一個美國研究團隊在新一期醫(yī)學刊物《自然醫(yī)學》上發(fā)表論文說,，他們發(fā)現(xiàn)了兩種變異基因,，通過它們可預測因放射治療兒童霍奇金淋巴瘤引發(fā)的復發(fā)性癌癥。
美國芝加哥大學、南加州大學等機構的研究人員分析了178名兒童霍奇金淋巴瘤治愈患者的基因組,，這些患者兒童時期患該病,，并曾長期接受放療和化療。在治療后的30年內,，治愈患者中又新增96例癌癥病例,。通過分組對比研究，研究人員發(fā)現(xiàn),，復發(fā)性癌癥患者基因組中有兩種變異基因明顯增多,。
研究人員說，上述變異基因與癌癥復發(fā)風險增加密切相關,。這一發(fā)現(xiàn)意味著可以更容易檢測出受放療危害的兒童霍奇金淋巴瘤患者,，調整他們的治療方案，避免其他癌癥的發(fā)生,。
霍奇金淋巴瘤是常見的惡性腫瘤,，結合放射和化學治療，絕大多數(shù)患者可以治愈,。但研究表明,，受放療影響，許多兒童霍奇金淋巴瘤治愈患者在30年內會癌癥復發(fā),，并且兒童患者接受放療的年齡越低,，治療劑量越大，癌癥復發(fā)的風險也越大,。(生物谷 Bioon.com)
doi:10.1038/nm.2407
PMC:3006442
PMID:16153702
Variants at 6q21 implicate PRDM1 in the etiology of therapy-induced second malignancies after Hodgkin's lymphoma
Timothy Best, Dalin Li ,Andrew D Skol, Tomas Kirchhoff,，Sarah A Jackson，Yutaka Yasui,，Smita Bhatia,，Louise C Strong，Susan M Domchek,，Katherine L Nathanson,， Olufunmilayo I Olopade， R Stephanie Huang,，Thomas M Mack,，David V Conti， Kenneth Offit,，Wendy Cozen,，Leslie L Robison，Kenan One
Many persistent pain states (pain lasting for hours, days, or longer) are poorly treated because of the limitations of existing therapies. Analgesics such as nonsteroidal anti-inflammatory drugs and opioids often provide incomplete pain relief and prolonged use results in the development of severe side effects. Identification of the key mediators of various types of pain could improve such therapies. Here, we tested the hypothesis that hitherto unrecognized cytokines and chemokines might act as mediators in inflammatory pain. We used ultraviolet B (UVB) irradiation to induce persistent, abnormal sensitivity to pain in humans and rats. The expression of more than 90 different inflammatory mediators was measured in treated skin at the peak of UVB-induced hypersensitivity with custom-made
