据Feinstein医学研究所的一项研究表明，当某些人不幸携带了一个可导致其患换精神分裂症(schizophrenia)的基因后，该基因或许能够防止此人患其他癌症的可能。
之前有研究表明，人类的多种恶性肿瘤的发生都与MET原癌基因被激活有关。最近的一些研究将该基因与自闭症产生的原因联系起来。在一项由Katherine E. Burdick主持的研究中，他们对MET原癌基因与精神分裂症联系起来。该研究报告发表在American Journal of Psychiatry杂志上。
研究人员对173名精神分裂症患者和137名正常人的MET基因进行分析，以研究MET原癌基因的单核苷酸多态性(SNPs)进行研究。他们发现MET基因中，有几个变异可增加患精神分裂症和一般性认知障碍的风险。研究人员再对另外一份包括107名患者和112名健康人的样本进行研究，发现两份报告的结果相似。
目前，研究人员还不十分清楚MET基因如何在增加精神分裂症患病风险的同时如何降低癌症的患病风险。但是从MET基因与自闭症相关性的研究中或许能为科学提供一些思路，当肿瘤发生时，MET被激活能够增加癌细胞增殖和侵润其他组织的能力。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
