0)[26] grade 2 from previous anti-cancer therapy Alanine aminotra

0)[26] grade 2 from previous anti-cancer therapy Alanine aminotransferase (ALT), aspartate aminotransferase (AST), or alkaline phosphatase (ALP) >5× Upper Limit of Normal (ULN), serum

bilirubin >1.5× ULN or serum creatinine >185 µmol/L Leukocytes <4.0 10 9/l and/or platelet count <150 10 9/l Significant cardiac event (e.g. myocardial Selleckchem SRT1720 infarction, superior vena cava (SVC) syndrome, New York Heart Association (NYHA) classification of heart disease ≥2 within 3 months before entry, or presence of cardiac disease that, in the opinion of the investigator, increases the risk of ventricular arrhythmia Pregnancy or breast feeding Comorbidity with a grave prognosis (estimated survival <3 months) and/or worse than the basic disease for which the patients will be included in the study Abnormalities of the bile ducts (such as stents) with an increased chance of infection Diseases with an increased chance of liver toxicity, such as primary biliary cirrhosis or xeroderma pigmentosum Patients who are declared

incompetent or have a psychiatric disorder that makes a comprehensive judgement impossible, such as psychosis, hallucinations and/or depression Previous enrolment in the present study or previous treatment with radioembolization Treatment with an investigational Ion Channel Ligand Library research buy agent within 42 days prior to enrolment Female patients who are not using an acceptable method of contraception or are less than 1 year postmenopausal or surgically sterile during their participation in this study (from the time the consent form is signed) to prevent pregnancy Male patients who are not surgically sterile or do not use an acceptable

method of contraception during their participation in this study to prevent pregnancy in a partner Evidence of portal hypertension, splenomegaly or ascites Body weight >150 kg Active hepatitis (B and/or Fossariinae C) Liver weight >3 kg (determined by software using CT data) Allergy for intravenous contrast agent used (Visipaque ®) General MRI contra-indications (severe claustrophobia, metal implants, implanted pacemaker and/or neurostimulators) Patients who have arterial variations that will not allow whole liver treatment by a single administration via the hepatic artery Acknowledgements The authors thank Ms. Tjitske Bosma (clinical research coordinator, University Medical Center Utrecht) for her contribution to the study design and coordination, and Mr. Remmert de Roos for his assistance in the preparation of the microspheres. This study was selleck financially supported by the Dutch Cancer Society (KWF Kankerbestrijding), under grant UU2009-4346. References 1. Choti MA, Bulkley GB: Management of hepatic metastases. Liver Transpl Surg 1999, 5:65–80.PubMedCrossRef 2. Russell AH, Tong D, Dawson LE, Wisbeck W: Adenocarcinoma of the proximal colon. Sites of initial dissemination and patterns of recurrence following surgery alone.

So, there is a suggestion that mutation in OCCR is less penetrate

So, there is a suggestion that mutation in OCCR is less penetrate for breast LY2874455 cancer at younger ages. In the current study, RAD001 in vitro the BRCA2 mutation in exon 9 is outside the

OCCR. This explains why all the Egyptian breast cancer patients having this mutation are of young age, less than forty. In our study, the identified repeated mutation in exon 13 of BRCA1 gene is a nonsense mutation (4446 C–T). It was detected in 20% of families. This mutation was found frequently in French-Canadian families and two families in France [35]. These multiple instances of mutation did not represent a founder effect many generations in the past. There was evidence for multiple independent BRCA1 mutational events and so multiple origins [41]. The 4446 C–T mutation is one of the most common mutations found in the Breast Cancer Information Core Data base. These mutations are likely to have arisen independently owing to the presence of mutational hot spots in the coding sequence of the gene [42]. The last investigated exon in BRCA1 gene see more for detection of mutation was exon 8. It has been found that 13.3% of index patients and half their asymptomatic relatives have mutation in exon 8(738 C–A). This mutation is a missense mutation predicted to destroy the protein ring-finger. Hamann et al. [37] found one missense mutation in exon 8 of BRCA1 gene in Germany.

