4 research outputs found
Vitality and nature in psychiatric spaces: Challenges and prospects for ‘healing architecture’ in the design of inpatient mental health environments
No full textHistorically, nature has been considered central to healing and recovery in institutional mental health settings, with inpatient spaces designed to mirror the restorative forces nature may afford. Within contemporary healthcare architecture, the discourse surrounding nature’s role has once again become prominent, especially in the concept of ‘healing architecture’. While the literature on ‘healing architecture’ primarily considers how to connect recovery to nature through interventions in the built environment, less interest has been directed towards how nature is configured in design processes and what implications that has for the everyday experiences of patients and staff. In this paper we consider the design and implementation of one particular psychiatric hospital in Denmark to show that the ‘nature’ brought into this healthcare space can be experienced as anything but ‘natural’ and may reduce rather than enhance a felt sense of ‘vitality’ amongst patients. Based on our analysis, we end the paper by suggesting four principles for future healthcare design
Sulphate reducing bacteria in wastewater treatment
No full textThe depletion of fresh water sources forces to design innovative integral solutions for the urban water cycle. Usual practice in most cities is to use drinking water to transport waste outside the city via sewer system. For toilet flushing the water quality is less important and seawater could be used as alternative to use of drinking water. Due to high sulphate content in seawater it usage for toilet flushing will increase the sulphate content of wastewater. Sulphate enrichment of wastewater may also origin from industrial wastewater discharges, seawater intrusion in the sewer network or from sulphate presence in the groundwater used for water supply. Sulphate-rich wastewater allows for alternative wastewater treatment solutions such as the novel Sulphate reduction Autotrophic denitrification and Nitrification Integrated (SANI) process, a sulphur-cycle based wastewater treatment process (Wang et al. 2009). The SANI process is a novel treatment concept developed by the Hong Kong University of Science and Technology and TU Delft. Previously, autotrophic (sulphide-based) denitrification has been studied intensively (Shao et al. 2010), also at relatively low temperatures (30°C) (Dries et al. 1998, Vallero et al. 2004). Therefore, the focus of this research was on sulphate reduction processes at lower temperatures and in the context of municipal wastewater treatment. Sulphate reducing bacteria (SRB) play a key role in the sulphur-cycle based wastewater treatment process (e.g. SANI), however SRB can also play a role in a conventional wastewater treatment process. The application of SRB is beneficial due to minimal sludge production, significant coliforms removal by their exposure to in the process produced sulphide, its applicability for selective heavy metal removal, and their ability to form granular sludge. The primary objective of this research was to study the kinetics of SRB found in domestic wastewater treatment plants (WWTPs) in moderate climate (e.g. the Netherlands), and in the temperature range of 10-20°C. A literature review revealed that temperature, carbon source, sulphide toxicity, sulphate and salt level are important parameters to understand the occurrence and performance of SRB in treating domestic wastewater. Consequently, these parameters