Oon Ming Liang, Hoppe Michal M, Fan Shuangyi, Phyu The, Phuong Hoang M, Tan Soo-Yong, Hue Susan Swee-Shan, Wang Shi, Poon Li M, Chan Hian L E, Lee Joanne, Chee Yen L, Chng Wee-Joo, de Mel Sanjay, Liu Xin, Jeyasekharan Anand D, Ng Siok-Bian
Department of Pathology, National University Hospital, National University Health System, Singapore, Singapore.
Cancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Leuk Lymphoma. 2019 Dec;60(13):3214-3224. doi: 10.1080/10428194.2019.1633629. Epub 2019 Jul 1.
Polo-like kinase-1 (PLK1) regulates the MYC-dependent kinome in aggressive B-cell lymphoma. However, the role of PLK1 and MYC toward proliferation in diffuse large B-cell lymphoma (DLBCL) is unknown. We use multiplexed fluorescent immunohistochemistry (fIHC) to evaluate the co-localization of MYC, PLK1 and Ki67 to study their association with proliferation in DLBCL. The majority (98%, 95% CI 95-100%) of MYC/PLK1-double positive tumor cells expressed Ki67, underscoring the key role of the MYC/PLK1 circuit in proliferation. However, only 38% (95% CI 23-40%) and 51% (95% CI 46-51%) of Ki67-positive cells expressed MYC and PLK1, respectively. Notably, 40% (95% CI 26-43%) of Ki67-positive cells are MYC- and PLK-negative. A stronger correlation exists between PLK1 and Ki67 expression ( = 0.74, < .001) than with MYC and Ki67 expression ( = 0.52, < .001). Overall, the results indicate that PLK1 has a higher association than MYC in DLBCL proliferation and there are mechanisms besides MYC and PLK1 influencing DLBCL proliferation.
Polo样激酶-1(PLK1)在侵袭性B细胞淋巴瘤中调节依赖MYC的激酶组。然而,PLK1和MYC在弥漫性大B细胞淋巴瘤(DLBCL)增殖中的作用尚不清楚。我们使用多重荧光免疫组织化学(fIHC)来评估MYC、PLK1和Ki67的共定位,以研究它们与DLBCL增殖的关联。大多数(98%,95%置信区间95-100%)MYC/PLK1双阳性肿瘤细胞表达Ki67,强调了MYC/PLK1回路在增殖中的关键作用。然而,分别只有38%(95%置信区间23-40%)和51%(95%置信区间46-51%)的Ki67阳性细胞表达MYC和PLK1。值得注意的是,40%(95%置信区间26-43%)的Ki67阳性细胞为MYC和PLK阴性。PLK1与Ki67表达之间的相关性(=0.74,<0.001)比MYC与Ki67表达之间的相关性(=0.52,<0.001)更强。总体而言,结果表明PLK1在DLBCL增殖中的关联性高于MYC,并且除了MYC和PLK1之外,还有其他机制影响DLBCL增殖。