Farnesyltransferase The coexistence of more than founder mutation has been reported in some Ashkenazi Jewish families [40]. In the current study, four families of the 60 Egyptian families were found to have inherited

mutation in both BRCA1 and BRCA2 genes, they are double heterozygote. Previous studies described an Ashkenazi Jewish patient found to have germline mutations in both BRCA1 and BRCA2 genes [43]. The potential explanation for the occurrence of the two mutations occurring in the same individual is that BRCA1 and BRCA2 have been implicated in the maintenance of genomic integrity [9, 11]. Collectively, it is obvious that BRCA1 and/or BRCA 2 mutations have been found to account for a greater proportion of breast cancer patients among the studied families. This observation might be due to the relatively young ages of diagnosis of breast cancer and that the hereditary cancers occur disproportionally in young women. The accumulation of BRCA1 and BRCA2 mutations data from sets of families revealed the prevalence of different mutations and the significance of the putative recurrent founder mutations in Egyptians. The high frequency of any recurrent mutation (frame shift), so far, suggest that there may be a strong BRCA1 and 2 founder effects in Egyptian population. The presence of putative founder mutations, which leading to reduce genetic heterogeneity of BRCA genes, facilitates carrier detection and genetic counseling.

Linear regression using least

Linear regression using least squares was used to determine the correlation and the equation of the best-fit line between the 16S rRNA gene percent identity and the shared proteins measure, and between the 16S rRNA gene percent identity and the average unique proteins measure. Preliminary results showed that genera having many very closely related isolates (such as many

isolates of the same species) had much higher correlations between 16S rRNA gene percent identity and the two proteomic similarity measures than genera having fewer very closely related isolates. Further analysis revealed that this phenomenon was caused by pairs

of these closely related isolates www.selleckchem.com/products/ew-7197.html “”anchoring”" the regression line, leading to an artificially good linear relationship. To avoid this bias, we initially tried excluding pairs of isolates from the same species. This approach was problematic, however, because the nomenclature for some pairs of isolates classifies them as belonging to different species even though their 16S rRNA genes are nearly identical. For example, the 16S rRNA gene of B. anthracis strain Sterne is 99.85% identical to that of Bacillus cereus strain ATCC 14579. Thus, we instead included pairs of isolates in the analysis only if their 16S rRNA genes were less than 99.5% identical, regardless of their www.selleckchem.com/products/MDV3100.html accepted species naming. To further compare 16S rRNA gene similarity EGFR inhibitor with our two proteomic similarity measures, we generated three phylogenetic trees, each of which was based on a different distance metric. The distance metric used for the first tree was 16S rRNA gene similarity. 16S rRNA gene alignments were created by downloading sequences from the RDP10 website that were pre-aligned based on secondary structure [49]. The evolutionary history was inferred using the maximum likelihood neighbour-joining method [50] within the Molecular

Evolutionary Genetics Analysis (MEGA) program [51]. Within MEGA, a bootstrap test with 1000 replicates was used. The second tree used the same metric employed Cell press by Snel et al. [13], which is 1 – S/P, where S is the number of shared proteins between two isolates and P is the size of the smaller proteome. The metric used for the third tree was simply the average unique proteins measure described above. For the protein-based distance metrics, trees were created using the unweighted pair group method with arithmetic mean (UPGMA). Graphical representations of the complete trees were created using Geneious [52], while those of the collapsed trees were created using MEGA [51].

