又一家中国 AI 医疗新锐崛起!视见科技完成 1 亿元 A 轮融资

新闻又一家中国 AI 医疗新锐崛起!视见科技完成 1 亿元 A 轮融资

近日,人工智能医疗公司视见科技宣布,已完成 A 轮追加融资,投资方为招商局创投。视见科技于 2018 年 3 月完成 A 轮融资,由深创投领投。至此,视见科技完成总额为 1 亿元人民币的 A 轮融资。 视见医疗科技是一家将人工智能应用于医学影像领域的创新型公司,核心是依托人工智能深度学习和计算机医学影像分析技术,开发出高质量的医学影像分析软件和大规模影像分析平台,对医学影像大数据进行智能化识别和分析,快速、精确地提供辅助诊疗方案建议,从而提高临床诊疗的精准度和效率。 据公司官网信息,视见医疗产品和服务涉及放射、病理和放疗三大领域,主要包括:大规模病理显微图像分析、肺癌早期 CT 筛查、放射靶区勾勒和规划、CT/MRI 三维器官建模、TCT 宫颈癌人工智能筛查系统、内窥镜影响分析等。 视见科技所提供的产品和服务可广泛应用于医院、独立影像和检验中心、远程诊断云平台、医学成像设备厂商、医学教研机构和患者等用户群体。目前,视见医疗已经获得香港创新科技署数百万港币资助和联想创投两千万元投资。视见医疗总部位于深圳,现设有深圳、香港、成都、北京四大研发中心。 视见科技的本轮融资将继续聚焦于产品研发,在团队组建和产品矩阵上持续追加投入,并加快推进临床应用场景探索,推动公司快速发展。 ▲视见科技创始人兼联席 CEO 陈浩博士(图片来源:视见科技官网) 对于视见科技本次融资,视见科技创始人兼联席 CEO 陈浩博士介绍道:“一方面说明视见科技成立一年多以来,公司的团队、产品和市场进度,得到了资本市场的充分认可;另一方面,人工智能在医疗领域的真正大规模落地应用,还需要一个较长的时间。从技术、产品、市场以及政策层面,都开始进入攻坚阶段,需要摒弃浮躁的心态。有了资本的助力,我们就更能沉下心来专注于把技术研发和产品开发做好,同时探索更多的临床应用场景。” 我们祝贺视见科技获得此次融资,也祝愿未来的中国医疗 AI 事业可以更加蓬勃发展。详情>>

2018-06-29 00:00:00
生物技术公司IPO大潮来势凶猛

新闻生物技术公司IPO大潮来势凶猛

【新闻事件】:继上周多个生物技术公司IPO共融资7.18亿美元后本周又有四家生物技术成功上市,共融资5.46亿,令过去10天的IPO总量达到12.7亿美元。今年半年不到美国已经上市30家生物技术企业,接近去年全年的31个,融资总量达到32.5亿美元。本周四个IPO各具特色,开发CKD的Tricida融资2.2亿,是少见的已经完成三期临床的IPO。开发mRNA药物的Translate Bio融资1.22亿,成为首家在美国上市的mRNA企业。开发CD47激动剂的Forty Seven 刚成立两年,这次融资1.12亿。另一家免疫疗法公司、开发肿瘤疫苗的Neon 融资1亿。 【药源解析】:资本以创纪录速度流入生物制药有多种因素,既有刚性需求也有一定泡沫成分。现在生物技术的大环境非常有利,是主要驱动力。FDA连续几年批准远高于历史平均水平的新分子药物,而且继续显示与制药工业合作尽快上市颠覆性新药的友好态度。现在只要产品没问题FDA极少会成为你赢利障碍。支付方面虽然压力很大,但受到挤压较多是传统me-too常见大众病药物。颠覆性疗法相比之下受到支付部门青睐,而这些药物是生物技术公司的主攻方向,所以资本大量涌入。另一个重要因素是虽然特朗普总统宣称要限制药价,但总是雷声大、雨点小,宣布限制药价新政当天制药股普遍上扬。 生物技术生存环境的另一个主要方面是技术进步本身。随着基础研究的进步和临床前、临床研究的精准化,现在研发效率有所改善。挣扎多年的几个主要技术如RNA、基因疗法、细胞疗法几乎同时进入收获季节,令投资者热情高涨。最近几年一个重要治疗板块是肿瘤免疫疗法,这种疗法不是直接杀死肿瘤、而是破坏肿瘤的生存环境,通常安全性比传统化疗要好。更重要的是免疫疗法的应答持久性远高于传统疗法,第一次令晚期肿瘤治愈成为触手可及的目标。免疫系统十分庞大复杂、介入点很多,所以吸引了大量资本从不同角度、不同通路调控这个天然抗癌系统。最后,近几年一个明显的趋势是开创新技术的著名大学教授纷纷下海、经验丰富的世界主要药厂高管也大量涌入初创生物技术公司,这令生物技术公司的技术和执行力都有较大提高,也成为吸引投资者的一个重要因素。 当然这些有利条件必然会导致一定程度泡沫。很多投资者怀着不想错过下一个PD-1的心理,类似当年淘金、有点赌博成分。现在投资进程不仅前移、A轮基本就是原来的天使,而且单项投入力度明显上升。很多临床证据不多、甚至没有临床数据的企业也参加IPO,虽然早期阳性数据相对容易得到但假阳性也更多,这可能会导致更高的失败率。早期项目区分更加困难,和买彩票类似、人的本性都认为自己投的项目最可能赢,但市场的容量是有限的,最后必须有人失败。目前制药业对有些高新技术的早期评价也存在不足,如免疫疗法现在还没有可靠的评价系统。这些因素可能导致重复盲目投入、甚至养育一些南郭先生,但大量资本涌入的确给颠覆性技术一个快速成长的机会。现在家喻户晓的PD-1药物五年前即使专业人员也没几个知道,这可能是现在生物技术IPO如此火爆的最核心因素。详情>>

