Search

The primary treatment for nasopharyngeal carcinoma (NPC) is radiotherapy. In rare cases, patients with NPC treated with radiotherapy may develop radiation-induced sarcoma (RIS), a malignant tumor, in the field of previous radiation. The prognosis is poor, and complete surgical resection is the only potentially curative treatment. We report a case of radiation-induced nasopharyngeal sarcoma after radiotherapy for NPC with suspected lung and liver metastases in a 69-year-old woman.

OBJECTIVE The aim of the study was to develop a methodology to identify the best use of a longitudinally measured biomarker in relevance to prognosis. MATERIALS AND METHODS Data of squamous cell carcinoma antigen (SCC-Ag) from 770 patients with cervical squamous cell carcinoma (SCC) were used. The pretreatment, nadir, and time-dependent SCC-Ag values were analyzed in relevance to disease relapse and death with univariate and multivariate analysis side by side with a variety of available clinicopathologic factors. The predictive power of the significant variates was evaluated by C-index with 5-fold cross validation. RESULTS The pretreatment, nadir, and time-dependent SCC-Ag were all significant risk factors for both relapse and death in the univariate analysis (p < .05), and the time-dependent SCC-Ag had the highest C-index in both events. The nadir and time-dependent SCC-Ag were both independently significant in response to relapse with International Federation of Gynecology and Obstetrics (FIGO) stage as the covariate, and the latter had a higher C-index (0.745). Only the time-dependent SCC-Ag was independently significant together with FIGO stage in response to death with the C-index at 0.844. CONCLUSIONS Increases in the serum level of SCC-Ag in cervical SCC patients suggest a higher risk of both relapse and death. The best use of serial SCC-Ag measurements is to include the time-dependent value in prognostic assessment with FIGO stage also accounted for. Cervical SCC patients should be followed up on their levels of SCC-Ag, and prognostic evaluation should be updated with recent measurements.

Triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancer as it shows a high capacity for metastasis and poor prognoses. Metabolic reprogramming is one of the hallmarks of cancer, and aberrant glycolysis was reported to be upregulated in TNBC. Thus, identifying metabolic biomarkers for diagnoses and investigating cross-talk between glycolysis and invasiveness could potentially enable the development of therapeutics for patients with TNBC. In order to determine novel and reliable metabolic biomarkers for predicting clinical outcomes of TNBC, we analyzed transcriptome levels of glycolysis-related genes in various subtypes of breast cancer from public databases and identified a distinct glycolysis gene signature, which included ENO1, SLC2A6, LDHA, PFKP, PGAM1, and GPI, that was elevated and associated with poorer prognoses of TNBC patients. Notably, we found a transcription factor named Y-box-binding protein 1 (YBX1) to be strongly associated with this glycolysis gene signature, and it was overexpressed in TNBC. A mechanistic study further validated that YBX1 was upregulated in TNBC cell lines, and knockdown of YBX1 suppressed expression of those glycolytic genes. Moreover, YBX1 expression was positively associated with epithelial-to-mesenchymal transition (EMT) genes in breast cancer patients, and suppression of YBX1 downregulated expressions of EMT-related genes and tumor migration and invasion in MDA-MB-231 and BT549 TNBC cells. Our data revealed an YBX1-glycolysis-EMT network as an attractive diagnostic marker and metabolic target in TNBC patients.

The tumor microenvironment plays an important role in tumor initiation and progression. It is well documented that nicotine participates in cigarette smoking-related malignancies. Previous studies focused on the effects of nicotine on tumor cells; however, the role of the microenvironment in nicotine-mediated tumorigenesis is poorly understood. Herein, we investigated the effect and molecular mechanism of nicotine on fibroblasts and its contribution to breast cancer. We found that nicotine induced the epithelial-mesenchymal transition (EMT) of breast cancer cells and promoted activation of fibroblasts. Interestingly, conditioned medium from nicotine-activated fibroblasts (Nic-CM) had a greater impact on promoting the EMT and migratory capability toward cancer cells than did treatment with nicotine alone. Production of connective tissue growth factor (CTGF) and transforming growth factor (TGF)-β by nicotine-treated fibroblasts was demonstrated to be crucial for promoting the EMT and cancer cell migration, and blocking of CTGF and TGF-β in Nic-CM-suppressed tumor motility. Moreover, nicotine induced expressions of CTGF, and TGF-β in fibroblasts as identified through α7 nicotinic acetylcholine receptor (nAChR)-dependent activation of the AKT/TAZ signaling mechanism. Together, our data showed for the first time that activation of fibroblasts is largely responsible for accelerating smoking-mediated breast cancer progression.