Immediately after administration of the intravenous infusion to a

Immediately after administration of the intravenous infusion to a subject, a balloon-type gas detector tube (Kitagawa Gas Detector Tube System; Komyo Rikagaku Kogyo KK, Kanagawa, Japan) was used click here to measure the concentration of ethanol in exhaled breath. The levels of aspartic acid aminotransferase (AST) and alanine aminotransferase (ALT) were noted from the medical records, and the alcohol drinking history was taken from each patient. Statistics Correlations LY2603618 between the total amount of ethanol administered and the ethanol concentration in exhaled breath, and between

the intravenous infusion speed and the ethanol concentration in exhaled breath, were calculated using Pearson’s correlation coefficient. Regression MK-0457 analysis was applied to each combination. Results Patient Characteristics, Treatment, and Breath Ethanol Concentrations

The patient characteristics, the amount of paclitaxel administered, the speed of the intravenous infusion, and the concentration of ethanol in exhaled breath are summarized in table I. The average ethanol concentration in exhaled breath immediately after the intravenous infusion of paclitaxel was 0.028 ± 0.015 mg/L (range 0.00–0.06). Table I Ethanol concentrations in exhaled breath of individual patients Hepatic function in all patients was assessed to be within the normal range, as indicated by AST and ALT values of 12–33 U/L and 12–62 U/L, respectively. Relationship between Ethanol Concentrations in Exhaled Breath and the Total Volume or Infusion Speed of Ethanol The correlation coefficient between the total amount of ethanol administered via the intravenous infusion and the ethanol concentration in exhaled breath was weak (R2 = 0.25; p = 0.055) [figure 1a]. In contrast, the intravenous infusion speed had a relatively stronger positive correlation with the concentration of exhaled ethanol (R2 = 0.49;

p = 0.11) [figure 1b]. Fig. 1 Relationship between the ethanol concentration in exhaled breath and (a) the total amount of ethanol administered via the intravenous paclitaxel infusion; and (b) the speed of the paclitaxel infusion. The data-point markers represent observed data. The oblique DCLK1 black data lines represent the fitted curves. Discussion More than 90% of ethanol is metabolized by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase 2 (ALDH2) in the liver[7] It has been reported that people with low ALDH2 activity show hereditary sensitivity to the effects of alcohol, and approximately 50% of Japanese people are poor alcohol metabolizers[8] Thus, the percentage of Japanese people who experience facial flush and heart palpitations in association with elevated blood aldehyde concentrations after drinking alcohol is larger than that of Europeans and Americans. Inter-individual differences in alcohol metabolism are also larger in the Japanese population.

2 0 2 3 1 0 465 1 0 3 0 0 099  Decreased musc activity T1-T3 10

2 0.2 3.1 0.465 1.0 3.0 0.099  Decreased musc. activity T1-T3 10.6 4.1 0.1 3.0 0.648 1.4 3.3 0.049*

Observed work ability: Dexterity/gross movements test  Decreased pain T1-T2 13.4 2.8 0.9 2.1 0.056 0.4 2.9 0.517  Decreased pain T1-T3 13.3 2.6 0.6 2.2 0.275 0.7 2.2 0.249  Decreased musc. activity T1-T2 13.9 2.0 0.5 1.8 0.118 0.4 1.9 0.181  Decreased musc. activity T1-T3 14.0 2.3 0.3 2.0 0.461 0.3 2.0 0.407 * P ≤ 0.05 Discussion The main results of this RCT study are lowered pain at follow-up among both intervention groups in Tipifarnib in vitro relation to the controls. Decreased pain was associated with increased self-rated and selleck kinase inhibitor indicated for observed work ability (P = 0.056). Both interventions showed positive results among female workers with chronic neck pain on long-term sick leave. Consequently, they could be beneficially developed for use in occupational health or primary care practice to decrease pain and increase work ability. The types of interventions were associated with different outcomes, which may illustrate their various time to effect of intervention and sustainability of effect. The results can be generalized to similar groups (regarding health status and societal context), taking into account

the below described considerations. Muscular strength training showed better results in terms of self-rated work ability and mental health. The majority of Selleckchem TPCA-1 participating women were employed in care of the elderly and disabled, where requirements regarding mental health and physical fitness are fairly high. Although longer periods of physical training might be needed to reduce chronic pain, the participants were encouraged to continue their training after the intensive program. The positive