2018-06-29 00:00:00
艾伯维与 Calibr 大合作,开发实体瘤 CAR- T 疗法

新闻艾伯维与 Calibr 大合作,开发实体瘤 CAR- T 疗法

今日,艾伯维(AbbVie)与 Calibr 宣布将合作开发 T 细胞疗法,主要针对实体瘤等癌症。此次合作拓宽了艾伯维的肿瘤学研究领域,使其获得先进的精准医学技术,从而扩大可改善癌症患者生活的治疗方法的开发。 Calibr 是一家致力于开发下一代药物的非营利性转化研究机构。作为 Scripps Research 的一部分,Calibr 位于美国圣地亚哥市的 Torrey Pines Mesa 生物医学研究中心,拥有从早期发现到临床项目的广泛研发产品线,在研新药类型包括小分子、多肽、生物治疗药物和细胞疗法等。 嵌合抗原受体 T 细胞(CAR-T)疗法利用癌症患者自身免疫系统的力量,来攻击和摧毁癌细胞。虽然该疗法在恶性血液病方面取得了令人鼓舞的结果,但目前针对实体瘤开发的 CAR- T 疗法依然存在局限性,它们由 CAR- T 细胞的快速激活和扩增引起,可能导致严重的不良事件。Calibr 的新型细胞疗法项目由 Calibr 蛋白质科学主管 Travis Young 博士领导,旨在通过使用一种专有的模块化“可切换”CAR- T 细胞(使用抗体开关分子来控制 CAR- T 细胞的激活和抗原特异性),来增强治疗的安全性、多功能性和功效。Calibr 的专利技术可以促进 CAR- T 通用疗法在多种类型的血液和实体肿瘤中的开发。 根据此次合作协议条款,艾伯维将向 Calibr 支付前期许可费,并获得 Calibr 可切换 CAR- T 平台的独家使用权,期限长达四年。两家机构将共同合作开发针对由艾伯维确定的实体瘤靶点的 T 细胞疗法。艾伯维还可以选择开发针对其提名靶点的其他细胞疗法,并获得正在开发的 Calibr 细胞治疗项目的许可(包括 Calibr 的主要候选药物),用于血液和实体癌症。Calibr 计划于 2019 年将该候选药物推向临床研究。此外,该协议还规定艾伯维有权在合作的头四年内获得 Calibr 可切换 CAR- T 平台和项目的独家许可。两家机构将分担临床前开发责任,艾伯维负责临床开发和推广,Calibr 有资格获得里程碑付款和特许权使用费。 “Calibr 组建了一支优秀的科学团队,开发了一种创新的细胞疗法技术,可以将我们带到癌症治疗的下一个前沿,”艾伯维副总裁兼肿瘤早期研发主管 Mohit Trikha 博士说:“艾伯维的肿瘤发现和早期研发专长与 Calibr 的新型可切换 CAR- T 治疗平台的结合,旨在推进当前的护理标准,并有可能为患者快速推出新的治疗方案。” “我们很高兴能与像艾伯维这样的强大合作伙伴一起工作,扩大 CAR- T 细胞领域对更广泛癌症的影响。”Calibr 和 Scripps Research 首席执行官 Peter Schultz 博士说。详情>>

