Division of Surgical Oncology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, Nagasaki 852-8501, Japan.
Lung Cancer. 2012 Aug;77(2):281-7. doi: 10.1016/j.lungcan.2012.04.003. Epub 2012 May 3.
Since multiple lung cancer treatment strategies differ, it is essential for clinicians to be able to distinguish between separate primary lesions and metastasis. In the present study, we used array comparative genomic hybridization (aCGH) and somatic mutation (epidermal growth factor receptor: EGFR) to analyze genomic alteration profiles in lung cancer patients. To validate the consistency among the pathological assessments and clarify the clinical differences between double primary lesions and metastasis, we also examined synchronous double lung cancer clinical data.
Between January 1970 and March 2010, 2215 patients with lung cancer underwent surgical resection at Nagasaki University Hospital. We performed molecular analysis of 12 synchronous double lung cancer patients without lymph node metastasis (intrapulmonary metastasis in the same lobe (pm1): n=6, primary: n=6). We then evaluated the clinical outcomes of patients with pathologically diagnosed synchronous double lung cancers (intrapulmonary metastasis (pm): n=80, primary: n=39) and other T3 tumors (n=230).
Examination of the concordance rate (CR) of the copy number changes (CNCs) for paired tumors showed that the metastasis group was larger than the primary group (55.5% vs. 19.6%, p=0.04). Pathological diagnosis and molecular classification were the same in 10 out of 12 cases (83%). As compared to the primary group, there tended to be an inferior 5-year survival curve for the pm group. However, in N0 patients, the survival curve for the pm group overlapped the primary group, while the survival rate of the pm1 group was much higher than that of other T3 group (p<0.01).
Both pathological and molecular assessment using aCGH adapted in the current study appeared to have a consistency. Pathological pm1(T3)N0 patients may have a better prognosis than other T3N0 patients.
由于多种肺癌治疗策略存在差异，临床医生能够区分单独的原发性病变和转移灶至关重要。本研究中，我们使用 array 比较基因组杂交（aCGH）和体细胞突变（表皮生长因子受体：EGFR）分析肺癌患者的基因组改变谱。为了验证病理评估之间的一致性，并阐明双原发性病变和转移之间的临床差异，我们还检查了同步双肺癌的临床数据。
1970 年 1 月至 2010 年 3 月，长崎大学医院对 2215 例肺癌患者进行了手术切除。我们对 12 例无淋巴结转移的同步双肺癌患者（同叶内肺转移（pm1）：n=6，原发性：n=6）进行了分子分析。然后，我们评估了病理诊断为同步双肺癌（肺内转移（pm）：n=80，原发性：n=39）和其他 T3 肿瘤（n=230）患者的临床结局。
对配对肿瘤的拷贝数变化（CNC）一致性（CR）的检查表明，转移组的 CNC 大于原发性组（55.5% vs. 19.6%，p=0.04）。12 例中有 10 例（83%）的病理诊断和分子分类相同。与原发性组相比，pm 组的 5 年生存率曲线较低。然而，在 N0 患者中，pm 组的生存曲线与原发性组重叠，而 pm1 组的生存率明显高于其他 T3 组（p<0.01）。
本研究中使用的 aCGH 进行的病理和分子评估似乎具有一致性。病理性 pm1（T3）N0 患者的预后可能优于其他 T3N0 患者。