results may therefore be due to changed behavior. Earlier studies have shown positive results from intensive training program, but there are few studies of how long time of coaching that is needed (Hartigan et al. 1996; Kay et al. 2005, Hurwitz et al. 2008). One review study recommended 4–6 weeks Edoxaban of intensive coaching, followed by 12–18 months of rehabilitation (Hartigan et al. 1996). Studies involving similar target groups have shown that both static strength and muscular endurance increased after an intervention with strength training among women with work-related trapezius myalgia (Andersen et al. 2008a; b). The same study series also indicates that strength training may alleviate pain in patients with trapezius myalgia. Another RCT showed that the threshold for perceived exertion and pain may be increased by muscular strength training (Hagberg et al. 2000). The myofeedback intervention was associated with increased vitality, increased performance in the cutlery wiping performance test. The results of our study regarding changed muscle activation showed increased gaps in more follow-up test after myofeedback compared to the controls and among participants in the intensive muscular strength training group (L. Sandsjö et al.


our study, we precisely characterized the composition


our study, we precisely characterized the composition of quinoa chromosomes by exposing only 1 ms of dwell time to avoid the radiation damage. Here we have shown for the first time the advantages of utilizing atomic force microscopy (AFM) and scanning electron microscopy (SEM) for the morphological characterization (at the atomic and nanoscale level) and STXM for the compositional characterization (at the nanoscale level) of chromosomes. The morphology and the biochemical properties inside a single quinoa chromosome were determined by utilizing nanoscale imaging tools such as STXM, AFM, SEM, and confocal laser scanning microscopy (CLSM). Methods Root tip preparation Chromosomes were isolated from the meristematic tissue of quinoa root tips. Seeds of Chenopodium quinoa were germinated on moist filter papers in petri dishes at room temperature in

XAV-939 molecular weight the dark over 48 h. For cytogenetic Sepantronium price analysis, primary root tips were pretreated with 2 mM 8-hydroxyquinoline for 4 h at room temperature, followed by incubation in ice-cold water overnight, fixed in methanol-glacial acetic acid (3:1 ratio), and stored at -4°C for further use. Cell suspension About 2-mm meristematic tips from each root were removed followed by dissection into the smallest possible sections. The root tip sections were macerated in a 200-μL enzyme reaction mixture for 4 h at 37°C. After the incubation time, the solution was filtered through a 50-μm gauze twice.

To this filtered solution, 2 ml of 75 mM KCl solution was added. This suspension was centrifuged for 70 min at 20°C at 760 rpm. The supernatant was discarded and the precipitate was re-suspended in 3 ml of the 3:1 fixative (methanol: acetic acid) and again centrifuged for 7 min at 760 rpm/75 g at 20°C. The above process was repeated five times. After discarding the supernatant from the final wash, the resulting pellet was re-suspended in 200 μL of the 3:1 fixative. AFM imaging In an attempt to prepare a full set of chromosomes, the samples were prepared not from the cell much suspension but using the maceration technique reported by Neethirajan et al. [14]. Briefly, the pretreated quinoa root tips were incubated in an enzyme solution of 2% cellulase, 2% pectolyase, and 1.5% macerozyme for 90 min at 37°C, followed by squashing on the glass slides by tapping with the tip of forceps in 30% acetic acid. The squashed specimens were further cleaned using 1X SSC to remove the cellular debris, before being imaged using AFM. The samples were first observed with an inverted phase contrast optical microscope (Nikon XMU-MP-1 research buy Eclipse Ti, Nikon Instruments, Tokyo, Japan) and photographed to determine the location of the chromosomes to be studied by AFM. The glass slides were marked underneath as a possible region of interest for AFM imaging.