Little is known about the effects of seamless hospital discharge planning on long-term care (LTC) costs and effectiveness. This study evaluates the cost and effectiveness of the recently implemented policy from hospital to LTC between patients discharged under seamless transition and standard transition. A total of 49 elderly patients in the standard transition cohort and 119 in the seamless transition cohort were recruited from November 2016 to February 2018. Data collected from medical records included the Multimorbidity Frailty Index, Activities of Daily Living Scale, and Malnutrition Universal Screening Tool during hospitalization. Multiple linear regression and Cox regression models were used to explore risk factors for medical resource utilization and medical outcomes. After adjustment for effective predictors, the seamless cohort had lower direct medical costs, a shorter length of stay, a higher survival rate, and a lower unplanned readmission rate compared to the standard cohort. However, only mean total direct medical costs during hospitalization and 6 months after discharge were significantly (p &lt, 0.001) lower in the seamless cohort (USD 6192) compared to the standard cohort (USD 8361). Additionally, the annual per-patient economic burden in the seamless cohort approximated USD 2.9–3.3 billion. Analysis of the economic burden of disability in the elderly population in Taiwan indicates that seamless transition planning can save approximately USD 3 billion in annual healthcare costs. Implementing this policy would achieve continuous improvement in LTC quality and reduce the financial burden of healthcare on the Taiwanese government.

Rationale: Small cell neuroendocrine carcinoma of the nasal cavity and paranasal sinuses is a rare but aggressive neoplasm with a poor prognosis and a strong propensity for regional recurrence and distant metastasis. Diagnosis is challenging and relies on immunohistochemical study. Treatment includes surgical resection, radiation therapy, chemotherapy, or a combination of these modalities. However, the optimal therapeutic strategy is still controversial. Due to its rarity, the complexity of the histological diagnosis, and the variety of the treatment regimens, we presented a case of primary small cell neuroendocrine carcinoma in the nasal cavity with description of the clinical manifestation, pathology features, and our treatment regimen. Patient concerns: An 82-year-old female patient with hypertension presented with right epistaxis on and off with nasal obstruction for several days. Diagnosis: An exophytic mass over the posterior end of the right inferior turbinate was found on nasopharyngoscope. Biopsy was done and the pathology confirmed small cell carcinoma, strongly positive for cytokeratin (AE1/AE3) and insulinoma-associated protein 1 (INSM-1), scatteredly positive for chromogranin A, synaptophysin and CD56. The final diagnosis was small cell neuroendocrine carcinoma of right nasal cavity, pT1N0M0, stage I. Interventions: The patient underwent wide excision of right intra-nasal tumor and post-operative radiotherapy with a dose of 6600 cGy in 33 fractions. Outcomes: No local recurrence or distant metastasis was noted during the 12 months of follow-up. Lessons: Multimodality treatment remains the most common therapeutic strategy, although no proven algorithm has been established due to the rarity of this disease. Further investigation is needed for providing evidence to standardize the treatment protocol.

Mutation of KRAS in non-small-cell lung cancer (NSCLC) shows a poor response to epidermal growth factor receptor (EGFR) inhibitors and chemotherapy. Currently, there are no direct anti-KRAS therapies available. Thus, new strategies have emerged for targeting KRAS downstream signaling. Panobinostat is a clinically available histone deacetylase inhibitor for treating myelomas and also shows potentiality in NSCLC. However, the therapeutic efficacy of panobinostat against gefitinib-resistant NSCLC is unclear. In this study, we demonstrated that panobinostat overcame resistance to gefitinib in KRAS-mutant/EGFR-wild-type NSCLC. Combined panobinostat and gefitinib synergistically reduced tumor growth in vitro and in vivo. Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Inhibition of TAZ by panobinostat or short hairpin RNA sensitized KRAS-mutant/EGFR-wild-type NSCLC to gefitinib through abrogating AKT/mammalian target of rapamycin (mTOR) signaling. Clinically, TAZ was positively correlated with EGFR signaling, and coexpression of TAZ/EGFR conferred a poorer prognosis in lung cancer patients. Our findings identify that targeting TAZ-mediated compensatory mechanism is a novel therapeutic approach to overcome gefitinib resistance in KRAS-mutant/EGFR-wild-type NSCLC.