2018-06-26 00:00:00
骨关节炎遗传学大数据

新闻骨关节炎遗传学大数据

The largest study to date on the genetics of hip and knee osteoarthritis (OA) has yielded new associations with genes encoding a cytokine, a kinase and a transcriptional repressor, as well as genetic correlations with other diseases. Can these clues help to unravel details of the pathogenesis of OA? Refers to Zengini, E. et al. Genome-wide analyses using UK Biobank data provide insights into the genetic architecture of osteoarthritis. Nat. Genet. 50, 549–558 (2018) Osteoarthritis (OA) is the most common joint disorder worldwide and a top contributor to global disability, yet no disease-modifying drugs exist to treat OA. To develop such drugs, a deeper understanding of the molecular pathogenesis of OA has been pursued through genetics, among other approaches, owing to the strong heritability of OA1,2. As of the end of 2017, 21 independent susceptibility loci for OA had been reported in various genome-wide association studies (GWAS) of hip, knee and hand OA, including a variety of phenotypes such as radiographic OA, total joint replacement and minimum joint space width (mJSW), a proxy for cartilage thickness1,2. These GWAS have yielded only a fragmented view of the molecular pathogenesis of OA, and one of the main hindrances has been the lower sample sizes used in these studies compared with GWAS in other complex diseases. However, the limitation caused by sample size has now been tackled by Zengini et al.3 in a new GWAS of knee and hip OA that illuminates many aspects of OA genetics, including the finding of novel genes associated with OA, that could open new areas of research in the pathogenesis of this disease. This impressive GWAS3 adds to what is known about the genetic architecture of hip and knee OA by contributing data from the UK Biobank that have been replicated and combined with data from individuals from Iceland. The UK Biobank data include the results of five GWAS on partially overlapping cohorts of self-reported and/or hospital-diagnosed patients with hip or knee OA and controls from the UK Biobank (~10,000 each of self-reported and hospital-diagnosed patients and ~40,000 controls). The top 200 single nucleotide polymorphisms (SNPs) were replicated in samples from the ~18,000 patients with OA and 246,000 controls from Iceland. The results of this study3 refine and confirm ideas that have already been derived from previous studies1,2, but also include the identification of nine new OA-associated loci and a wide exploration of genetic correlations between OA and other traits and diseases (Box 1). The genetic architecture of OA is that of a highly polygenic disease. The complexity of OA means that only ~30 loci have been identified so far, most of which are associated with hip or knee OA, that explain only a small fraction of the disease heritability. These loci mainly contain common variants that have a small effect, with the exception of two rare variants that have a strong effect1,2. These common variants are mainly found outside of gene coding sequences and possibly modify gene regulation, although the hypothesized effects of these variants are difficult to demonstrate. One notable result from this new GWAS3 is the strong genome-wide correlation between hip and knee OA (88%), which had not previously been suspected because loci identified in patients with OA were often joint specific1,2. However, despite this high degree of overall correlation between hip and knee OA, Zengini et al.3 also noted many results that were specific to the particular phenotypes included in this study. The heterogeneity of these phenotypes and the complexity of OA genetics are likely to have contributed to the modest reproducibility of the loci identified with genome-wide significance in previous studies. Zengini and co-workers3 found no strong causal relationships between the nine new loci and potentially important pathways in OA pathogenesis; however, evidence did suggest that three of the loci might be associated with genes that could potentially reveal new insights into OA. One SNP was located in an intron of TGFA, which encodes transforming growth factor-α (TGFα). Previously, this locus has been associated with hip mJSW and with the differential expression of TGFα between cartilage lesions and non-lesioned cartilage4. TGFα also induced many changes typical of OA in cultured rat chondrocytes5. The locus identified by Zengini et al. therefore reinforces the idea that TGFα might be an important cytokine in OA. Another