were studied to evaluate the applicability of SRB to domestic wastewater treatment. The present study comprises both analysis of kinetics of SRB (long and short term effects) and of microbial population (by application of Transcript Restriction Fragment Length Polymorphism (T-RFLP) and clone-sequencing) of SRB. The main conclusions of each chapter will be addressed below. Experimental methods Throughout this study different types of tests were performed, of which the main tests comprised long-term operation of reactors (months), execution of short-term batch experiments (6 hours) and microbiological population analyses. The reactors were operated for a long time at the following standard conditions: temperature of 20°C, hydraulic retention (HRT) of 10 hours, solid retention time (SRT) of 15 days, pH 7.6 and under non-aerated conditions (anaerobic). The influent of reactors contained: acetate and propionate as organic substrates (300 mgCODVFA/L), ammonium (100 mgN/L), phosphate (10 mgP/L), salinity (0.7%) and sulphate (500 mg/L). The effect of change of various operational parameters on SRB were compared to SRB in this standard reactor. In each reactor biomass was evaluated for the growth, conversion rates, morphology and microbial population present. Short-term experiments were conducted to study the separately effect of nutrients (nitrogen, phosphate, sulphide ions, different substrates, et cetera). Microbiological population analyses were performed by T-RFLP and clone sequencing to identify specific microorganisms present in the sludge. SRB in aerobic WWTP In chapter 3 the presence and activity of SRB in aerobic municipal WWTPs were studied, in order to investigate what type of SRB are naturally occurring in the conventional WWTPs. As SRB are strictly anaerobic microorganisms also the ability of SRB to cope with oxygen exposure was studied. Nine WWTPs were subject to sampling to compare the SRB population in the samples taken from biological tanks and influent by T-RFLP and sequencing techniques. The T-RFLP results revealed that the SRB populations were very similar in these nine WWTPs. Also the similarity between the activated sludge of the tanks and influent was high (>76%). Desulfobacter postgatei, Desulfobulbus propionicus, and Desulfovibrio intestinalis seems to be the most common detected SRB species among the nine selected WWTP in the Netherlands. Batch-activity tests (6 hours) using sludge from the WWTP, did not show any SRB activity. This indicated that likely the SRB where derived from the influent with hardly any enhanced cultivation occurring in the treatment plant itself. Furthermore, 2 long-term (>3 SRT) sequencing batch reactors were operated in presence and absence of oxygen, investigating whether SRB can be active in relatively low DO concentration. Firstly a sequencing batch reactor was operated in the absence of oxygen (anaerobically), resulting in a dominant SRB population, then the conditions were altered to low DO conditions achieved by oxygen transfer between the mixed liquor and the oxygen present in the headspace of the reactor. In both reactors biodegradable organic carbon was removed, partly based on SRB activity. Sulphate reducing activity was also obtained under aerobic condition due to the formation of granular sludge, a protective strategy of the bacteria protect against oxygen exposure. In conclusion, SRB are naturally occurring in conventional WWTP, however are not very active. SRB however, can be active under low DO conditions if growing into sludge granules or as biofilms. SRB at low temperatures The SANI process was