In the Paris System (TPS), standardized cytomorphological criteria and diagnostic categories were proposed for reporting urine cytology. To evaluate the diagnostic agreement and interobserver concordance for assessing TPS criteria, the Taiwan Society of Clinical Cytology organized an online survey with 10 atypical urine cytology cases. A total of 137 participants completed the survey. The mean agreement of diagnosis was 51.2%, ranging from 34.3% to 83.2% for each case. For 60% (6/10) of cases, the agreement was &lt, 50%. The interobserver concordance of diagnosis and cytological criteria assessment showed poor agreement. The nuclear-to-cytoplasmic (N/C) ratio had the highest kappa value of 0.386, indicating a significantly higher interobserver concordance and reproducibility than the other three TPS criteria. The correct rate of assessing the N/C ratio increased as the N/C ratio increased (correlation coefficient: 0.891, p &lt, 0.01). Three cases with an N/C ratio near 0.5 were overestimated. Poor interobserver concordance of diagnosis and TPS criteria was revealed. Compared with other cytological features, the N/C ratio assessment was quantitative and more reproducible, but a tendency to overestimate cells was noted when the N/C ratio was approximately 0.5. Continuing education programs should emphasize the accurate assessment of N/C ratio to improve the application of TPS.

Succinate dehydrogenase (SDH)–deficient renal cell carcinoma is a recently recognized distinct subtype of renal cell carcinoma in the 2016 World Health Organization classification. It is associated with SDH gene germline mutations, which also cause paraganglioma/pheochromocytoma, gastrointestinal stromal tumor, and pituitary adenoma. The tumor most commonly presents in young adulthood. The tumors are arranged in solid nests or in tubules and frequently show cystic change. The tumors are composed of cuboidal to oval cells with round nuclei, dispersed chromatin, and inconspicuous nucleoli. The cytoplasm is eosinophilic or flocculent but not truly oncocytic. The most distinctive histologic feature is the presence of cytoplasmic vacuoles or inclusions. Loss of SDH subunit B immunostaining is needed for a definite diagnosis. The prognosis is good for low-grade tumors but worse for tumors with high-grade nuclei, sarcomatoid change, or coagulative necrosis. Long-term follow-up is indicated.

Rationale: Cancer cells reprogram cellular metabolism to fulfill their needs for rapid growth and metastasis. However, the mechanism controlling this reprogramming is poorly understood. We searched for upregulated signaling in metastatic colorectal cancer and investigated the mechanism by which Glut3 promotes tumor metastasis. Methods: We compared RNA levels and glycolytic capacity in primary and metastatic colon cancer. The expression and association of Glut3 with clinical prognosis in colon cancer tissues was determined by immunohistochemistry. Glut3 gain-of-function and loss-of-function were established using colon cancer HCT116, HT29, and metastatic 116-LM cells, and tumor invasiveness and stemness properties were evaluated. Metabolomic profiles were analyzed by GC/MS and CE-TOF/MS. The metastatic burden in mice fed a high-fat sucrose diet was assessed by intravenous inoculation with Glut3 knockdown 116-LM cells. Results: Upregulation of glycolytic genes and glycolytic capacity was detected in metastatic colorectal cancer cells. Specifically, Glut3 overexpression was associated with metastasis and poor survival in colorectal cancer patients. Mechanistically, Glut3 promoted invasiveness and stemness in a Yes-associated protein (YAP)-dependent manner. Activation of YAP in turn transactivated Glut3 and regulated a group of glycolytic genes. Interestingly, the expression and phosphorylation of PKM2 were concomitantly upregulated in metastatic colorectal cancer, and it was found to interact with YAP and enhance the expression of Glut3. Importantly, a high-fat high-sucrose diet promoted tumor metastasis, whereas the inhibition of either Glut3 or YAP effectively reduced the metastatic burden. Conclusion: Activation of the Glut3-YAP signaling pathway acts as a master activator to reprogram cancer metabolism and thereby promotes metastasis. Our findings reveal the importance of metabolic reprogramming in supporting cancer metastasis as well as possible therapeutic targets.