newly associated SNP3 was located in an intron of MAP2K6, which encodes dual specificity mitogen-activated protein kinase (MAPK) kinase 6 (MP2K6), a central member of the p38 MAPK pathway. This pathway is involved in the signal transduction of a plethora of cellular processes, including inflammation and chondrocyte apoptosis, and its inhibition has been proposed to be beneficial for OA. However, the overall inhibition of the p38 MAPK pathway has resulted in aggravated disease in mouse models of OA6. The possibility that MP2K6 could provide clues about how to modulate the p38 MAPK pathway in a selective and beneficial way merits additional studies. The third promising gene, BACH1, is located in the vicinity of another newly associated SNP, rs116882138, and showed increased RNA expression in degraded cartilage3. Previous mouse studies have shown that deficiency of Bach1 prevents the development of OA by a combination of reduced oxidative damage and decreased amounts of extracellular matrix-degrading enzymes7, suggesting that this locus could be the first to be related to reactive oxygen species in OA. Understanding the genetic relationships between OA and other traits or clinical conditions can help elucidate cause and effect, as inherited genetic risks cannot be subject to reverse causation. To this end, Zengini and co-workers3 investigated the genetic relationship between OA and other traits using two methods. First, they estimated genetic correlations using cross-trait linkage disequilibrium score regression to assess the heritability explained by common SNPs. This method distinguishes between population stratification and polygenicity in GWAS8. Zengini et al.3 found a genome-wide genetic correlation between OA and 35 of the 219 investigated traits and diseases. The 35 genetically correlated phenotypes fell into several broad categories: BMI and obesity-related traits, type 2 diabetes mellitus, education, depression, parents’ longevity, reproductive phenotypes, smoking and lung cancer. Zengini et al.3 also applied Mendelian randomization to the data sets, in which significantly associated SNPs are used as instrumental variables to quantify causal relationships between risk factors and disease9. The only consistent evidence for causal genetic correlation was identified in obesity-related traits (Box 1). In other words, genetic factors that predispose to various measures of obesity also cause an increased risk of OA, a fact that had previously been reported in smaller data sets than those used by Zengini et al.3 and only for a single obesity-related gene2. Interestingly, Zengini et al.3 did not find a causal effect between metabolic syndrome-related phenotypes (other than obesity) and OA, although an association between metabolic syndrome and OA has been postulated10. These data are relevant as they suggest that although there are likely to be common pathogenic pathways between traits such as dyslipidaemia and OA or type 2 diabetes mellitus and OA, these conditions do not seem to be causally linked. In conclusion, this truly large-scale GWAS3 confirms the complexity of OA at a genetic level and provides some clues that could help to define the molecular pathogenesis of this disease. Among these clues, genetic factors related to obesity but not to other aspects of metabolic syndrome are important as causative contributors to OA in large joints. Box 1 Current understanding of the genetics of hip and knee osteoarthritis Genetic structure The genetics of hip and knee osteoarthritis (OA) are highly polygenic with ~30 known loci explaining only a small fraction (~25%) of the heritability. These loci predominantly involve common risk alleles of small effect and the known loci show modest reproducibility. Phenotype specificity The OA loci are specific to particular OA phenotypes defined by joint, clinical or radiographic assessment, sex and other factors. Zengini et al.3 found a strong genetic correlation between OA in the hip and knee joints. Function of risk variants The function of most putative risk variants is difficult to discern. Available evidence for the function of risk variants includes expression quantitative trait loci and epigenetic modifications that are suggestive of regulatory functions. Disease or trait correlations OA genetics correlate with many other traits, including causal correlations with obesity, height and lumbar spine bone mineral density. No causal genetic links exist between OA and type 2 diabetes mellitus or triglyceride levels.详情>>