The bands were detected with EzWest Lumi plus (ATTO, Tokyo, Japan

The bands were detected with EzWest Lumi plus (ATTO, Tokyo, Japan) and ImageQuant LAS 4000mini (GE Healthcare UK Ltd, Little Chalfont, UK). Liquid chromatography (LC)/mass spectrometry (MS) analysis Protein spots in gels were compared and

analyzed by visual inspection. The gel spots were stored in 1% acetic acid and were subjected to LC/MS/MS analysis. Identification of proteins was carried out using Mascot server (Matrix Science) with datasets of rodent and Leptospira proteomes. A protein score of >40 was used to select proteins with significant matching. The difference between the theoretical and experimental mass and pI was also used to determine significant matching. Acknowledgments This study was supported by a grant of the Science and Technology Research Partnership for Sustainable Development (SATREPS) program from Japan Science and Technology Agency (JST) and Japan International Cooperation Agency (JICA). We thank selleck chemicals Dr. H. Sumimoto and colleagues of the Research Support Center, Graduate

School of Medical Sciences, Kyushu University for their technical support and advice. We also thank Sayaka Akiyoshi, Takayoshi Yamaguchi, Hideko Kameyama, and Naomi Hidaka for their technical cooperation. Electronic supplementary material Additional file 1: Table S1: Amino acid sequence coverage of leptospiral HADH by LC/MS/MS. (DOC 33 KB) References 1. Levett PN: Leptospirosis. Selleck SYN-117 Clin Microbiol Rev 2001,14(2):296–326.PubMedCentralPubMedCrossRef

2. Bharti AR, Nally JE, Ricaldi JN, Matthias MA, Diaz MM, Lovett MA, Levett PN, Gilman RH, Willig MR, Gotuzzo E, Vinetz JM, Peru-United States Leptospirosis Consortium: Leptospirosis: a zoonotic disease of global importance. mTOR inhibitor Lancet Infect Dis 2003,3(12):757–771.PubMedCrossRef 3. Picardeau M: Diagnosis and epidemiology of leptospirosis. Med Mal Infect 2013,43(1):1–9.PubMedCrossRef 4. Adler B, de la Pena MA: Leptospira and leptospirosis. Vet Microbiol 2010,140(3–4):287–296.PubMedCrossRef 5. Toyokawa T, Ohnishi ADP ribosylation factor M, Koizumi N: Diagnosis of acute leptospirosis. Expert Rev Anti Infect Ther 2011,9(1):111–121.PubMedCrossRef 6. Vijayachari P, Sugunan AP, Shriram AN: Leptospirosis: an emerging global public health problem. J Biosci 2008,33(4):557–569.PubMedCrossRef 7. Camargo ED, da Silva MV, Batista L, Vaz AJ, Sakata EE: An evaluation of the ELISA-IgM test in the early diagnosis of human leptospirosis. Rev Inst Med Trop Sao Paulo 1992,34(4):355–357.PubMedCrossRef 8. Fonseca Cde A, Teixeira MM, Romero EC, Tengan FM, Silva MV, Shikanai-Yasuda MA: Leptospira DNA detection for the diagnosis of human leptospirosis. J Infect 2006,52(1):15–22.PubMedCrossRef 9. Balassiano IT, Vital-Brazil JM, Pereira MM: Leptospirosis diagnosis by immunocapture polymerase chain reaction: a new tool for early diagnosis and epidemiologic surveillance. Diagn Microbiol Infect Dis 2012,74(1):11–15.PubMedCrossRef 10.

Nearly 40% of the starting suspension of yeast cells were recover

Nearly 40% of the starting suspension of yeast cells were recovered when cells were slowly frozen in an 8% DMSO-containing solution and this procedure was selected for long term storage of mutant pools. Although specialized Poziotinib clinical trial cooling apparatuses can be used to control the freezing rate, we found that simple placement of vials of cells within readily and cheaply obtained styrofoam containers (such as those used for shipments of molecular biology enzymes) was sufficient. Figure 2 Gradual freezing in DMSO maximizes recovery of cryopreserved Histoplasma yeast. R428 mouse WU15 yeast were frozen in varying concentrations of glycerol (A) or DMSO (B). Histoplasma yeast were grown

to late log/early stationary phase in rich medium and added to the appropriate glycerol- or DMSO-containing solutions before freezing. Final cryoprotectant concentrations