The major obstacle in current cancer therapy is the existence of cancer stem cells (CSCs), which are responsible for therapeutic resistance and contribute to metastasis and recurrence. Identification of reliable biomarkers for diagnostic and therapeutic targets is necessary for drug development and cancer treatment. In this study, we identified that the antipsychotic chlorpromazine (CPZ) exhibited potent anti-breast cancer and anti-CSC capabilities. Treatment with CPZ suppressed stemness properties including mammosphere formation, aldehyde dehydrogenase (ALDH) activity, and stemness-related gene expressions in breast cancer cells and CSCs. Moreover, CPZ increased the susceptibility of breast cancer MCF7 cells and drug-resistant MCF7/ADR cells when combined with chemotherapies. Mechanistically, we identified that CPZ suppressed yes-associated protein (YAP) through modulating Hippo signaling and promoting proteasomal degradation of YAP. Elevated expression of YAP was confirmed to be crucial for stemness-related gene expressions, and was associated with invasiveness and stem-like signatures in breast cancer patients. Moreover, overexpression of YAP conferred poor outcomes particularly of basal-like breast cancer patients. Our data showed that YAP is a promising therapeutic target for breast CSCs, and CPZ has the potential to be a repurposed drug for breast cancer treatment.

Colon cancer is the third most common cancer in the world and the second most common cause of cancer-related mortality. Molecular biomarkers for colon cancer have undergone vigorous discovery and validation. Recent studies reported that overexpression of podocalyxin-like protein 1 (PODXL) is associated with distant metastasis and poor prognosis across several types of malignancies. Its role and underlying molecular mechanism, however, are not yet fully understood. In the present study, we revealed that the Hippo transducer, the transcriptional coactivator with PDZ-binding motif (TAZ), acts as a downstream mediator of PODXL in colon cancer. Inhibition of PODXL resulted in the suppression of TAZ signaling and the downregulation of Hippo downstream genes. Moreover, PODXL plays a critical role in cancer stemness, invasiveness, and sensitivity to chemotherapies in colon cancer HCT15 cells. Notably, expression of PODXL showed a positive correlation with stem-like and epithelial-mesenchymal transition (EMT) core signatures, and was associated with poor survival outcomes in patients with colon cancer. These findings provide novel insights into the molecular mechanism of PODXL-mediated tumorigenesis in colon cancer.

Robots can deal with different kinds of challenges using tactile sensing arrays as a primary resource. This paper demonstrates the ability of robotic hands to recognize objects' shapes using only a flexible tactile sensor arrays attached to the robotic hand's surface without building the 3D models of objects. A telemanipulation module was developed to achieve a co-moving mechanism between the robotic hand and human hands so that the robotic hand can directly learn the best way to grasp objects from human hands without additional path planning process. Tactile array data were collected while the robotic hand was performing a reiterative grasping process. By extracting the proper features from the tactile sensor array data, the support vector machines (SVMs) were employed to perform object classification. From experiments, the proposed method can achieve 96.67% classification accuracy based on sensory data and SVMs.

SummaryObjectiveTo determine whether acid aspiration provokes the development of multidrug-resistant Acinetobacter baumannii (MDRAB) pneumonia in its host.MethodsGroups of mice were inoculated intratracheally (IT) with 50μl of 0.1N HCl and 1×108 colony-forming units (CFU) Ab396 (A+Ab group), or 50μl of 0.1N HCl and 20μl of 0.9% saline (A+S group), or 20μl of 0.9% saline and 1×108 CFU of Ab396 (S+Ab group), or 50μl of 0.9% saline and 20μl of 0.9% saline (S+S group). Cytokines, bacterial loads in the bronchoalveolar lavage fluid (BALF), lung permeability, histopathology of the lungs, and survival rates were evaluated.ResultsOnly the A+Ab mice developed extensive Ab396 pneumonia and had significantly elevated bacterial loads, increased lung leakage, and lower levels of tumor necrosis factor alpha (TNF-α) compared with the other three groups (p