Nature Reviews Rheumatology
2018-06-14 00:00:00
增速放缓、数量下滑:2018全球新药研发大数据体现了哪些新趋势?

新闻增速放缓、数量下滑:2018全球新药研发大数据体现了哪些新趋势?

近年来,全球医药产业呈现出稳健发展的势头,新的药物作用靶标以及新的治疗方式不断被发现和应用,2018年全球新药研发也呈现出诸多新的特点。通过对国际知名咨询机构Informa Pharma Intelligence公司的Pharmaprojects数据库数据进行分析,可以帮助我们全面了解2018年全球在研新药市场的一些新变化,及时发现全球新药研发领域的一些新趋势。 在研项目数量: 增速放缓,与化学合成药开发难度增大有关 Pharmaprojects数据库收录的在研药品信息,特指目前处于在研状态的药品研发项目,纳入了处于临床前研究阶段的项目、处于不同临床研究阶段的项目、处于注册阶段的项目,以及增加新适应症的已上市药物。根据最新数据,截至2018年1月,全球在研新药数量为15267个,与2017年的14872个相比,同比增幅仅为2.7%。 从2001-2018年数据看,全球在研新药数量保持持续增长态势,尤其是2011年以来,全球在研新药数量呈现明显增长势头。然而需要特别注意的是,虽然2014年以来全球在研新药数量同比增幅均超过8.0%,但近两年增速逐年放缓,2016年、2017年、2018年全球在研新药数量增幅分别为11.5%、8.4%和2.7%。 2018年全球在研药物数量仅增加395个,与2017年1154个的增量相比,出现了较大幅度的下滑。近年来,化学合成小分子药物开发难度逐年增加,一些在研项目出现了项目终止的状况,进而导致化学合成药物呈现净增长数量下滑,并对全球在研药物数量的下滑产生了一定的影响。 通常,制药业产品管线数量的持续增长与制药业的产出有内在关联。需要注意的是,产品管线扩张速度下滑在2015年时即已出现。以全球上市的NAS(新活性物质)数量为例,其已从2014年的63个下降至2015年的46个,2016年该数字进一步下降至41个,这也是自2011年以来NAS数量连续两次出现下滑。 值得庆幸的是,这种局面在2017年得到了扭转,2017年全球上市的NAS数量为54个,包括47个新分子实体NMEs和7个疫苗类药物。其中,仅美国FDA在2017年批准的新分子实体NMEs药物就已高达34个,这也创造了1997年以来FDA批准NMEs药物数量的峰值。尽管整个制药行业仍未完全走出低谷,但全球在研药物数量继续保持整体增长,仍然是一个积极信号。 不同阶段对比: 注册前和上市阶段项目数减少 从制药研发流程来看,新药研发大概可以分为三个阶段:首先,通过临床前研究发现并确认候选药物;其次,通过临床研究验证候选药物的有效性和安全性;最后,顺利通过注册及上市环节,最终实现候选药物的临床价值。 通过对比2018年和2017年处于不同研发阶段的在研药物规模后发现,所有阶段的在研药物数量基本维持不变或仅有小幅变动。 其中,处于临床前研究阶段的药物数量变化相对明显,2018年处于该阶段的药物数量为8040个,较2017年数量(7493个)增加了547个候选药物,同比增幅为7.3%,远超全球在研药物平均增速,数量更是首次突破8000大关。据统计,2018年统计数据中新进入临床前研究阶段的药物数量为3807个,与去年同期数据(4005个)相比略有下降。在这些临床前研究项目中,许多项目来自小型创业公司。 处于临床研究阶段(包括Ⅰ期、Ⅱ期和Ⅲ期临床阶段)和注册阶段的在研药物数量分别为5493个和150个,同比增幅分别为0.86%和29.3%。 而处于注册前和上市阶段的在研药物数量则出现下滑趋势,在研药物数量分别为214和1199,同比增幅分别为-2.7%和-14.0%。 处于上市阶段的在研药物,一般是指开发新的治疗领域或增加新的适应症的已上市药物,如果没有进一步的研发进展,则会被视为完全上市的药物,并从该类别中移出不再进行统计。进一步分析发现,2018年新增的进入上市阶段的在研药物数量约为100个,但最终处于活跃状态的药物数量却下降了约200个左右,这意味着约有300个项目因为无新的研发进展而被移出统计范畴。 后期项目流失率: Ⅲ期项目数量下滑,影射流失率仍高 对处于临床研究阶段的在研药物数据进一步分析后发现,2018年处于Ⅰ期、Ⅱ期和Ⅲ期临床研究阶段的药物数量分别为2127、2360和1006个,增幅分别为3.1%、0.1%和-1.9%。处于临床Ⅱ期的药物数量基本无变化,但处于临床Ⅲ期的药物数量则出现了小幅下滑,因此不难看出,处于研发后期的品种仍存在流失率较高的情况,应引起注意。 其实,2017年处于Ⅱ期和Ⅲ期临床研究阶段的药物数量增幅已有所放缓,2018年该趋势仍在延续。但这种情况未必完全是件坏事。临床试验往往需要巨大的费用支持,如果不能保证上市药物的持续增加,那么临床阶段药物数量的稳定增长也是无法保证的。从近十年的数据来看,2018年处于各临床研究阶段的药物数量都约为10年前数据的2倍,但上市药物数量却没有这样高的增幅。 获批上市的可能性: 注册前>Ⅲ期临床 对于在研药物市场的评估,在研药物数量情况是一方面,项目质量同样重要。对项目的临床和注册进度进行分析,可评估一种药物获得FDA批准的可能性,并确定一种药物是否较其他同类药物更易获得批准。 从统计数据来看,2018年“注册前”药物获得批准的可能性高于行业平均水平的药物比例约为52.5%,较2017年(49.3%)有所升高;临床Ⅲ期情况则相反,2018年获得批准的可能性高于行业平均水平的药物比例为24.2%,较2017年(25.3%)有所下降。从临床研究阶段的整体数据看,2018年在研药物获批可能性的分布情况,与2017年数据基本一致。详情>>

2018-06-01 00:00:00

论文生物标志物作为药物开发的工具:发现、验证、鉴定和使用

The 21st Century Cures Act, approved in the USA in December 2016, has encouraged the establishment of the national Precision Medicine Initiative and the augmentation of efforts to address disease prevention, diagnosis and treatment on the basis of a molecular understanding of disease. The Act adopts into law the formal process, developed by the FDA, of qualification of drug development tools, including biomarkers and clinical outcome assessments, to increase the efficiency of clinical trials and encourage an era of molecular medicine. The FDA and European Medicines Agency (EMA) have developed similar processes for the qualification of biomarkers intended for use as companion diagnostics or for development and regulatory approval of a drug or therapeutic. Biomarkers that are used exclusively for the diagnosis, monitoring or stratification of patients in clinical trials are not subject to regulatory approval, although their qualification can facilitate the conduct of a trial. In this Review, the salient features of biomarker discovery, analytical validation, clinical qualification and utilization are described in order to provide an understanding of the process of biomarker development and, through this understanding, convey an appreciation of their potential advantages and limitations.展开>><<收起

Nature Reviews Rheumatology,Published: 14 May 2018  0
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新的呼吸和尿液检测可更准确地检测早期乳腺癌