indicated along the x-axis of each graph. Vials were placed immediately Adriamycin at -80°C (rapid freeze) or were placed into a styrofoam container before placement at -80°C (slow freeze). Frozen cell aliquots were thawed after 1 week or 9 weeks and recovery measured as the number of viable cfu relative to the number present before freezing. Generation of mutant pools Insertion mutants were generated in the NAm 2 Histoplasma strain WU15 by co-cultivation of Agrobacterium tumefaciens and Histoplasma yeast cells. Co-cultures were plated onto filters and Histoplasma transformants selected Glycogen branching enzyme by transferring filters to medium containing hygromycin to which resistance is provided by sequences within the T-DNA element [23]. Transformant yeast cells were collected and suspensions from individual plates combined to create pools derived from 100 to 200 independent mutant colonies. Yeast cell suspensions were diluted into fresh medium and allowed to grow for 24-48 hours. Twenty-four pools were prepared representing roughly 4000 insertion mutants. A portion of each culture was reserved for nucleic acid isolation and the remainder frozen in aliquots and stored at -80°C. Nucleic acids were purified from

each pool, diluted to 50 ng/ul, and stored at -20°C until analysis by PCR. With an estimated 9000-10,000 genes encoded by the Histoplasma genome, this collection does not represent the number of insertion mutants required for saturation of the genome. We used two probability functions to estimate the size of the library required for a 95% chance of isolating an insertion in a particular locus in the 40 megabase NAm 2 genome. Both calculations assume no bias in insertion sites. Based on the number of predicted genes, the Poisson approach estimates a library of approximately 30,000 insertions would be required. The single study in which multiple alleles of a single locus were isolated in Histoplasma (five AGS1 alleles isolated in a screen of 50,000 insertions; [23]) supports the Poisson calculation; five alleles would be the most probable number of alleles based on a 9000 or 10,000 target estimate.

2), the non-relaxed fraction of quantum yield after 30 min in dar

2), the non-relaxed fraction of quantum yield after 30 min in dark (q i) was 0.30 ± 0.04 in the sun leaves and 0.39 ± 0.07 in the shade leaves. Increase

of relative variable fluorescence at 2 ms (V J) indicates stronger limitation of electron transport from QA to QB as shown also numerically by the Selleck AG-881 values of probability (ψET2o) of trapped PSII electron transfer from reduced QA to QB (Table 4). The variable Chl fluorescence increase from I to P represents the measure of electron transport from QB beyond PSI (Munday and Govindjee 1969; Schansker et al. 2003). As is evident by the values of the probability with which the electron moves toward PRIMA-1MET purchase PSI end acceptors, ψRE1o, the electron transport between PSII and PSI after HL treatment becomes 3 Methyladenine less limited (Table 4), especially in shade leaves. (For a detailed discussion on the interpretation of the J–I–P rise (the so-called thermal phase of fast ChlF kinetics), see a review by Stirbet and Govindjee 2012). Another explanation for the above results is that HL treatment affects the post-illumination redox state of the PQ pool, and the activation state of the PS I acceptor side (e.g., due to FNR activity) probably does not decay within the 30-min dark period that was used before the measurements. Stromal

components can donate electrons to the PQ pool in the dark. Reduction in the dark can be substantially stimulated by pre-illumination with strong light (Asada et al. 1992). An increase of PQ-pool reduction with respect to the control will induce an increase of the J-step (Toth et al. 2007) and, hence, of all the parameters based on the values of V J. This

is also supported by increased values of F 0 in samples 30 min after HL treatment. The changes of connectivity parameters (p 2G, p, ω) after HL treatment were mostly insignificant (Table 4); moreover, according to Laisk and Oja (2013), estimates of p parameter can be strongly influenced by the redox status of the PQ pool. Since F 0 value may increase in samples after HL treatment, calculated values of connectivity parameters may not be used as a measure of true PSII connectivity. Nevertheless, the insignificant differences between the F 0 values Pregnenolone before and after HL treatment and the maintained significance of differences between the sun and shade leaves suggest that the estimate of connectivity parameters could not be as prone to errors due to PQ redox status as expected. The membrane model parameters (Table 4) show energy flux parameters per active RC. A higher value of the inferred absorbance per RC (ABS/RC) in shade leaves before HL treatment (~2.6) as compared to the sun leaves (~2.2) seems to indicate increased antenna size per active RC (Strasser et al. 2000; Stirbet and Govindjee 2011). However, a correction for connectivity (Suppl. Table 2; see information given in parentheses), i.e., multiplying the ABS/RC by 1 + C where C is the curvature constant of the relative variable fluorescence curve (Force et al.