Mutation of KRAS in non-small-cell lung cancer (NSCLC) shows a poor response to epidermal growth factor receptor (EGFR) inhibitors and chemotherapy. Currently, there are no direct anti-KRAS therapies available. Thus, new strategies have emerged for targeting KRAS downstream signaling. Panobinostat is a clinically available histone deacetylase inhibitor for treating myelomas and also shows potentiality in NSCLC. However, the therapeutic efficacy of panobinostat against gefitinib-resistant NSCLC is unclear. In this study, we demonstrated that panobinostat overcame resistance to gefitinib in KRAS-mutant/EGFR-wild-type NSCLC. Combined panobinostat and gefitinib synergistically reduced tumor growth in vitro and in vivo. Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Inhibition of TAZ by panobinostat or short hairpin RNA sensitized KRAS-mutant/EGFR-wild-type NSCLC to gefitinib through abrogating AKT/mammalian target of rapamycin (mTOR) signaling. Clinically, TAZ was positively correlated with EGFR signaling, and coexpression of TAZ/EGFR conferred a poorer prognosis in lung cancer patients. Our findings identify that targeting TAZ-mediated compensatory mechanism is a novel therapeutic approach to overcome gefitinib resistance in KRAS-mutant/EGFR-wild-type NSCLC.

BACKGROUND: Carbonic anhydrase IX (CAIX) is a hallmark of metabolic change in cancer cells. The aim was to evaluate the utility of CAIX expression for the detection of malignant pleural effusions by enzyme-linked immunosorbent assay (ELISA) and immunocytochemistry. METHODS: A total of 97 pleural effusions including 54 benign effusions, 10 atypical effusions, and 33 malignant effusions, classified based on cytological diagnosis and etiology, were subjected to ELISA to measure protein level and to immunocytochemistry in cell blocks to determine CAIX expression. RESULTS: CAIX levels were significantly higher in the malignant group compared with the benign group. Receiver operating characteristic curve analysis of benign and malignant pleural effusion for CAIX indicated an area under the curve of 0.82 with a value of 1882 pg/dL as the best threshold for distinguishing benign from malignant effusions, which yields a sensitivity, specificity, and accuracy of 63.6%, 94.4%, and 82.8%, respectively. None of the benign effusion expressed CAIX by immunocytochemistry. Malignant effusion cell blocks expressed CAIX in 63.6% of cases with 100% specificity. Upon combination of CAIX level and immunocytochemistry to detect malignant pleural effusions, the sensitivity and accuracy increased to 81.8% and 89.7%, respectively. The CAIX level determined by ELISA and the CAIX expression detected by immunocytochemistry were positively correlated. In atypical effusions, 5 cases (50%) exhibited CAIX levels higher than the cutoff value or were highlighted by CAIX immunocytochemistry. CONCLUSIONS: ELISA and immunocytochemistry methods for determination of CAIX protein are potential additional tests for detection of malignant pleural effusions. Cancer (Cancer Cytopathol) 2012;. © 2012 American Cancer Society.

BACKGROUND: The sensitivity of conventional cytology for the detection of malignant cells in pleural effusion is insufficient. GLUT1 and CAIX are the hallmarks of metabolic change in cancer cells. The aim of this study was to evaluate the usefulness of GLUT1 and CAIX expression to the detection of cancer cells in pleural effusions. METHODS: A total of 150 pleural effusions were subjected to immunocytochemical staining for GLUT1 and CAIX expression. According to their cytological diagnosis and etiology, these included 58 benign effusions, 38 probable malignant effusions, 7 atypical effusions, and 47 malignant effusions,. RESULTS: None of the benign effusions showed GLUT1 or CAIX expression, but probable malignant effusions and malignant effusions significantly expressed GLUT1 and CAIX with a positive result in 74.5% and 63.8% of the malignant effusions, respectively, with 100% specificity. When the combination of both markers was evaluated, GLUT1 and CAIX displayed a higher diagnostic performance, ie, a sensitivity of 76.6%, specificity of 100%, and accuracy of 89.5%. A statistically significant positive correlation between GLUT1 and CAIX expression was observed. In addition, 18% of cases with cells resembling mesothelial cell hyperplasia in probable malignant effusions and 71.4% of cases with atypical cells of uncertain significance in atypical effusions were highlighted on GLUT1 or/and CAIX immunocytochemical stains. CONCLUSIONS: Immunocytochemical staining for GLUT1 and CAIX may be a complementary tool for the detection of malignant pleural effusions and is helpful in distinguishing cancer cells from reactive mesothelial cells. A combination of GLUT1 and CAIX immunocytochemical staining can give a higher diagnostic performance. Cancer (Cancer Cytopathol) 2011;. © 2011 American Cancer Society.

