-1 was found to be frequently decreased, and significantly correlated with tumor invasion and an advanced clinical stage (P = 0.022 and P = 0.028, respectively). In addition, functional assays revealed that miR-1 inhibited cell proliferation, clonogenicity, cell invasion and migration. Bioinformatics analyses identified the major biological processes that were targeted by miR-1. These results suggest that miR-1 has a tumor-suppressive effect on the development and progression of ESCC. The findings of this study may contribute to the further understanding of the functions of miR-1 in ESCC.

Loss of heterozygosity at D8S262: an early genetic event of hepatocarcinogenesis.

BACKGROUND: Hepatocellular carcinoma (HCC) is a multi-factor, multi-step, multi-gene and complicated process resulting from the accumulation of sequential genetic and epigenetic alterations. An important change among them is from precancerous lesions to HCC. However, only few studies have been reported about the sequential genetic changes during hepatocarcinogenesis. METHODS: We observed firstly molecular karyotypes of 10 matched HCC using Affymetrix single-nucleotide polymorphism (SNP) 6.0 arrays, and found chromosomal fragments with high incidence (more than 70%) of loss of heterozygosity (LOH). Then, we selected 28 microsatellite markers at some gene spanning these chromosomal fragments, and examined the frequency of LOH of 128 matched HCC and 43 matched precancerous lesions-dysplastic nodules (DN) by a PCR-based analysis. Finally, we investigated the expression of proteins encoded by these genes in HCC, DN and the surrounding hepatic tissues. RESULTS: The result of Affymetrix SNP6.0 arrays demonstrated that more than 70% (7/10) cases had chromosomal fragment deletion on 4q13.3-35.1, 8p23.2-21.2, 16q11.2-24.3, and 17p13.3-12. Among 28 microsatellite markers selected, LOH frequencies at D8S262 for DN and HCC were found to be the highest, 51.2% and 72.7%, respectively. Immunohistochemically, the positive rate of its adjacent gene CSMD1 in HCC, DN, and the surrounding hepatic tissues were 27.3% (35/128), 75% (33/44), and 82% (105/128), respectively. CONCLUSIONS: LOH at D8S262 may be associated with an early genetic event of hepatocarcinogenesis, and a predictor for the monitor and prevention of HCC. VIRTUAL SLIDES: The virtual slides for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1557074981159099 .

Thymic TFH cells involved in the pathogenesis of myasthenia gravis with thymoma.

Follicular helper CD4+ T (TFH) cells are the specialized providers of B cell help in germinal centers (GCs). Formation of GCs in thymi is the primary thymi characteristic in MG patients. TFH cells are involved in the pathogenic process of many autoimmune diseases including systemic lupus erythematosus, rheumatoid arthritis and autoimmune thyroid disease. The role thymic TFH cells played in MG with thymoma has not been elucidated. Here, we analyzed surface markers CXCR5, Bcl-6, ICOS and IL-21 on TFH cells in thymus derived from thymoma patients with ocular MG (OMG), generalized MG (GMG) or without MG using immunohistochemical staining, immunofluorescence, western blotting, and real-time PCR analysis. We show that clinical severity of MG is correlated with higher mRNA expression of the four markers. Indeed, results show higher expression of all four markers in thymoma with GMG patients compared with both OMG and non-MG patients. We found no significant difference in the expression of CXCR5, Bcl-6 and ICOS in OMG compared with non-MG patients. Regression analysis shows a positive correlation between thymic CXCR5, BCL-6, ICOS and IL-21 levels and quantitative MG score (QMGS) in GMG patients. In addition, we found no significant correlation between TFH cell expression and QMGS in OMG patients. Our findings show that higher expression of TFH cells in the thymoma is related to the clinical severity of MG and suggests a role in the pathogenesis of MG. However, the real source of these TFH cells is still uncertain and needs further study.

Dysplastic nodules with glypican-3 positive immunostaining: a risk for early hepatocellular carcinoma.

Glypican-3 (GPC3) has been reported to be a novel serum and histochemical marker for HCC. The positivity or negativity for GPC3 in hepatic precancerous lesions, such as dysplastic nodules (DN), has also been described. Moreover, our previous studies have demonstrated that some DN in liver cirrhosis represent monoclonal hyperplasia, and confirmed their neoplastic nature. However, additional studies must be performed to investigate further the relationship between DN with GPC3 positivity and HCC. Thus, we first investigated the expression of GPC3 in 136 HCC and 103 small DN (less than 1 cm in diameter) by immunohistochemical staining and determined the clonality of 81 DN from female patients using X-chromosome inactivation mosaicism and polymorphism of androgen receptor (AR) gene. Then we examined these samples for chromosomal loss of heterozygosity (LOH) at 11 microsatellite polymorphism sites. The results demonstrated that GPC3 immunoreactivity was detected in 103 of 136 HCC (75.7%) and 19 of 103 DN (18.4%), and the positive ratio correlated with HBsAg positivity. Clonality assays showed that 15 GPC3-positive DN from female patients, including 12 high-grade DN (HGDN), and 28 (42.4%) of 66 GPC3-negative DN, were monoclonal. In addition, among 19 GPC3-positive DN, chromosomal LOH was found at loci D6S1008 (100%, 19/19), D8S262 (52.6%, 10/19) and D11S1301 (57.9%, 11/19). However, the LOH frequency in GPC3-negative DN was 5.95% (5/84), 23.8% (20/84), and 4.76% (4/84) in three loci, respectively. Thus, we concluded that GPC3-positive DN, especially GPC3-positive HGDN, was really a late premalignant lesion of HCC.

Stat3 inhibits PTPN13 expression in squamous cell lung carcinoma through recruitment of HDAC5.