developed in Hong Kong at relatively high sewage temperature (30°C). The question whether SRB, as part of the SANI-process, could also be applied successfully in moderate climates, was central in chapter 4. Since temperature is a key-parameter in many biological processes, its kinetic effect on SRB performance, as well as the effect on SRB population was studied. Two sequencing batch reactors were operated, for more than 3 SRTs under sufficiently stable conditions, at 10°C and 20°C, to simulate winter and summer conditions of moderate climate, respectively. The study revealed that at 20°C complete readily biodegradable organic substrate (volatile fatty acids: VFA) removal was achieved, while at 10°C only 2/3 of the CODVFA content was removed. A decrease in rate of approximately a factor 2, caused the incomplete CODVFA removal at 10°C. Despite acetate was the only substrate in the effluent, batch experiments indicated that the acetate and propionate consumption rate were equally affected by a temperature decrease from 20°C to 10°C. Increasing the HRT to 13.3 hours assured a complete CODVFA removal also for operations at 10°C. Microbial population analyses (T RFLP and sequencing) revealed that barely any alteration in SRB population occurred, as response on a temperature decrease from 20 to 10°C, in both laboratory reactors (chapter 4). Also in a full-scale WWTP the SRB population hardly altered due to temperature changes in the range of 10-20°C (chapter 3). Temperature in the range of 10-20°C seems therefore not favouring proliferation of other SRB species. The marginal effect of temperature on SRB population and the opportunity to prolong the HRT for temperatures of 10°C in order to achieve complete VFA COD removal, indicate that SRB may be applied in moderate climate successfully. As for normal wastewater treatment process design, the design should be based on the conversion at the lowest temperature. Acetate and propionate feeding The competition between SRB and methanogens is a point of concern for stable process design; both can convert the organic carbon in absence of oxygen or nitrate. Methanogens, however produce methane, which would not be easy to use in the subsequent denitrification step of the SANI process. Along many other factors, the organic substrate type is suggested to play a key-role for this competition. Hence, the effect of acetate, propionate and a mixture of both substrates on the proliferation and activity of both microbial groups were evaluated in chapter 5. Three sequencing batch reactors were operated to investigate the effect of these feed procedures. In the acetate fed reactor, methanogens became dominant, while in the propionate reactor SRB were the dominant population. In the mixed substrate fed reactor both substrates were fully converted by SRB. All operational characteristics such as the substrate consumption rate, yield and growth rate were similar for SRB from the propionate fed and mixed substrate-fed reactors. Nonetheless, low similarity (3 SRTs) were operated. The reactors were fed with 400 or 800 mgCODVFA/L, resulting in respectively 200 or 400 mg/L sulphide. After changing the feed composition from 400 to 800 mgCODVFA/L, no additional CODVFA was consumed indicating the sludge suffered from sulphide toxicity. However, after a month of operation, all CODVFA was oxidized by SRB. Clone sequencing results revealed that the SRB species differ between the 400 and 800 mgCODVFA/L fed reactors, indicating that a SRB were able to resist higher sulphide level were selected to achieve complete organic carbon removal. The