Cancer Research UK

About: Cancer Research UK is a nonprofit organization based out in London, United Kingdom. It is known for research contribution in the topics: Cancer & Gene. The organization has 1025 authors who have published 777 publications receiving 148154 citations. The organization is also known as: CRUK.

Evidence of Linkage to Chromosome 9q22.33 in Colorectal Cancer Kindreds from the United Kingdom

Abstract: About 30% of all colorectal cancers are thought to have a genetic basis and the known predisposing genes can only account for a small fraction of cases A previous report suggested that a colorectal cancer candidate gene, explaining at least 20% of colorectal cancer cases with family history, was located within a 25 cM region on chromosome 9q222-q313 We typed 16 polymorphic markers encompassing the region of putative linkage in 57 colorectal tumor families from the United Kingdom Known Mendelian syndromes had been excluded We found suggestive evidence of linkage, as positive parametric (HLOD = 123) and nonparametric (NPL = 121, P = 011) LOD scores were obtained by analysis of the whole family set Enrichment for cases with a priori genetic etiology by analyzing families with at least one person affected at 167 (P 24, P < 001), the linked region was 17 cM between D9S971 and D9S272/D9S173 Exclusion from the analysis of kindreds with a phenotype of multiple polyposis also found evidence of linkage in the same region (NPL = 247 at close to D9S277, P = 0009) The type I transforming growth factor-beta receptor, a prime candidate gene, was excluded as a cause of disease The results presented here further support the existence of a colorectal cancer susceptibility gene on chromosome 9q and refine its likely location

The European Cancer Patient’s Bill of Rights, update and implementation 2016

Abstract: In this implementation phase of the European Cancer Patient’s Bill of Rights (BoR), we confirm the following three patient-centred principles that underpin this initiative: The right of every European citizen to receive the most accurate information and to be proactively involved in his/her care. The right of every European citizen to optimal and timely access to a diagnosis and to appropriate specialised care, underpinned by research and innovation. The right of every European citizen to receive care in health systems that ensure the best possible cancer prevention, the earliest possible diagnosis of their cancer, improved outcomes, patient rehabilitation, best quality of life and affordable health care. The key aspects of working towards implementing the BoR are: Agree our high-level goal. The vision of 70% long-term survival for patients with cancer in 2035, promoting cancer prevention and cancer control and the associated progress in ensuring good patient experience and quality of life. Establish the major mechanisms to underpin its delivery. (1) The systematic and rigorous sharing of best practice between and across European cancer healthcare systems and (2) the active promotion of Research and Innovation focused on improving outcomes; (3) Improving access to new and established cancer care by sharing best practice in the development, approval, procurement and reimbursement of cancer diagnostic tests and treatments. Work with other organisations to bring into being a Europe based centre that will (1) systematically identify, evaluate and validate and disseminate best practice in cancer management for the different countries and regions and (2) promote Research and Innovation and its translation to maximise its impact to improve outcomes.

Nerve growth factor induced stimulation of Ras requires Trk interaction with Shc but does not involve phosphoinositide 3-OH kinase

Abstract: The TrkA receptor protein tyrosine kinase is involved in signalling PC12 cell differentiation and cessation of cell division in response to nerve growth factor (NGF). To assess the importance of adaptor proteins and Ras in NGF control of phosphoinositide 3-OH kinase (PI 3-kinase), specific receptor mutations in Trk have been employed. We show that phosphorylation of tyrosine 490, but not 785, of Trk is essential for activation of both Ras and PI 3-kinase in vivo, correlating with tyrosine phosphorylation of Shc and binding of Shc to the adaptor Grb2 and the Ras exchange factor Sos. A mutant receptor that lacks Y490 and Y785, but contains an introduced YxxM motif which binds the regulatory domain of PI 3-kinase, is unable to activate Ras despite causing increased PI 3-kinase activity. This indicates clearly that activation of PI 3-kinase by itself is not sufficient to cause activation of Ras, arguing against a model in which PI 3-kinase acts upstream of Ras. The Shc site of Trk is thus crucial for the activation of Ras and PI 3-kinase.