據(jù)Feinstein醫(yī)學(xué)研究所的一項(xiàng)研究表明,，當(dāng)某些人不幸攜帶了一個(gè)可導(dǎo)致其患換精神分裂癥(schizophrenia)的基因后,，該基因或許能夠防止此人患其他癌癥的可能。
之前有研究表明,，人類的多種惡性腫瘤的發(fā)生都與MET原癌基因被激活有關(guān),。最近的一些研究將該基因與自閉癥產(chǎn)生的原因聯(lián)系起來。在一項(xiàng)由Katherine E. Burdick主持的研究中,，他們對MET原癌基因與精神分裂癥聯(lián)系起來,。該研究報(bào)告發(fā)表在American Journal of Psychiatry雜志上。
研究人員對173名精神分裂癥患者和137名正常人的MET基因進(jìn)行分析,，以研究MET原癌基因的單核苷酸多態(tài)性(SNPs)進(jìn)行研究,。他們發(fā)現(xiàn)MET基因中，有幾個(gè)變異可增加患精神分裂癥和一般性認(rèn)知障礙的風(fēng)險(xiǎn),。研究人員再對另外一份包括107名患者和112名健康人的樣本進(jìn)行研究,，發(fā)現(xiàn)兩份報(bào)告的結(jié)果相似。
目前,，研究人員還不十分清楚MET基因如何在增加精神分裂癥患病風(fēng)險(xiǎn)的同時(shí)如何降低癌癥的患病風(fēng)險(xiǎn),。但是從MET基因與自閉癥相關(guān)性的研究中或許能為科學(xué)提供一些思路，當(dāng)腫瘤發(fā)生時(shí),，MET被激活能夠增加癌細(xì)胞增殖和侵潤其他組織的能力,。（生物谷Bioon.com）
生物谷推薦原始出處：
Am J Psychiatry Published January 15, 2010
Association of Genetic Variation in the MET Proto-Oncogene With Schizophrenia and General Cognitive Ability
Katherine E. Burdick, Ph.D., Pamela DeRosse, Ph.D., John M. Kane, M.D., Todd Lencz, Ph.D., and Anil K. Malhotra, M.D.
OBJECTIVE: Despite increased exposure to cancer risk factors, several studies have demonstrated a lower incidence of cancer in schizophrenia patients than in the general population. Lower cancer rates in first-degree relatives of schizophrenia patients suggest that the inverse relationship between cancer and schizophrenia may be related to genetic factors. Few studies of schizophrenia have focused on cancer-related genes. The MET proto-oncogene is primarily linked to tumor metastasis, but MET is also involved in neurodevelopment and influences risk for autism. Thus, MET may be of particular interest as a candidate gene for neuropsychiatric diseases with a developmental etiology, including schizophrenia. METHOD: The authors examined the relationship between 21 single-nucleotide polymorphisms in MET and schizophrenia in 173 Caucasian patients and 137 comparison subjects. They then genotyped a second independent sample (107 patients and 112 comparison subjects) for replication. Finally, they tested for MET's effects on general cognitive ability (g). RESULTS: In the initial cohort, the authors identified four haplotype blocks and found one block to be globally associated with schizophrenia. In block 3, the most common haplotype was overrepresented in comparison subjects (frequency, 47%) relative to schizophrenia patients (frequency, 33%) (p=4.0x10–4; odds ratio=0.56). The authors replicated the block 3 finding in the second sample with similar frequencies: 46% in comparison subjects and 36% in schizophrenia patients (p=0.03; odds ratio=0.66). Moreover, the protective haplotype was associated with a higher g in the combined comparison sample. CONCLUSIONS: These data suggest that MET variation influences schizophrenia risk and neurocognition, supporting a neurodevelopmental role across CNS-relevant phenotypes. These results add to the growing evidence suggesting an intriguing relationship between cancer-related genes and schizophrenia susceptibility.