achieved adaption of SRB to sulphide was accomplished by the occurrence of a new dominant species within the reactor. In conclusion, since 400 mg/L CODVFA is usual for domestic wastewater (resulting in 200 mg/L sulphide), no sulphide toxicity issues are expected for the application of SRB in domestic wastewater treatment. Final remarks This research contributed to a better understanding of SRB application in (domestic) wastewater treatment. It revealed that SRB could perform well at moderate climate additions, and no major bottlenecks were identified regarding saline black water treatment. Furthermore, fluctuation of acetate and propionate in the influent does not seem to affect the performance of SRB, and propionate seems even beneficial for SRB in preventing methanogenesis. In the future more attention should be given to the integration of these findings with the SANI process, as well as on the overall seawater toilet-flushing concept.BiotechnologyApplied Science
Recurrent Genomic Alterations In Sequential Progressive Leukoplakia And Oral Cancer: Drivers Of Oral Tumorigenesis?
No full textA significant proportion (up to 62%) of oral squamous cell carcinomas (OSCCs) may arise from oral potential malignant lesions (OPMLs), such as leukoplakia. Patient outcomes may thus be improved through detection of lesions at a risk for malignant transformation, by identifying and categorizing genetic changes in sequential, progressive OPMLs. We conducted array comparative genomic hybridization analysis of 25 sequential, progressive OPMLs and same-site OSCCs from five patients. Recurrent DNA copy number gains were identified on 1p in 20/25 cases (80%) with minimal, high-level amplification regions on 1p35 and 1p36. Other regions of gains were frequently observed: 11q13.4 (68%), 9q34.13 (64%), 21q22.3 (60%), 6p21 and 6q25 (56%) and 10q24, 19q13.2, 22q12, 5q31.2, 7p13, 10q24 and 14q22 (48%). DNA losses were observed in >20% of samples and mainly detected on 5q31.2 (35%), 16p13.2 (30%), 9q33.1 and 9q33.29 (25%) and 17q11.2, 3p26.2, 18q21.1, 4q34.1 and 8p23.2 (20%). Such copy number alterations (CNAs) were mapped in all grades of dysplasia that progressed, and their corresponding OSCCs, in 70% of patients, indicating that these CNAs may be associated with disease progression. Amplified genes mapping within recurrent CNAs (KHDRBS1, PARP1, RAB1A, HBEGF, PAIP2, BTBD7) were selected for validation, by quantitative real-time PCR, in an independent set of 32 progressive leukoplakia, 32 OSSCs and 21 non-progressive leukoplakia samples. Amplification of BTBD7, KHDRBS1, PARP1 and RAB1A was exclusively detected in progressive leukoplakia and corresponding OSCC. BTBD7, KHDRBS1, PARP1 and RAB1A may be associated with OSCC progression. Protein-protein interaction networks were created to identify possible pathways associated with OSCC progression. © The Author 2014. Published by Oxford University Press. All rights reserved.231026182628Parkin, D.M., Global cancer statistics in the year 2000 (2001) Lancet Oncol., 2, pp. 533-543Jemal, A., Bray, F., Center, M.M., Ferlay, J., Ward, E., Forman, D., Global cancer statistics (2011) CA Cancer J. Clin., 61, pp. 69-90Carvalho, A.L., Nishimoto, I.N., Califano, J.A., Kowalski, L.P., Trends in incidence and prognosis for head and neck cancer in the United States: a site-specific analysis of the SEER database (2005) Int. J. Cancer, 114, pp. 806-816Atula, T., Silvoniemi, P., Kurki, T., Varpula, M., Grénman, R., The evaluation and treatment of the neck in carcinoma of the oral cavity (1997) Acta Otolaryngol. Suppl., 529, pp. 