OBJECTIVES: This study aimed to compare the real-world outcomes of segmentectomy and lobectomy for lung cancer after adjusting for background factors and the extent of lymphadenectomy. METHODS: This retrospective cohort study used a nationwide database in Japan. The data of patients with clinical stage 0/IA lung cancer who underwent segmentectomy or lobectomy between 2017 and 2019 were retrieved. Short-term postoperative outcomes were compared between the segmentectomy and lobectomy groups using propensity score-matched analysis. RESULTS: In the total cohort of 59 663 patients, 11 975 and 47 688 patients were in the segmentectomy and lobectomy groups, respectively. After propensity score matching, 8426 matched patients from each group were retrieved. All confounders including age, sex, comorbidities, smoking history, respiratory function, tumour size, clinical stage, affected lobe and extent of lymphadenectomy were appropriately adjusted. The overall complication rate and the cardiopulmonary complication rate were lower in the segmentectomy group than in the lobectomy group (8.5% vs 11.2%, P < 0.001 and 7.5% vs 10.3%, P < 0.001, respectively). The incidence of prolonged air leak was also lower after segmentectomy than after lobectomy (3.6% vs 5.3%). Surgical mortality, operative time and blood loss volume were comparable between the 2 groups. CONCLUSIONS: The postoperative complication rate was lower with segmentectomy than with lobectomy for early-stage lung cancer.

CADM1, a member of the immunoglobulin superfamily cell adhesion molecule, acts as a tumor suppressor in a variety of human cancers. CADM1 is also ectopically expressed in adult T‐cell leukemia (ATL), conferring an invasive phenotype characteristic to ATL. Therefore, CADM1 plays dual roles in human oncogenesis. Here, we investigate the roles of CADM1 in small cell lung cancer (SCLC). Immunohistochemistry demonstrates that 10 of 35 (29%) primary SCLC tumors express CADM1 protein. Western blotting and RT‐PCR analyses reveal that CADM1 is significantly expressed in 11 of 14 SCLC cells growing in suspension cultures but in neither of 2 SCLC cells showing attached growth to plastic dishes, suggesting that CADM1 is involved in anchorage‐independent growth in SCLC. In the present study, we demonstrate that SCLC expresses a unique splicing variant of CADM1 (variant 8/9) containing additional extracellular fragments corresponding to exon 9 in addition to variant 8, a common isoform in epithelia. Variant 8/9 of CADM1 is almost exclusively observed in SCLC and testis, although this variant protein localizes along the membrane and shows similar cell aggregation activity to variant 8. Interestingly, both variant 8/9 and variant 8 of CADM1 show enhanced tumorigenicity in nude mice when transfected into SBC5, a SCLC cell lacking CADM1. Inversely, suppression of CADM1 expression by shRNA reduced spheroid‐like cell aggregation of NCI‐H69, an SCLC cell expressing a high amount of CADM1. These findings suggest that CADM1 enhances the malignant features of SCLC, as is observed in ATL, and could provide a molecular marker specific to SCLC. (Cancer Sci 2012; 103: 1051–1057)

Somatic mutations are accumulated in normal human tissues with aging and exposure to carcinogens. If we can accurately count any passenger mutations in any single DNA molecule, since their quantity is much larger than driver mutations, we can sensitively detect mutation accumulation in polyclonal normal tissues. Duplex sequencing, which tags both DNA strands in one DNA molecule, enables accurate count of such mutations, but requires a very large number of sequencing reads for each single sample of human-genome size. Here, we reduced the genome size to 1/90 using the Bam HI restriction enzyme and established a cost-effective pipeline. The enzymatically cleaved and optimal sequencing (EcoSeq) method was able to count somatic mutations in a single DNA molecule with a sensitivity of as low as 3 × 10 ⁻⁸ per base pair (bp), as assessed by measuring artificially prepared mutations. Taking advantages of EcoSeq, we analyzed normal peripheral blood cells of pediatric sarcoma patients who received chemotherapy ( n = 10) and those who did not ( n = 10). The former had a mutation frequency of 31.2 ± 13.4 × 10 ⁻⁸ per base pair while the latter had 9.0 ± 4.5 × 10 ⁻⁸ per base pair ( P < 0.001). The increase in mutation frequency was confirmed by analysis of the same patients before and after chemotherapy, and increased mutation frequencies persisted 46 to 64 mo after chemotherapy, indicating that the mutation accumulation constitutes a risk of secondary leukemia. EcoSeq has the potential to reveal accumulation of somatic mutations and exposure to environmental factors in any DNA samples and will contribute to cancer risk estimation.