DNA damage and repair represent important biological processes that are targets of various chemotherapies against cancer. In many ways, chemotherapeutic agents can induce DNA damage in cancerous as well as normal cells. However, DNA damage induced by chemotherapeutic agents can be intrinsically repaired by normal physiologic responses, which hampers inhibition of tumor growth and cause drug-resistance. Base excision repair (BER) is one such physiologic process that is important in the cellular response to many chemotherapeutic agents, specifically those agents that target DNAs. Once the BER pathway is triggered, damaged DNA bases undergo a series of chemical modifications resulting in the formation of abasic or apurinic/apyrimidinic (AP) site, which serves as key intermediates in the excision of damaged DNA bases and restoration of regular bases. To monitor BER-conferred intrinsic drug-resistance to chemotherapeutic agents such as DNA-alternating temozolomide (TMZ), pemetrexed (Alimta®), and fludarabine, we have developed a F-18 labeled fluoroethoxyamine ([11C]FEX) as an imaging agent for positron emission tomography (PET) imaging of DNA damage and repair in vivo. In this work, we report the synthesis, radiolabeling, and evaluation of [18F]FEX in vivo in mice. We have shown that [18F]FEX-PET can be used to monitor DNA damage and repair in tumor xenograft mouse models including an uracil DNA glycosylase (UDG)-knockout tumor mouse model of non-small cell lung cancer (NSCLC).

Primary small cell neuroendocrine carcinoma of the base of the tongue is a rare site for extra pulmonary small cell carcinomas. Histopathologically it is similar to small cell carcinoma of the lung with focal positivity for pancytokeratin and immune reactivity for the neuroendocrine markers. Here we present a case of limited stage small cell neuroendocrine carcinoma of the base of the tongue in a middle aged smoker male for the first time in literature. We discuss its clinicopathological, radiological findings and management of extra pulmonary small cell carcinoma.

Biological materials such as cells, DNA, RNA, and proteins can be recovered from blood, urine, feces, pancreatic juice and sputum of patients. Here, they described a method for free plasma DNA extraction used in our laboratory, compared it to one of the most reproduced in the literature, and also verified the effects of short time storage of plasma on DNA quantification. This is a new method for DNA extraction. Also, they verified that fast processing after plasma collection was necessary to produce realistic results of plasma DNA.

Lung cancer accounts for an estimated 1.4 million deaths globally that is, 18.4% of all cancer deaths. More than 35,000 people died from lung cancer in 2008 in the UK. In males this was almost a quarter of all cancer deaths and in females just over a fifth. By comparison, 16% of female cancer deaths were from breast cancer and the second commonest cause of cancer death overall (colorectal) accounts for 10% of all cancer deaths. The majority of people with lung cancer (three quarters in the UK) present with stage IIIb or IV disease where cure is impossible and so survival low in comparison with other common cancers. Low dose CT screening of high risk populations has been shown to substantially reduce mortality and the remaining questions here centre on the exact design of CT screening programs to ensure cost effectiveness, defining the population that may benefit, including those at lower risk, and establishing the optimum management of screen detected nodules.

Prostate cancer is a leading cause of cancer death in men, with an estimate of about 241,000 new cases and 34,000 deaths due to prostate cancer in the United States in 2011. Prostate cancer is dependent on the androgen receptor (AR); the androgen axis shown to be a key driver of the disease. This principle was first established more than 70 years ago by the demonstration that surgical castration will retard the progression of disease. Prostate cancer typically responds well to suppression of testosterone. Surgical castration is effective in lowering testosterone production but suffers from its psychological impact and irreversibility; thus treatment of the early stages of advanced disease in the Western world is typically based on ‘chemical’ castration with luteinising hormone releasing hormone (LHRH) agonists. These agents suppress luteinising hormone release and markedly reduce testicular testosterone production. Even with effective surgical or chemical castration, however, some residual androgen production persists (perhaps within tumor cells themselves or from extra-testicular sources); hence there has been a search for other agents to manage the disease.

Ceramide is composed of sphingosine and a fatty acid found in large concentration within the cell membrane and often acts as a signaling molecule for various functions including programmed cell death. In the present investigation, we observed that C6-ceramide induces p53-dependent apoptosis and effectively killed the Astrocytoma grade4 (Glioblastoma Multiforme) HTB12 cell lines. Ceramide-induced cell death was confirmed by Trypan blue assay which showed about 65% cells dying from ceramide treatment. Apoptosis was confirmed by Caspase3 ELISA assay and DNA fragmentation assay. The p53 induction was confirmed by immunoblot studies. Since C6 Ceramide induces apoptosis in Glioblastoma cells, it may be employed in chemotherapeutic strategy to treat this highly malignant brain cancer.

The purpose of this study was to investigate the association between haplotype-tagging single nucleotide polymorphisms (SNPs) within the Aurora Kinase A (AURKA) gene and prostate cancer outcomes in patients with clinically localized prostate cancer. Four intronic haplotype-tagging SNPs within the AURKA gene were individually selected and examined in regard to their influence on clinical outcomes in 212 patients who underwent radical prostatectomy as first-line treatment. Haplotype-tagging SNPs were selected using the ABI SNP Browser to cover SNPs with an r2 of 0.90 or greater in the AURKA gene with a minor allele frequency of at least 0.25. This study demonstrates no evidence for intronic AURKA SNPs in predictingrecurrence-free survivalin patients with prostate cancer.