223-225Brunin, F., Mosseri, V., Jaulerry, C., Point, D., Cosset, J.M., Rodriguez, J., Cancer of the base of the tongue: past and future (1999) Head Neck, 21, pp. 751-759Forastiere, A., Koch, W., Trotti, A., Sidransky, D., Head and neck cancer (2001) N. Engl. J. Med., 345, pp. 1890-1900Silverman, S., Sugerman, P.B., Oral premalignancies and squamous cell carcinoma (2000) Clin. Dermatol., 18, pp. 563-568Lee, J.J., Hong, W.K., Hittelman, W.N., Mao, L., Lotan, R., Shin, D.M., Benner, S.E., Papadimitrakopoulou, V.M., Predicting cancer development in oral leukoplakia: ten years of translational research (2000) Clin. Cancer Res., 6, pp. 1702-1710Schepman, K., der Meij, E., Smeele, L., der Waal, I., Concomitant leukoplakia in patients with oral squamous cell carcinoma (1999) Oral Dis., 5, pp. 206-209Reibel, J., Prognosis of oral pre-malignant lesions: significance of clinical, histopathological, and molecular biological characteristics (2003) Crit. Rev. Oral Biol. Med., 14, pp. 47-62Mithani, S.K., Mydlarz, W.K., Grumbine, F.L., Smith, I.M., Califano, J.A., Molecular genetics of premalignant oral lesions (2007) Oral Dis., 13, pp. 126-133Tsui, I.F.L., Rosin, M.P., Zhang, L., Ng, R.T., Lam, W.L., Multiple aberrations of chromosome 3p detected in oral premalignant lesions (2008) Cancer Prev. Res. (Phila), 1, pp. 424-429Garnis, C., Chari, R., Buys, T.P.H., Zhang, L., Ng, R.T., Rosin, M.P., Lam, W.L., Genomic imbalances in precancerous tissues signal oral cancer risk (2009) Mol. Cancer, 8, p. 50Smith, J., Rattay, T., McConkey, C., Helliwell, T., Mehanna, H., Biomarkers in dysplasia of the oral cavity: a systematic review (2009) Oral Oncol., 45, pp. 647-653Huang, D.W., Sherman, B.T., Lempicki, R.A., Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources (2009) Nat. Protoc., 4, pp. 44-57Huang, D.W., Sherman, B.T., Lempicki, R.A., Bioinformatics enrichment tools: paths toward the comprehensive functional analysis of large gene lists (2009) Nucleic Acids Res., 37, pp. 1-13Rhodes, D.R., Yu, J., Shanker, K., Deshpande, N., Varambally, R., Ghosh, D., Barrette, T., Chinnaiyan, A.M., ONCOMINE: a cancer microarray database and integrated data-mining platform (2004) Neoplasia, 6, pp. 1-6Cervigne, N.K., Reis, P.P., Machado, J., Sadikovic, B., Bradley, G., Galloni, N.N., Pintilie, M., Gilbert, R., Identification of a microRNA signature associated with progression of leukoplakia to oral carcinoma (2009) Hum. Mol. Genet., 18, pp. 4818-4829Brown, K.R., Otasek, D., Ali, M., McGuffin, M.J., Xie, W., Devani, B., Toch, I.L., Jurisica, I., NAViGaTOR: Network Analysis, Visualization and Graphing Toronto (2009) Bioinformatics, 25, pp. 3327-3329Paris, P.L., Sridharan, S., Scheffer, A., Tsalenko, A., Bruhn, L., Collins, C., High resolution oligonucleotide CGH using DNA from archived prostate tissue (2007) Prostate, 67, pp. 1447-1455Johnson, N.A., Hamoudi, R.A., Ichimura, K., Liu, L., Pearson, D.M., Collins, V.P., Du, M.-Q., Application of array CGH on archival formalin-fixed paraffin-embedded tissues including small numbers of microdissected cells (2006) Lab. Invest., 86, pp. 968-978Albertson, D.G., Pinkel, D., Genomic microarrays in human genetic disease and cancer (2003) Hum. Mol. Genet., 12 (SPEC NO.), pp. R145-R152Forozan, F., Mahlamäki, E.H., Monni, O., Chen, Y., Veldman, R., Jiang, Y., Gooden, G.C., Kallioniemi, O.P., Comparative genomic hybridization analysis of 38 breast cancer cell lines: a basis for interpreting complementary DNA microarray data (2000) Cancer Res., 60, pp. 4519-4525Lucito, R., Healy, J., Alexander, J., Reiner, A., Esposito, D., Chi, M., Rodgers, L., Troge, J., Representational oligonucleotide