Hypoxia and acidosis are microenvironmental selection forces during somatic evolution in breast carcinogenesis. The effect of cobalt chloride (CoCl(2))-induced hypoxia on the expression of hypoxia-inducible factor (HIF)-1alpha, glucose transporter 1 (GLUT1), and carbonic anhydrase IX (CAIX) was assessed in breast cancer cells derived from primary sites (HCC1395 and HCC1937) and metastatic sites (MCF-7 and MDA-MB-231) by reverse transcriptase-polymerase chain reaction and immunoblotting. We analyzed these proteins' expression in tissue samples from normal breast tissue, usual ductal hyperplasia (DH), atypical ductal hyperplasia (ADH), ductal carcinoma in situ (DCIS), and invasive ductal carcinoma (IDC) using immunohistochemistry. CAIX mRNA was expressed constitutively in MDA-MB-231 cells but not in the other three cell lines. CAIX mRNA expression was increased after CoCl(2)-induced hypoxia in all four breast cancer cell lines. The expression of HIF-1alpha and GLUT1 proteins was increased after CoCl(2)-induced hypoxia in all breast cancer cell lines tested. Hypoxia significantly increased CAIX protein expression in primary cancer cells but not in metastatic ones. HIF-1alpha was not expressed in benign breast tissue, whereas it was significantly expressed in DH, ADH, DCIS, and IDC (p0.001). GLUT1 and CAIX were expressed only in DCIS (56.8% and 25.0%) and IDC (44.1% and 30.5%), with higher expression in high grade DCIS than low/intermediate grade DCIS (79.2% vs. 30.0%, p = 0.001 and 37.5% vs. 10.0%, p = 0.036, respectively). High CAIX expression was significantly associated with poor histological grade of IDC (p = 0.005). During breast carcinogenesis, the role of HIF-1alpha changes from response to proliferation to tumor progression. GLUT1 expression (glycolytic phenotype) and CAIX expression (acid-resistant phenotype) may result in a powerful adaptive advantage and represent an aggressive phenotype.

Oncocytic carcinoma arising in the submandibular gland is an extremely rare tumor and only 11 cases have been reported previously. We report on a 51-year-old man with a previously benign oncocytoma in the submandibular gland that transformed from a benign morphology to malignant cellular atypia and mitosis. To our knowledge, the current report is the first published case of a malignant transformation from benign oncocytoma to oncocytic carcinoma of the submandibular gland. The proliferative activity of the tumor cells was evaluated immunohistochemically using antibodies against Ki-67.

Background: Malignant myoepitheliomas of the breast are extremely rare. There has been a limited number of published reports of myoepithelial carcinomas originating from the breast. Case Report: We describe a malignant myoepithelioma of the breast in a 56-year-old woman. Histological examination showed polygonal epithelioid cells and spindle cells with moderate to marked nuclear atypia. Immunohistochemistry showed reactivity in the spindle cells for smooth muscle actin, cytokeratin (AE1/AE3), and p63, indicating a myoepithelial cell lineage of tumor cells. The patient underwent radical surgical excision of the lesion and axillary lymph node dissection. She demonstrated no evidence of recurrence over an 11-month follow-up. Conclusions: We suggest myoepithelial carcinomas of the breast be managed with appropriate surgical clearance. A multidisciplinary approach is usually required.

