Bodipy photosensitizer linked hybrid nanomaterials for photodynamic therapy

Photodynamic therapy (PDT) is an alternative clinically approved treatment method to obliterate the cancerous lesion by producing reactive oxygen species (ROS) via activated photosensitizer (PS) molecule at a certain wavelength1. In recent years, Bodipy (4,4-difluoro-4-bora-3a,4a-diaza-s-indacene) as a photosensitizer molecule has been extensively investigated in PDT2,3. However, the use of many Bodipy PS in PDT has been limited due to their insolubility in aqueous solutions. Therefore, nanotechnology offers tremendous solutions to building up nano-carrier systems for insoluble molecules. We have herein developed a stable formulation of hybrid Bodipy PS via conjugation of TiO2 nanoparticles to the Bodipy PS. In this study, a heavy metal substituted Bodipy PS molecule has been synthesized and linked to polyethyleneimine (PEI) functionalized TiO2 nanoparticles to increase the stability and biocompatibility of the photosensitizer in physiological conditions (pH:7.4) as a potential photodynamic therapy agent and investigated PDT effect on CRL-4010 and MDA-MB-231 cancer cells.No sponso

Bodipy photosensitizer linked hybrid nanomaterials for photodynamic therapy

Photodynamic therapy (PDT) is an alternative clinically approved treatment method to obliterate the cancerous lesion by producing reactive oxygen species (ROS) via activated photosensitizer (PS) molecule at a certain wavelength1. In recent years, Bodipy (4,4-difluoro-4-bora-3a,4a-diaza-s-indacene) as a photosensitizer molecule has been extensively investigated in PDT2,3. However, the use of many Bodipy PS in PDT has been limited due to their insolubility in aqueous solutions. Therefore, nanotechnology offers tremendous solutions to building up nano-carrier systems for insoluble molecules. We have herein developed a stable formulation of hybrid Bodipy PS via conjugation of TiO2 nanoparticles to the Bodipy PS. In this study, a heavy metal substituted Bodipy PS molecule has been synthesized and linked to polyethyleneimine (PEI) functionalized TiO2 nanoparticles to increase the stability and biocompatibility of the photosensitizer in physiological conditions (pH:7.4) as a potential photodynamic therapy agent and investigated PDT effect on CRL-4010 and MDA-MB-231 cancer cells.No sponso

Personalized treatment options in Non-small Cell Lung Cancer

Lung cancer is the leading cause of cancer related death among both men and women worldwide [1-3]. There are two major groups of lung cancer based on the histological features and response to therapy; non small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). NSCLC is also divided to the histological subtypes, and which accounts 80% of lung cancer patients [3, 4] . Despite advances in diagnosis, 5-year survival rates are approximately 15% for all cases [5] . Since EGFR (epidermal growth factor receptors) is overexpressed in more than 80% of NSCLC patients, its overexpression is correlated with poor prognosis and chemoresistance. However, only 10% of EGFR1 overexpressing patients respond to EGFR1 TKI (tyrosine kinase inhibitor) therapy implying that EGFR1 overexpression may not be the main factor responsible for NSCLC development [6, 7]. Therefore, new therapeutic strategies that specifically target other molecular pathways must be considered as alternative options. In this review, we tried to summarize the most recent studies in treatment of NSLC, and made suggestions on the basis of our results and clinical studies

Epithelial mesenchymal transition regulator TWIST1 transcription factor stimulates glucose uptake through upregulation of GLUT1, GLUT3, and GLUT12 in vitro

TWIST1 is a major regulator of epithelial mesenchymal transition process, essential in cancer metastasis. Cancer cells increase glucose uptake capabilities to meet their high energy requirements. In this study, we explored the potential role of TWIST1 on glucose transport into the 293T cells in an insulin-dependent and insulin-independent manner. For this purpose, the ectopic expression of TWIST1 was successfully performed by electroporation. The altered mRNA expressions of GLUT-1, -3, -4, and -12, insulin receptor (InsR), and insulin receptor substrate (IRS)-1 and -2 were assessed in control and TWIST1-overexpressing cells. Glucose uptake rates of the cells were evaluated by fluorometric glucose uptake assay. Our findings showed that the transcriptional expression levels of GLUT-1, -3, and -12 genes were significantly upregulated by TWIST1. However, TWIST1 did not alter the mRNA and protein expressions of the InsR, its substrates (IRS-1 and -2), and GLUT-4 genes in 293T cells which are main factors for insulin-stimulated glucose uptake pathway. Also, the glucose transport activities were significantly increased in TWIST1-overexpressing cells compared to controls due to fetal bovine serum (FBS) stimulation, but there was a slight non-significant difference in insulin stimulation. Thus, our data suggest that TWIST1 could promote glucose uptake independently of insulin and is possible to be evaluated as a metabolic marker in cancer. Further investigations are needed to clarify the precise molecular mechanisms underlying the cells' glucose uptake and consumption during tumorigenesis

Clinicogenetic Study of Turkish Patients With Syndromic Craniosynostosis and Literature Review

BACKGROUND: Fibroblast growth factor receptor 2 mutations have been associated with the craniosynostotic conditions of Apert, Crouzon, Pfeiffer, Saethre-Chotzen, Jackson-Weiss, Beare-Stevenson cutis gyrata, and Antley-Bixler syndromes in various ethnic groups. METHODS: Thirty-three unrelated Turkish patients (12 with Apert syndrome, 14 with Crouzon syndrome, six with Pfeiffer syndrome, and one with Saethre-Chotzen syndrome) and 67 nonsyndromic craniosynostosis patients were screened for mutations in exons Ilia and IIIc of the FGFR2 gene by denaturing high-performance liquid chromatography and confirmed by direct sequencing. RESULTS: We detected several pathogenic mutations in 11/33 (33%) patients with Apert syndrome (four with p.Pro253Arg; seven with p.Ser252Trp) and 8/33 (24%) patients with Crouzon syndrome (three with p.Trp290Arg, one with p.Cys342Tyr, p.Cys278Phe, p.G1n289Pro, and a novel p.Tyr340Asn mutation) and five (15%) with Pfeiffer syndrome (p.Cys342Arg, p.Pro253Arg, p.Trp290Arg, and p.Ser351Cys). No FGFR2 gene mutation was detected in any of the patients with Saethre-Chotzen syndrome and nonsyndromic craniosynostosis. CONCLUSIONS: Our results indicate that the majority of Turkish patients with syndromic craniosynostosis have detectable genetic changes with an overall frequency of 72.7%. Because this is the first molecular genetic report from a Turkish cohort, the identified spectrum profile of FGFR2 mutations of the syndromic craniosynostotic patients would be very helpful for understanding the genotype phenotype relationship and has a great value for diagnosis, prognosis, and genetic counseling