microarray analysis: a high-resolution method to detect genome copy number variation (2003) Genome Res., 13, pp. 2291-2305Schwab, M., Amplification of the MYCN oncogene and deletion of putative tumour suppressor gene in humanneuroblastomas (1990) Brain Pathol., 1, pp. 41-46Ha, P.K., Benoit, N.E., Yochem, R., Sciubba, J., Zahurak, M., Sidransky, D., Pevsner, J., Califano, J., A transcriptional progression model for head and neck cancer (2003) Clin. Cancer Res., 9, pp. 3058-3064Siebers, T.J.H., Bergshoeff, V.E., Otte-Hö ller, I., Kremer, B., Speel, E.J.M., van der Laak, J.A.W.M., Merkx, M.A.W., Slootweg, P.J., Chromosome instability predicts the progression of premalignant oral lesions (2013) Oral Oncol., 49, pp. 1121-1128Saraswathi, T.R., Ranganathan, K., Shanmugam, S., Sowmya, R., Narasimhan, P.D., Gunaseelan, R., Prevalence of oral lesions in relation to habits: cross-sectional study in South India (2006) Indian J. Dent. Res., 17, pp. 121-125Ahmadi-Motamayel, F., Falsafi, P., Hayati, Z., Rezaei, F., Poorolajal, J., Prevalence of oral mucosal lesions in male smokers and nonsmokers (2013) Chonnam Med. J., 49, pp. 65-68Sujatha, D., Hebbar, P.B., Pai, A., Prevalence and correlation of oral lesions among tobacco smokers, tobacco chewers, areca nut and alcohol users (2012) Asian Pac. J. Cancer Prev., 13, pp. 1633-1637Bockmühl, U., Schwendel, A., Dietel, M., Petersen, I., Distinct patterns of chromosomal alterations in high-and low-grade head and neck squamous cell carcinomas (1996) Cancer Res., 56, pp. 5325-5329Califano, J., van der Riet, P., Westra, W., Nawroz, H., Clayman, G., Piantadosi, S., Corio, R., Koch, W., Genetic progression model for head and neck cancer: implications for field cancerization (1996) Cancer Res., 56, pp. 2488-2492Soder, A.I., Hopman, A.H., Ramaekers, F.C., Conradt, C., Bosch, F.X., Distinct nonrandom patterns of chromosomal aberrations in the progression of squamous cell carcinomas of the head and neck (1995) Cancer Res., 55, pp. 5030-5037Van Dyke, D.L., Worsham, M.J., Benninger, M.S., Krause, C.J., Baker, S.R., Wolf, G.T., Drumheller, T., Carey, T.E., Recurrent cytogenetic abnormalities in squamous cell carcinomas of the head and neck region (1994) Genes Chromosomes Cancer, 9, pp. 192-206Graveland, A.P., Bremmer, J.F., de Maaker, M., Brink, A., Cobussen, P., Zwart, M., Braakhuis, B.J.M., Leemans, C.R., Molecular screening of oral precancer (2013) Oral Oncol., 49, pp. 1129-1135Akervall, J.A., Jin, Y., Wennerberg, J.P., Zätterström, U.K., Kjellén, E., Mertens, F., Willén, R., Mitelman, F., Chromosomal abnormalities involving 11q13 are associated with poor prognosis in patients with squamous cell carcinoma of the head and neck (1995) Cancer, 76, pp. 853-859Hu, N., Wang, C., Ng, D., Clifford, R., Yang, H.H., Tang, Z.-Z., Wang, Q.-H., Goldstein, A.M., Genomic characterization of esophageal squamous cell carcinoma from a high-risk population in China (2009) Cancer Res., 69, pp. 5908-5917Paris, P.L., Sridharan, S., Hittelman, A.B., Kobayashi, Y., Perner, S., Huang, G., Simko, J., Collins, C., An oncogenic role for the multiple endocrine neoplasia type 1 gene in prostate cancer (2009) Prostate Cancer Prostatic Dis., 12, pp. 184-191Lee, J.-J., Au, A.Y.M., Foukakis, T., Barbaro, M., Kiss, N., Clifton-Bligh, R., Staaf, J., Robinson, B.G., Array-CGH identifies cyclin D1 and UBCH10 amplicons in anaplastic thyroid carcinoma (2008) Endocr. Relat. Cancer, 15, pp. 801-815Tanaka, Y., Kanai, F., Tada, M., Tateishi, R., Sanada, M., Nannya, Y., Ohta, M., Shiina, S., Gain of GRHL2 is associated with early recurrence of hepatocellular carcinoma (2008) J. Hepatol., 49, pp. 746-757Hwang, K.