Cancer Gene Ther 2000, 7:66–73 PubMedCrossRef 21 Yu YA, Shabahan

Cancer Gene Ther 2000, 7:66–73.PubMedCrossRef 21. Yu YA, Shabahang S, Timiryasova TM, Zhang Q, Beltz R, Gentschev I, Goebel W, Szalay AA: Visualization of tumors and metastases in live animals with bacteria and vaccinia virus encoding light-emitting proteins. Nat Biotechnol 2004, 22:313–320.PubMedCrossRef 22. Hingorani M, Spitzweg C, Vassaux G, Newbold HSP990 manufacturer K, check details Melcher A, Pandha H, Vile R, Harrington K: The biology of the

sodium iodide symporter and its potential for targeted gene delivery. Curr Cancer Drug Targets 2010, 10:242–267.PubMedCrossRef 23. Lee YJ, Chung JK, Shin JH, Kang JH, Jeong JM, Lee DS, Lee MC: In vitro and in vivo properties of a human anaplastic thyroid carcinoma cell line transfected with the sodium iodide symporter gene. Thyroid 2004, 14:889–895.PubMedCrossRef 24. Cengic N, Baker CH, Schutz M, Goke B, JQ-EZ-05 supplier Morris JC, Spitzweg C: A novel therapeutic strategy for medullary thyroid cancer based on radioiodine therapy following tissue-specific sodium iodide symporter gene expression. J Clin Endocrinol Metab 2005, 90:4457–4464.PubMedCrossRef 25. Kakinuma H, Bergert ER, Spitzweg C, Cheville JC, Lieber MM, Morris JC: Probasin promoter (ARR(2)PB)-driven, prostate-specific expression of the human sodium iodide symporter (h-NIS) for targeted radioiodine therapy of prostate cancer. Cancer

Res 2003, 63:7840–7844.PubMed 26. Scholz IV, Cengic N, Baker CH, Harrington KJ, Maletz K, Bergert ER, Vile R, Goke B, Morris JC, Spitzweg C: Radioiodine therapy of colon cancer following tissue-specific oxyclozanide sodium iodide symporter gene transfer. Gene Ther 2005, 12:272–280.PubMedCrossRef 27. Dwyer RM, Bergert ER, O’Connor

MK, Gendler SJ, Morris JC: In vivo radioiodide imaging and treatment of breast cancer xenografts after MUC1-driven expression of the sodium iodide symporter. Clin Cancer Res 2005, 11:1483–1489.PubMedCrossRef Competing interests No competing financial interests exist for Kyong-Hwa Jun, Tae-Jin Song, Sepideh Gholami, Joyce Au, Dana Haddad, Carson Joshua, Chun-Hao Chen, Kelly Mojica, Pat Zanzonico, and Yuman Fong. Nanhai G. Chen, Qian Zhang, and Aladar A. Szalay are affiliated with Genelux Corporation. Authors’ contributions SG assisted with the write up of the manuscript. TS assisted in the in vivo experiments and contributed to the study design. JA contributed to the cytotoxicity assay. DH contributed to the in vivo PET and SPECT imaging. JC contributed to fluorescent imaging. CC contributed to the statistical analysis of the data. KM contributed to the viral replication assay. PZ contributed to the study design and radioactive imaging experiments. NC and QZ contributed to the viral sequence and construct. AS and YF contributed to the study design and completion of the manuscript. All authors read and approved the final manuscript.