The 6th Annual Meeting of the United States Chinese Anti-Cancer Association(USCACA) was held in conjunction with the 50 th Annual Meeting of American Society of Clinical Oncology(ASCO) on May 30, 2014 in Chicago, Illi...The 6th Annual Meeting of the United States Chinese Anti-Cancer Association(USCACA) was held in conjunction with the 50 th Annual Meeting of American Society of Clinical Oncology(ASCO) on May 30, 2014 in Chicago, Illinois, the United States of America. With a focus on personalized medicine, the conference featured novel approaches to investigate genomic aberrations in cancer cells and innovative clinical trial designs to expedite cancer drug development in biomarker-defined patient populations. A panel discussion further provided in-depth advice on advancing development of personalized cancer medicines in China. The conference also summarized USCACA key initiatives and accomplishments, including two awards designated to recognize young investigators from China for their achievements and to support their training in the United States. As an effort to promote international collaboration, USCACA will team up with Chinese Society of Clinical Oncology(CSCO) to host a joint session on "Breakthrough Cancer Medicines" at the upcoming CSCO Annual Meeting on September 20 th, 2014 in Xiamen, China.展开更多
Tumors and cancers of the gastrointestinal tract and pancreas are commonly derived from precursor lesions so that understanding the physiological, cellular, and molecular mechanisms underlying the pathogenesis of prec...Tumors and cancers of the gastrointestinal tract and pancreas are commonly derived from precursor lesions so that understanding the physiological, cellular, and molecular mechanisms underlying the pathogenesis of precursor lesions is critical for the prevention and treatment of those neoplasms. Pancreatic neuroendocrine tumors(PNETs) can also be derived from precursor lesions. Pancreatic α cell hyperplasia(ACH), a specific and overwhelming increase in the number of α cells, is a precursor lesion leading to PNET pathogenesis. One of the 3 subtypes of ACH, reactive ACH is caused by glucagon signaling disruption and invariably evolves into PNETs. In this article, the existing work on the mechanisms underlying reactive ACH pathogenesis is reviewed. It is clear that the liver secretes a humoral factor regulating α cell numbers but the identity of the liver factor remains elusive. Potential approaches to identify the liver factor are discussed.展开更多
文摘The 6th Annual Meeting of the United States Chinese Anti-Cancer Association(USCACA) was held in conjunction with the 50 th Annual Meeting of American Society of Clinical Oncology(ASCO) on May 30, 2014 in Chicago, Illinois, the United States of America. With a focus on personalized medicine, the conference featured novel approaches to investigate genomic aberrations in cancer cells and innovative clinical trial designs to expedite cancer drug development in biomarker-defined patient populations. A panel discussion further provided in-depth advice on advancing development of personalized cancer medicines in China. The conference also summarized USCACA key initiatives and accomplishments, including two awards designated to recognize young investigators from China for their achievements and to support their training in the United States. As an effort to promote international collaboration, USCACA will team up with Chinese Society of Clinical Oncology(CSCO) to host a joint session on "Breakthrough Cancer Medicines" at the upcoming CSCO Annual Meeting on September 20 th, 2014 in Xiamen, China.
基金Supported by National Cancer Institute of the National Institutes of Health,No.R00CA138914(YT)National Natural Science Foundation,No.81372216(YT)
文摘Tumors and cancers of the gastrointestinal tract and pancreas are commonly derived from precursor lesions so that understanding the physiological, cellular, and molecular mechanisms underlying the pathogenesis of precursor lesions is critical for the prevention and treatment of those neoplasms. Pancreatic neuroendocrine tumors(PNETs) can also be derived from precursor lesions. Pancreatic α cell hyperplasia(ACH), a specific and overwhelming increase in the number of α cells, is a precursor lesion leading to PNET pathogenesis. One of the 3 subtypes of ACH, reactive ACH is caused by glucagon signaling disruption and invariably evolves into PNETs. In this article, the existing work on the mechanisms underlying reactive ACH pathogenesis is reviewed. It is clear that the liver secretes a humoral factor regulating α cell numbers but the identity of the liver factor remains elusive. Potential approaches to identify the liver factor are discussed.