-T., Han, W., Cho, J., Lee, J.W., Ko, E., Kim, E.K., Jung, S.-Y., Kang, J.J., Genomic copy number alterations as predictive markers of systemic recurrence in breast cancer (2008) Int. J. Cancer, 123, pp. 1807-1815Higgins, M.E., Claremont, M., Major, J.E., Sander, C., Lash, A.E., CancerGenes: a gene selection resource for cancer genome projects (2007) Nucleic Acids Res., 35, pp. D721-D726Tsui, I.F.L., Poh, C.F., Garnis, C., Rosin, M.P., Zhang, L., Lam, W.L., Multiple pathways in the FGF signaling network are frequently deregulated by gene amplification in oral dysplasias (2009) Int. J. Cancer, 125, pp. 2219-2228Duran, A., Linares, J.F., Galvez, A.S., Wikenheiser, K., Flores, J.M., Diaz-Meco, M.T., Moscat, J., The signaling adaptor p62 is an important NF-kappaB mediator in tumorigenesis (2008) Cancer Cell, 13, pp. 343-354Shimada, K., Uzawa, K., Kato, M., Endo, Y., Shiiba, M., Bukawa, H., Yokoe, H., Tanzawa, H., Aberrant expression of RAB1A in human tongue cancer (2005) Br. J. Cancer, 92, pp. 1915-1921Bos, P.D., Zhang, X.H.-F., Nadal, C., Shu, W., Gomis, R.R., Nguyen, D.X., Minn, A.J., Foekens, J.A., Genes that mediate breast cancer metastasis to the brain (2009) Nature, 459, pp. 1005-1009Teramoto, T., Kawamata, H., Fujimori, T., How does adenosquamous carcinoma arise in the small intestine? (2003) J. Gastroenterol., 38, pp. 810-811Wang, Z., The role of COX-2 in oral cancer development, and chemoprevention/treatment of oral cancer by selective COX-2 inhibitors (2005) Curr. Pharm. Des., 11, pp. 1771-1777Pontes, H.A.R., Pontes, F.S.C., Fonseca, F.P., de Carvalho, P.L., Pereira, E.M., de Abreu, M.C., de Freitas Silva, B.S., dos Santos Pinto, D., Nuclear factor kB and cyclooxygenase-2 immunoexpression in oral dysplasia and oral squamous cell carcinoma (2013) Ann. Diagn. Pathol., 17, pp. 45-50Kalyankrishna, S., Grandis, J.R., Epidermal growth factor receptor biology in head and neck cancer (2006) J. Clin. Oncol., 24, pp. 2666-2672Taoudi Benchekroun, M., Saintigny, P., Thomas, S.M., El-Naggar, A.K., Papadimitrakopoulou, V., Ren, H., Lang, W., Feng, L., Epidermal growth factor receptor expression and gene copy number in the risk of oral cancer (2010) Cancer Prev. Res. (Phila), 3, pp. 800-809Sheu, J.J.-C., Hua, C.-H., Wan, L., Lin, Y.-J., Lai, M.-T., Tseng, H.-C., Jinawath, N., Lin, C.-F., Functional genomic analysis identified epidermal growth factor receptor activation as the most common genetic event in oral squamous cell carcinoma (2009) Cancer Res., 69, pp. 2568-2576Pan, W., Zhang, Q., Xi, Q.S., Gan, R.B., Li, T.P., FUP1, a gene associated with hepatocellular carcinoma, stimulates NIH3T3 cell proliferation and tumor formation in nude mice (2001) Biochem. Biophys. Res. Commun., 286, pp. 1033-1038Rodríguez, M.I., Peralta-Leal, A., O'Valle, F., Rodriguez-Vargas, J.M., Gonzalez-Flores, A., Majuelos-Melguizo, J., López, L., Rodríguez-Manzaneque, J.C., PARP-1regulates metastatic melanoma through modulation of vimentin-induced malignant transformation (2013) PLoS Genet., 9, pp. e1003531Costello, E., Greenhalf, W., Neoptolemos, J.P., New biomarkers and targets in pancreatic cancer and their application to treatment (2012) Nat. Rev. Gastroenterol. Hepatol., 9, pp. 435-444Onodera, T., Sakai, T., Hsu, J.C., Matsumoto, K., Chiorini, J.A., Yamada, K.M., Btbd7 regulates epithelial cell dynamics and branching morphogenesis (2010) Science, 329, pp. 562-565Wicki, A., Lehembre, F., Wick, N., Hantusch, B., Kerjaschki, D., Christofori, G., Tumor invasion in the absence of epithelial-mesenchymal transition: podoplanin-mediated remodeling