新闻新的呼吸和尿液检测可更准确地检测早期乳腺癌

A new method for early and accurate breast cancer screening has been developed by researchers at Ben-Gurion University of the Negev and Soroka University Medical Center, using commercially available technology. The researchers were able to isolate relevant data to more accurately identify breast cancer biomarkers using two different electronic nose gas sensors for breath, along with gas-chromatography mass spectrometry (GC-MS) to quantify substances found in urine. In their study published in Computers in Biology and Medicine, researchers detected breast cancer with more than 95 percent average accuracy using an inexpensive commercial electronic nose (e-nose) that identifies unique breath patterns in women with breast cancer. In addition, their revamped statistical analyses of urine samples submitted both by healthy patients and those diagnosed with breast cancer yielded 85 percent average accuracy. "Breast cancer survival is strongly tied to the sensitivity of tumor detection; accurate methods for detecting smaller, earlier tumors remains a priority," says Prof. Yehuda Zeiri, a member of Ben-Gurion University's Department of Biomedical Engineering. "Our new approach utilizing urine and exhaled breath samples, analyzed with inexpensive, commercially available processes, is non-invasive, accessible and may be easily implemented in a variety of settings." The study reports breast cancer is the most commonly diagnosed malignancy among females and the leading cause of death around the world. In 2016, breast cancer accounted for 29 percent of all new cancers identified in the United States and was responsible for 14 percent of all cancer-related deaths. Mammography screenings, which are proven to significantly reduce breast cancer mortality, are not always able to detect small tumors in dense breast tissue. In fact, typical mammography sensitivity, which is 75 to 85 percent accurate, decreases to 30 to 50 percent in dense tissue. Current diagnostic imaging detection for smaller tumors has significant drawbacks: dual-energy digital mammography, while effective, increases radiation exposure, and magnetic resonance imaging (MRI) is expensive. Biopsies and serum biomarker identification processes are invasive, equipment-intensive and require significant expertise.  "We've now shown that inexpensive, commercial electronic noses are sufficient for classifying cancer patients at early stages," says Prof. Zeiri. "With further study, it may also be possible to analyze exhaled breath and urine samples to identify other cancer types, as well." Story Source: Materials provided by American Associates, Ben-Gurion University of the Negev. Note: Content may be edited for style and length. Journal Reference: Or Herman-Saffar, Zvi Boger, Shai Libson, David Lieberman, Raphael Gonen, Yehuda Zeiri. Early non-invasive detection of breast cancer using exhaled breath and urine analysis. Computers in Biology and Medicine, 2018; 96: 227 DOI: 10.1016/j.compbiomed.2018.04.002详情>>

2018-04-27 00:00:00
研究发现新型生物标志物对类风湿性关节炎具有显著特异性

新闻研究发现新型生物标志物对类风湿性关节炎具有显著特异性

Rheumatoid arthritis (RA) is an autoimmune disorder that occurs when the immune system mistakenly attacks the body's tissues. Unlike the wear-and-tear damage of osteoarthritis, rheumatoid arthritis affects the lining of the joints, causing painful swelling that can eventually result in bone erosion and joint deformity. Most RA patients are positive for anticitrullinated protein antibodies (ACPA), and these antibodies are highly specific for RA diagnosis. ACPA recognizes various citrullinated proteins, such as fibrinogen, vimentin and glucose- 6-phosphate isomerase. Citrullinated proteins are proteins that have the amino acid arginine converted into the citrulline, which is not one of the 20 standard amino acids encoded by DNA in the genetic code. Autoreactivity to citrullinated protein may increase susceptibility to RA. While many candidate citrullinated antigens have been identified in RA joints, the involvement of citrullinated proteins in blood serum remains mostly uninvestigated. To that end, a team of University of Tsukuba-centered researchers set out to explore the expression and commonality of citrullinated proteins in peptide glucose-6-phosphate isomerase-induced arthritis (pGIA) and patients with RA, and went one step further to investigate its correlation with RA disease activity. The researchers recently published their findings in Arthritis Research & Therapy. "We examined serum citrullinated proteins from pGIA by western blotting, and the sequence was identified by mass spectrometry. With the same methods, serum citrullinated proteins were analyzed in patients with RA, primary Sjögren's syndrome, systemic lupus erythematosus, and osteoarthritis as well as in healthy subjects," study corresponding author Isao Matsumoto explains. "In patients with RA, the relationship between the expression of the identified protein inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) and clinical features was also evaluated, and the levels of citrullinated ITIH4 were compared before and after biological treatment." The researchers found that citrullinated ITIH4 was highly specific to patients with RA, compared with patients with other autoimmune and arthritic diseases or in healthy subjects, indicating a potential role for citrullinated ITIH4 in RA pathogenesis. Notably, its levels were decreased in correlation with the reduction of disease activity score after effective treatment in patients with RA. Moreover, antibody response to citrullinated epitope in ITIH4 was specifically observed in patients with RA. "Our results suggest that citrullinated ITIH4 might be a novel biomarker to distinguish RA from other rheumatic diseases and for assessing disease activity in patients with RA," Matsumoto says. "To our knowledge, this is the first report of its kind in the literature."详情>>