Objectives. Malignant phenotypic traits are caused by microenvironmental selection pressures during carcinogenesis. Hypoxia can drive a tumor toward a more aggressive malignant phenotype. The objective was to better understand the role of the hypoxia-regulated genes in cervical carcinogenesis. Methods. We analyzed the expression of the hypoxia-regulated genes, including hypoxia-inducible factor-1α (HIF-1α), erythropoietin (Epo), vascular endothelial growth factor (VEGF), glucose transporter 1 (GLUT1), carbonic anhydrase IX (CAIX), and MET, in cervical cell lines and human tissue samples of cervical intraepithelial neoplasia (CIN I–III) and invasive squamous cell carcinoma (ISCC). Results. CAIX and MET were expressed in cervical carcinoma cell lines, but not in normal or human papillomavirus-immortalized cervical cells. In clinical tissue samples, Epo, VEGF, GLUT1, and CAIX were not detected in normal squamous epithelia. GLUT1 was expressed in nearly all cases of CIN and ISCC, however, CAIX was expressed only in CIN III and ISCC. HIF-1α and MET expression was confined to the basal cells in normal squamous epithelia and was detected in the dysplastic cells of CIN and ISCC. Conclusions. The role of HIF-1α and MET changes from response to proliferation to tumor progression during cervical carcinogenesis. GLUT1 expression, a glycolytic phenotype adaptive to glycolysis, occurs early during cervical carcinogenesis and is a specific marker for dysplasia or carcinoma. MET and CAIX may contribute tumor progression in later stage. CAIX expression, an acid-resistant phenotype, may be a powerful adaptive advantage during carcinogenesis. Successful adaptation to the hypoxia–glycolysis–acidosis sequence in a microenvironment is crucial during carcinogenesis.

Background Understanding mothers’ economic conditions and postpartum depression (PPD) is important for determining how they will take care of themselves and their infants during the postnatal period, especially for low-income families. This study examined the relationship between economic conditions and PPD to elucidate the effect of economic contraction on PPD. Methods Our population-based nationwide study used 2000–2013 the National Health Insurance Research Database of Taiwan. A total of 1240 newly diagnosed PPD patients were recruited. We used the database of the Directorate General of Budget, Accounting, and Statistics of Executive Yuan of Taiwan for national economic indicators. The correlation between economic indicators and PPD was examined. Results The PPD incidence was positively correlated with yearly unemployment rate, consumer price index, and gross domestic product. During the great recession of 2008–2009, PPD was positively correlated with inflation rate. Consumer price index had a positive correlation with PPD incidence per month when comparing PPD in 2010 with the economic indicators during the great recession. Limitations As this retrospective study evaluated macroeconomic indicators, it is unclear whether the macroeconomic indicators’ effect on PPD totally reflects the effect of true personal economic status on PPD. Conclusions There was a significant association between PPD and economic conditions. This study shows that mothers’ familial environment plays an important role in the development of PPD. The impact of the worldwide economic downturn of the great recession on women is persistent. This useful finding may give health policy planners a hint of early discovering and dealing with PPD when worldwide economic downturn

Cytomegalovirus (CMV) colitis usually occurs in immunocompromised patients with human immunodeficiency virus infection, organ transplantation, and malignancy receiving chemotherapy or ulcerative colitis receiving immunosuppressive agents. However, CMV colitis is increasingly recognized in immunocompetent hosts. Notably, CMV colitis coexisting with Clostridium difficile infection (CDI) in apparently healthy individuals has been published in recent years, which could result in high morbidity and mortality. CMV colitis is a rare but possible differential diagnosis in immunocompetent patients with abdominal pain, watery, or especially bloody diarrhea, which could be refractory to standard treatment for CDI. As a characteristic of CDI, however, pseudomembranous colitis may be only caused by CMV infection. Real-time CMV-polymerase chain reaction (PCR) for blood and stool samples may be a useful and noninvasive diagnostic strategy to identify CMV infection when treatment of CDI eventually fails to show significant benefits. Quantitative CMV-PCR in mucosal biopsies may increase the diagnostic yield of traditional histopathology. CMV colitis is potentially life-threatening if severe complications occur, such as sepsis secondary to colitis, massive colorectal bleeding, toxic megacolon, and colonic perforation, so that may necessitate pre-emptive antiviral treatment for those who are positive for CMV-PCR in blood and/or stool samples while pending histological diagnosis.