of the actin cytoskeleton (2006) Cancer Cell, 9, pp. 261-272De Vicente, J.C., Rodrigo, J.P., Rodriguez-Santamarta, T., Lequerica-Fernández, P., Allonca, E., García-Pedrero, J.M., Podoplanin expression in oral leukoplakia: tumorigenic role (2013) Oral Oncol., 49, pp. 598-603Wu, I., Moses, M.A., BNF-1, a novel gene encoding a putative extracellular matrix protein, is overexpressed in tumor tissues (2003) Gene, 311, pp. 105-110Ellermeier, C., Smith, G.R., Cohesins are required for meiotic DNA breakage and recombination in Schizosaccharomyces pombe (2005) Proc. Natl Acad. Sci. USA, 102, pp. 10952-10957Kalejs, M., Ivanov, A., Plakhins, G., Cragg, M.S., Emzinsh, D., Illidge, T.M., Erenpreisa, J., Upregulation of meiosis-specific genes in lymphoma cell lines following genotoxic insult and induction of mitotic catastrophe (2006) BMC Cancer, 6, p. 6Severino, P., Alvares, A.M., Michaluart, P., Okamoto, O.K., Nunes, F.D., Moreira-Filho, C.A., Tajara, E.H., Global gene expression profiling of oral cavity cancers suggests molecular heterogeneity within anatomic subsites (2008) BMC Res. Notes, 1, p. 113Nasser, W., Flechtenmacher, C., Holzinger, D., Hofele, C., Bosch, F.X., Aberrant expression of p53, p16INK4a and Ki-67 as basic biomarker for malignant progression of oral leukoplakias (2011) J. Oral Pathol. Med., 40, pp. 629-635Meric, F., Hunt, K.K., Translation initiation in cancer: a novel target for therapy (2002) Mol. Cancer Ther., 1, pp. 971-979Weber, A., Wittekind, C., Tannapfel, A., Genetic and epigenetic alterations of 9p21 gene products in benign and malignant tumors of the head and neck (2003) Pathol. Res. Pract., 199, pp. 391-397Brito, J.A.R., Gomes, C.C., Guimarães, A.L.S., Campos, K., Gomez, R.S., Relationship between microRNA expression levels and histopathological features of dysplasia in oral leukoplakia (2013) J. Oral Pathol. Med.Yang, C.-C., Hung, P.-S., Wang, P.-W., Liu, C.-J., Chu, T.-H., Cheng, H.-W., Lin, S.-C., miR-181 as a putative biomarker for lymph-node metastasis of oral squamous cell carcinoma (2011) J. Oral Pathol. Med., 40, pp. 397-404Sadikovic, B., Andrews, J., Carter, D., Robinson, J., Rodenhiser, D.I., Genome-wide H3K9 histone acetylation profiles are altered in benzopyrene-treated MCF7 breast cancer cells (2008) J. Biol. Chem., 283, pp. 4051-4060Devries, S., Nyante, S., Korkola, J., Segraves, R., Nakao, K., Moore, D., Bae, H., Waldman, F., Array-based comparative genomic hybridization from formalin-fixed, paraffin-embedded breast tumors (2005) J. Mol. Diagn., 7, pp. 65-71Paris, P.L., Albertson, D.G., Alers, J.C., Andaya, A., Carroll, P., Fridlyand, J., Jain, A.N., Krijtenburg, P.-J., High-resolution analysis of paraffin-embedded and formalin-fixed prostate tumors using comparative genomic hybridization to genomic microarrays (2003) Am. J. Pathol., 162, pp. 763-770Bohlander, S.K., Espinosa, R., Le Beau, M.M., Rowley, J.D., Díaz, M.O., A method for the rapid sequence-independent amplification of microdissected chromosomal material (1992) Genomics, 13, pp. 1322-1324Livak, K.J., Schmittgen, T.D., Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) method (2001) Methods, 25, pp. 402-408Brown, K.R., Jurisica, I., Online predicted human interaction database (2005) Bioinformatics, 21, pp. 2076-2082Brown, K.R., Jurisica, I., Unequal evolutionary conservation of human protein interactions in interologous networks (2007) Genome Biol., 8, pp. R95Shirdel, E.A., Xie, W., Mak, T.W., Jurisica, I., NAViGaTing the micronome-using multiple microRNA prediction databases to identify signalling pathway-associated microRNAs (2011) PLoS ONE, 6, pp. e1742