2018-04-27 00:00:00
“基因医生计划”正式发布!基因科技助力精准医学

新闻“基因医生计划”正式发布!基因科技助力精准医学

4月18日,由树兰医疗集团管理有限公司、深圳华大基因科技有限公司共同发起的“基因医生计划”(GeneDoctor Project)在杭州良渚新城正式发布。该计划旨在推动精准医学新技术在医院的转化应用,通过培养复合型“基因医生”人才,为成果的快速转化“破局”,开创医疗的新模式,为我国精准医学的发展抢占先机。 本次发布的“基因医生计划”将以开放性项目平台致力推动包括基因组学、代谢组学、免疫组学、蛋白质组学等在内的跨组学(Trans-Omics)数据的获得与解读纳入临床常规,建立临床标准与指南,发现疾病新知,促进临床转化与应用,实现平台、技术、人才的共同发展,实现医疗模式的创新。 活动现场,树兰医疗发起人、中国工程院李兰娟院士,华大联合创始人、董事长汪建,余杭区委副书记、区长陈如根,副区长许玲娣,华大执行副总裁杨爽,华大执行副总裁、国内区域规划与发展中心主任路军,树兰医疗集团总裁郑杰,树兰(杭州)医院院长叶再元,华大国际高级副总裁、董事长特别助理何亦武等相关领导出席了发布会。 陈如根在致辞中表示,余杭将全力支持“基因医生计划”的实施与推广,推动基因科技成果在余杭的转化和应用,并提供一流的服务和环境,推动合作不断深化。   余杭区委副书记、区长陈如根致辞 李兰娟院士指出,十九大明确提出了实施“健康中国”的战略,在近期结束的海南博鳌亚洲论坛中,习总书记也提出大力发展健康事业的指导意见。树兰医疗希望通过“基因医生计划”践行总书记改革开放的要求,创建一些新的医学模式来满足人民群众不断增长的医疗卫生需求。未来,“基因医生计划”将构建个人生命健康云,提供全人全程、全方位全周期的健康医疗服务。   树兰医疗发起人、中国工程院李兰娟院士致辞 汪建强调,此次华大与树兰医疗合作,双方均具备优秀的团队和领先的科研技术,强强联合,优势互补,将能够为余杭区、杭州市乃至浙江省精准医学的发展起到核心支撑作用,继续助推我国医疗卫生健康事业的发展。   华大联合创始人、董事长汪建致辞 在发布会上,还进行了三项签约活动——余杭区政府、树兰医疗、华大共同签署战略合作意向书,在良渚国际生命科技小镇共同建设民生、科研、产业三环联动为承载的国际基因谷。树兰医疗与良渚新城管委会、良渚新城管委会与树兰旗下杭州医景股权投资基金管理有限公司也签署了合作协议。 基因科技应用临床 推动医疗模式创新转化 近年来,以基因检测为基石的“精准医学”愈发受到世界各国的高度重视,这种将个人基因、环境与生活习惯差异考虑在内的疾病预防与处置的新兴方法与医疗模式正在逐渐兴起。据了解,自2015年我国将“精准医学”计划上升为“国家战略”后,相关产业及市场正在基因组测序技术、生物医学分析技术和大数据分析工具的驱动之下不断快速发展。而相比全球,不少国家已经形成了以肿瘤为主要对象,覆盖从早期筛查、辅助诊断、伴随诊断到精准治疗全流程的精准医学产业。 业内人士则建议,我国“精准医学”应借助基因测序技术锁定个人病变基因,实现精准的预测预防、治疗和康复,同时结合“基因+质谱+临床”大数据,发现疾病新知,促进临床转化,推动医疗模式创新转化,为我国在精准医学领域的发展抢占先机。 “基因医生计划”启动 助力我国精准医学快速发展 正如业内人士所言,精准医学成果需要通过医院及医生等载体实现转化与应用,为普通民众、医院、医生和患者等提供辅助诊断的工具与平台,争取在全球推进的“精准医学”大产业中拥有话语权,最终为民族大健康事业服务。 此次树兰医疗与华大首提的“基因医生计划”在国际竞争中独树一帜。该计划的发起旨在推动精准医学新技术在医院转化应用,将通过多方共同参与,构建跨组学工具与平台,推动基因组学等检测纳入临床常规,通过对样本和基因组学等数据进行标准化存储、分析与解读,促进数据共享,为医生与患者提供个人健康状况的完整数据。同时,也将通过实践培养出一批复合型“基因医生”人才,实现平台、技术、人才共同发展,实现医学模式的创新,为成果的快速转化“破局”,为我国精准医学的发展抢占先机。 树兰医疗将为“基因医生计划”提供平台支撑 据悉,树兰将依托自身的医疗资源优势为“基因医生计划”提供平台支撑。同时,该计划将在余杭国际基因谷、良渚先导基地开展“健康余杭”万人队列研究项目,开展人群大样本的基于真实世界数据的生物信息、临床医学和卫生经济学研究。 树兰医疗作为医疗领域中国社会化办医的标杆,一直致力于积极探索大生命科学领域的研究、创新和孵化,培养以健康医学为核心的跨学科人才,建立“临床、科研、教学、产业”四位一体的生态体系,积极推动医疗健康产业生态的数据开放。目前已集聚了50余名临床医学院士级专家及2000余名国内外著名专家,目前已建设和委托管理的医院已达8家,运行良好,其中2家医院已通过国际JCI标准认证,托管的博鳌超级医院更是外界备受关注。树兰医疗建立专业的实验诊断中心和医疗智能信息化服务闭环,发起OMAHA联盟,推动健康医疗数据的标准化及共享,提高患者对自身健康医疗数据使用的完整性、可及性和可用性。 华大将为“基因医生计划”提供技术驱动 透过“基因医生计划”发布会得知,此次计划开启后,华大将提供工具、科技与人才支撑,并将推动跨组学数据与临床实践的全面融合,从提高就医个性化、精准化程度等多方面助推“基因医生计划”的开展。 据了解,作为全球领先的基因组学研发机构,华大近年来在基因测序领域取得了长足的发展,以科教、科研、科服、科普四大支柱服务于生命科学研究的各个领域。尤其在基因测序临床应用方面,华大已开发出一系列基于跨组学技术的检测服务,形成了贯穿生命孕育、出生、发育、成长、衰老等全过程的全时全景产品图谱,可用于出生缺陷防控、肿瘤精准诊疗与康复、传染感染性疾病精准治疗、心脑血管及代谢类疾病防控等。华大将充分发挥基因测序技术优势,为我国“精准医学”产业的发展贡献力量。 此次“基因医生计划”的正式发布具有划时代的意义,它将促进“基因医生”群体的蓬勃发展,帮助国家在精准医学领域实现跨越式发展,助力国家基因科技产业的发展与腾飞,并共同探索有效的医学模式,为人类健康服务。详情>>