Proteins of the protein tyrosine phosphatase (PTP) family are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, and apoptosis. PTPN13 (also known as FAP1, PTPL1, PTPLE, PTPBAS, and PTP1E), a putative tumor suppressor, is frequently inactivated in lung carcinoma through the loss of either mRNA or protein expression. However, the molecular mechanisms underlying its dysregulation have not been fully explored. Interleukin-6 (IL-6) mediated Stat3 activation is viewed as crucial for multiple tumor growth and progression. Here, we demonstrate that PTPN13 is a direct transcriptional target of Stat3 in the squamous cell lung carcinoma. Our data show that IL-6 administration or transfection of a constitutively activated Stat3 in HCC-1588 and SK-MES-1 cells inhibits PTPN13 mRNA transcription. Using luciferase reporter and ChIP assays, we show that Stat3 binds to the promoter region of PTPN13 and promotes its activity through recruiting HDAC5. Thus, our results suggest a previously unknown Stat3-PTPN13 molecular network controlling squamous cell lung carcinoma development.

[Expression and clinical significance of HAb18G/CD147 in malignant tumors].

OBJECTIVE: To explore the clinical relevance between HAb18G/CD147 expression and malignant tumors, including esophageal cancer, colon cancer, cervical cancer, lung cancer, ovarian cancer, and hepatocellular carcinoma. METHODS: The expression and localization of CD147 in six kinds of malignant tumors, their adjacent tissues, and lymph node metastasis specimens were studied by immunohistochemical SP staining. Then the relationships between CD147 expression and degree of tumor differentiation, depth of invasion, lymph node metastasis were analyzed. RESULTS: CD147 expression was significantly elevated in tumors compared with their adjacent tissues. CD147 expression was positively correlated with the degree of tumor differentiation, depth of invasion, and lymph node metastasis. CD147 expression was significantly increased in infiltrating deep tissues of colon cancer, cervical cancer, and esophageal cancer (P<0.05). The expression of CD147 was significantly increased in lymph node metastatic tissues in cervical cancer, esophageal cancer, lung cancer, and ovarian cancer (P<0.05), but not in colon cancer. CD147 expression was significantly increased in poorly differentiated tissues in colon cancer, cervical cancer, esophageal cancer and lung cancer (P<0.05). CONCLUSION: CD147 expression was significantly higher in tissues of poor differentiation, deep invasion, and lymph node metastasis. This indicated that CD147 may be a prognostic indicator for malignant tumors.

EMMPRIN/CD147 expression is associated with disease-free survival of patients with colorectal cancer.

EMMPRIN/CD147 has been proved to be associated with tumor invasion and metastasis in various human malignancies. In the present study, we investigated the expression of CD147 and its association with disease-free survival of colorectal cancer patients. CD147 expression was investigated in 328 cases of colorectal cancer by immunohistochemistry assay. Statistical analysis was utilized to evaluate the association of CD147 expression with disease-free survival of colorectal cancer patients. CD147 expression was proved to be increased in colorectal cancer (P < 0.001) and related to tumor invasion (P < 0.001), metastasis (P < 0.001), and TNM stage (P < 0.001). Kaplan-Meier showed CD147 was associated with disease-free survival of patients with colorectal cancer for patients with higher CD147 expression tend to have shorter disease-free survival (P < 0.001). Multivariate analysis also proved CD147 to be an independent prognostic factor for disease-free survival of colorectal cancer patients (P < 0.05). These results suggested the potential role of CD147 in relapse of human colorectal cancer. It might be a novel molecular marker to predict relapse of patients with colorectal cancer.

Identification of genuine primary pulmonary NK cell lymphoma via clinicopathologic observation and clonality assay.

Extranodal natural killer (NK)/T-cell lymphoma, nasal type, is an uncommon lymphoma associated with the Epstein-Barr virus (EBV). It most commonly involves the nasal cavity and upper respiratory tract. Primary pulmonary NK/T cell lymphoma is extremely rare. If a patient with a NK or T-cell tumor has an unusual reaction to treatment or an unusual prognosis, it is wise to differentiate NK from T-cell tumors. The clinicopathologic characteristics, immunophenotype, EBV in situ hybridization, and T cell receptor (TCR) gene rearrangement of primary pulmonary NK cell lymphoma from a 73-year-old Chinese woman were investigated and the clonal status was determined using female X-chromosomal inactivation mosaicism and polymorphisms at the phosphoglycerate kinase (PGK) gene. The lesion showed the typical histopathologic characteristics and immunohistochemical features of NK/T cell lymphoma. However, the sample was negative for TCR gene rearrangement. A clonality assay demonstrated that the lesion was monoclonal. It is concluded that this is the first recorded case of genuine primary pulmonary NK cell lymphoma. The purpose of the present work is to recommend that pathologists carefully investigate the whole lesion to reduce the likelihood that primary pulmonary NK cell lymphoma will be misdiagnosed as an infectious lesion. In addition, TCR gene rearrangement and clonal analysis, which is based on female X-chromosomal inactivation mosaicism and polymorphisms at PGK and androgen receptor (AR) loci, were found to play important roles in differentiating NK cell lymphoma from T cell lymphoma. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/5205300349457729.

A rare case of malignant triton tumor in the cerebellopontine angle.

Malignant triton tumor (MTT) is defined as malignant peripheral nerve sheath tumor with rhabdomyoblastic differentiation. Intracranial MTT is extremely rare, and only four cases have been reported in the literature. Here, we report a case of MTT occurring in the cerebellopontine angle, and describe its histopathological characteristics, immunohistochemical features, and prognosis. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1336227313684480.