Thank you, Alex, and good afternoon, everyone. On today's call, we will provide our third business update and review progress with our clinical development priorities particularly in our transcriptional regulation program with CYC065, our lead CDK inhibitor drug candidate. Our business strategy has two drugs firstly using our CDK inhibitors to interfere with transcription and overcome resistance of cancer cells or break the addiction to oncogenes. We are executing on this strategy by achieving the objectives of Phase 1 study with CYC065 including determination of a recommended Phase 2 dose, initiating part 2 of the Phase 1, study incorporating patients with solid tumors, including those with cyclin E make NCL one oblification and filing a phase 1/2 study or CYC065 in combination with [indiscernible]. Secondly, employing our sapacitabine and CDK inhibitor regimen to disrupt the ability of cancer cell to repair damage to the DNA also called DNA damage response or DDR and thus restore their sensitivity to anticancer therapy. We are currently evaluating this strategy as a non-part based treatment alternative in a Phase 1/2 study of an all oral regimen of sapacitabine administered sequentially with seliciclib, our first generation CDK inhibitor in a targeted population of BRCA positive patients. At ASCO 2016 we reported promising clinical data from parts one and two of this study, including durable CR, PR and stable disease in patients with breast, ovarian and pancreatic cancers. The CYC065 phase 1 clinical results and establishment of a recommended phase 2 dose provide the basis to progress clinical evaluation of the drug along and in combinations in both liquid and solid cancers. We've evaluated CYC065 in an ongoing first in human single agent ascending dose phase 1 study in patients with advance solid cancers. The aims of the study are to set safety the pharmacokinetics, pharmacodynamics and identify a recommended Phase 2 dose which was achieved in the sixth dosing level. In part one of this study prolong reduction of the Mcl-1 biomarker was observed in 11 out of 13 evaluable patients treated at the recommended phase 2 dose following a single intravenously administered dose of CYC065 which was generally well-tolerated. Although in such early clinical studies we typically do not expect to see much in the way of an efficacy signal we encouraged to observe preliminary anti-cancer activity in five patients. Four of these patients were treated at the recommended Phase 2 dose and three out of four were reported by investigators to have molecular features of the cancers associated with the drug's mechanism action, these included overexpression or amplification of Mcl-1, MYC and/or cyclin E. After achieving the goals in part one of the study we're working with investigators to open part two with the objective of evaluating additional schedules in patients with advanced solid tumors and in particular cyclin E amplified tumors. Such tumor features are frequently reported among others in patients with high grade serious ovarian and uterine cancers. Of note key opinion leaders have pointed out that patients with cyclin E amplified tumors do not carry BRCA mutations. As such they're not candidates for treatment with standard of care PARP inhibitors. Our top clinical development priority is to finalize designs for a Phase1/2 study starting CYC065 in combination with venetoclax in relapsed/refractory chronic lymphocytic leukemia or CLL, but we believe that Mcl-1 suppression maybe beneficial. Venetoclax is a Bcl-2 inhibitor approved for relapsed/refractory CLL. However, it has been reported that venetoclax does not affect levels of Mcl-1 which is often associated with the emergence of resistance to Bcl-2 inhibitors. In parallel discussions with principle investigators and/or cooperative groups are progressing with the objective of evaluating CYC065 in both pediatric and adult patients in other indications supported by strong preclinical data. One such study to be conducted as an investigator sponsored trial will evaluate the drug in patients with leukemias, including AML, and in particular those with mixed lineage leukemia rearrangements, or MLL-r. In parallel, the Company is discussing with investigators a potential evaluation of CYC065 in patients with neuroblastoma, a mostly pediatric life-threatening malignancy, frequently associated with MYC amplification. There're no available drugs with significant activity against MYC. We will report on the progress of these collaborations as they develop. Turning to our DDR or DNA Damage Response program, enrollment has been completed in an extension of the Phase 1 study evaluating the combination regimen of sapacitabine and seliciclib, our first generation CDK inhibitor, in an enriched population of BRCA positive patients with advanced breast cancer. Part 3 of this study has been recently opened for enrolment with the objective of testing a revised dosing schedule in additional patients, including BRCA positive, ovarian and pancreatic cancer patients. Finally let us turn to the report of the SEAMLESS Phase 3 data, which was selected for oral presentation at the 59th American Society of Hematology or ASH Annual Meeting on December 11, 2017………… The presentation will include additional data from a comprehensive analysis of the seamless data set will be objective of characterizing the specified sub group of patients EG those with low peripheral white blood cell count who appear to have clinically relevant benefit from the investigation of treatment regimen. As previously reported in the intensive population, the investigational arm of the seamless study did not reach the particular significant improvement in medium and overall survival versus active control. However, improvement in medium overall survival was observed is a stratified sub group of patients with low base lines peripheral white blood cell counts. The subgroup comprised approximately two thirds of the study's population. Following analysis of the full seamless data set and database lock the company is developing submission materials to support consultations with European and U.S. authorities with the objective of determining potential regulatory pathways. Consistently with our CYC065focus strategy the company is not planning any additional studies with sapacitabine and AML at this time. Our future catalysts include initiate CYC065 phase 1B in relapsed refractory CLO in combination with venetoclax, a Bcl-2 inhibitor. Update CYCO65 phase 1 data in solid tumors. Update mature data from the part 1 extension sapacitabine/seliciclib DDR study in BRCA positive breast cancer cohort. Complete part 3 in the sapacitabine/seliciclib DDR study in patient with BRCA positive breast cancers including ovarian pancreatic. Submit CYC140 BLK 1 inhibitor IND application and conduct regulatory authority meetings regarding the seamless study of sapacitabine/seliciclib in AML. Before handing over to Paul to take us through the financials, let us summarize the highlights of Cyclacel's business. CDK inhibitors are a validated drug class generating sizable revenues and profits. We believe in Cyclacel has CYC065, a differentiated and promising candidate in this space. Cyclacel's strategy is to target molecularly defined patient populations ensuring treatments are administered to those patients more likely to benefit. Our compounds aim to overcome cancer cell resistances, addiction to oncogenes or interfere with the ability of cancer cells to recur damage to the DNA. We believe our compounds are competitively positioned who have potential to address large markets. For those of you who are interested further details on our strategy, pipeline and programs, are described in the September 2017 Corporate Presentation available in the Investor Relations page of our website. We will now review our financials. Paul?
