英国研究人员周三表示，严重恶性癌症患者可以通过检测干细胞标记蛋白——核纤层蛋白A来及早确认。这意味着一种更精确定位恶性肠癌的新方法问世，改进病人存活率的定制疗法成为可能。
目前正在研发中的新测试手段可以帮助医生确定如何以及何时治疗不同类型的癌症，这一发现就是最新的一个例子。
在肠癌四阶段的最早两个阶段，病人往往进行手术切除肿瘤，但是很少进行化疗，因为这种毒性疗法可能引起很大伤害。
尽管如此，新的研究显示大约1/3的早期病人拥有核纤层蛋白A干细胞标记，这表示他们得的是一种更严重的癌症，因此进行化疗对他们很可能大有好处。该研究小组得出结论指，核纤层蛋白A检测呈阳性的病人在手术之外还应该进行化疗，以便增加他们的存活率。
达拉谟大学(Durham University)和东北英格兰干细胞研究所如今准备开发一种功能强大的检测工具，该工具最终可能广泛用于医院中。
他们的研究发表在《公共科学图书馆·综合》上。（生物谷Bioon.com）
生物谷推荐原始出处：
PLoS ONE 3(8): e2988. doi:10.1371/journal.pone.0002988 Willis ND, Cox TR, Rahman-Casañs SF, Smits K, Przyborski SA, et al. (2008) Lamin A/C Is a Risk Biomarker in Colorectal Cancer.
Lamin A/C Is a Risk Biomarker in Colorectal Cancer
Naomi D. Willis1, Thomas R. Cox1, Syed F. Rahman-Casañs2, Kim Smits3, Stefan A. Przyborski1, Piet van den Brandt3, Manon van Engeland4, Matty Weijenberg3, Robert G. Wilson2, Adriaan de Bruïne4, Christopher J. Hutchison1*
Background
A-type lamins are type V intermediate filament proteins encoded by the gene LMNA. Mutations in LMNA give rise to diverse degenerative diseases related to premature ageing. A-type lamins also influence the activity of the Retinoblastoma protein (pRb) and oncogenes such a β-catenin. Consequently, it has been speculated that expression of A-type lamins may also influence tumour progression.
Methodology/Principal Findings
An archive of colorectal cancer (CRC) and normal colon tissue was screened for expression of A-type lamins. We used the Cox proportional hazard ratio (HR) method to investigate patient survival. Using CRC cell lines we investigated the effects of lamin A expression on other genes by RT-PCR; on cell growth by FACS analysis; and on invasiveness by cell migration assays and siRNA knockdown of targeted genes. We found that lamin A is expressed in colonic stem cells and that patients with A-type lamin-expressing tumours have significantly worse prognosis than patients with A-type lamin negative tumours (HR = 1.85, p = 0.005). To understand this finding, we established a model system based upon expression of GFP-lamin A in CRC cells. We found that expression of GFP-lamin A in these cells did not affect cell proliferation but did promote greatly increased cell motility and invasiveness. The reason for this increased invasiveness was that expression of lamin A promoted up-regulation of the actin bundling protein T-plastin, leading to down regulation of the cell adhesion molecule E-cadherin.
Conclusions
Expression of A-type lamins increases the risk of death from CRC because its presence gives rise to increased invasiveness and potentially a more stem cell-like phenotype. This report directly links A-type lamin expression to tumour progression and raises the profile of LMNA from one implicated in multiple but rare genetic conditions to a gene involved in one of the commonest diseases in the Western World.