2018-04-20 00:00:00
“重新定义”阿尔兹海默症?科学家建议,按照生物标志物来!

新闻“重新定义”阿尔兹海默症?科学家建议,按照生物标志物来!

4月10日,Alzheimer’s & Dementi协会发布一份报告建议,“重新定义”阿尔兹海默症,即根据大脑的变化,而不是记忆衰退等认知症状定义这一疾病。这一改变有望建立“通用语言”,加快药物研发以及诊疗方案的及早干预。 “症状是疾病的结果,并不能成为疾病的定义。”报告者之一、梅奥诊所的脑成像专家Clifford Jack如此强调。这份由全球阿尔兹海默症协会、国家衰老研究所完成的新提议以论文的形式发表在《Alzheimer's & Dementia: The Journal of the Alzheimer's Association.》期刊。 科学家们建议,阿尔兹海默症患者应该依据体内生物标志物(例如β-淀粉样蛋白、Tau蛋白)分类。 DOI: https://doi.org/10.1016/j.jalz.2018.02.018 目的 2017年,FDA批准默沙东PD-1抗体Keytruda用于治疗携带一种特定基因特征的任何一种实体瘤,使其成为首个依据生物标志物进行区分的抗肿瘤疗法,在抗癌史上画上浓墨一笔。 现在,针对阿尔兹海默症的这一定义“变革”有望通过更客观的标准(例如脑部扫描)挑选患者进行相关研究,并有助于在疾病初期(症状尚未明显之前)筛选并给予有效干预。 This table shows the eight biomarker profiles (left column) and corresponding categories (right column) outlined in a new biomarker-based framework that could be used to group research participants. The biomarker profiles can be sorted into three broader categories: Normal Alzheimer's biomarkers, Alzheimer's continuum, and non-Alzheimer's pathologic change. [NIA-AA Research Framework] 意义 不可否认的是,“重新定义”将产生一个惊人的效果:更多的人会被考虑患有阿尔兹海默症,因为在症状出现之前的15-20年,大脑病变就已经发生。这也意味着,阿尔兹海默症患者数量将急剧增加。 “在70岁以上、无认知障碍的老年人中,有1/3人的大脑内实际上已经出现AD迹象。” Clifford Jack表示道。 全球约有5000万阿尔兹海默症患者。作为常见的神经性衰退疾病,AD已经成为威胁老年人健康和生命的主要病因。遗憾的是,抗AD药物研发一直鲜有成效,迄今已有超200项围绕AD药物的临床试验失败。这些研究多集中于治疗已经出现记忆丧失、交流困难等典型痴呆症状的患者。不少科学家们认为失败的一个原因可能是,当记忆衰退、认知退化等症状出现时,大脑中已经存在病斑了。 “依据典型病症确诊时,已经太晚了。” 衰老研究所的神经科学主任Eliezer Masliah博士说道。所以,他认为,阿尔兹海默症的诊疗时间应该“更早”。 这一指南“跳脱”认知衰退的传统范畴,通过生物标志物反映生病初期的大脑变化。但是,专家们强调,因为这一建议尚未得到证实,现在利用这些扫描、检测标准进行日常护理还为时尚早。目前,医生们仍将通过认知评估等主要方法诊断大多数病例。 责编:悠然 参考资料: Alzheimer’s Should be Characterized by Biomarkers: Report New way of defining Alzheimer's aims to find disease sooner详情>>

2018-04-17 00:00:00