Table 4 Summary of mutational analysis in NSCLC patients with E2A-PBX1 fusion transcripts Total (%) K-P-E- K + P-E- K-P + E- K + P + E-
K-P + E+ K-P-E+ K + P-E+ K + P + E+ Total 22 (100) 12 (54.5) 7 (31.8) 1 (4.5) 1 (4.5) 1 (4.5) Gender F 15 (100) 7 (46.7) 5 (33.3) 1 (6.7) 1 (6.7) 1 (6.7) M 7 (100) 5 (71.4) 2 (28.6) Race Caucasian 16 (100) 8 (50.0) 5 (31.3) 1 (6.3) 1 (6.3) 1 (6.3) High Content Screening Asian 3 (100) 2 (66.7) 1 (33.3) Middle eastern 1 (100) 1 (100) Hispanic 2 (100) 1(50.0) 1 (50.0) Smoking status NS 4 (100) 4 (100) S 18 (100) 8 (44.4) 7 (38.9) 1 (5.6) 1 (5.6) 1 (5.6) Stage I 12 (100) 8 (66.7) 3 (25.0) 1 (8.3) II 2 (100) 1 (50.0) 1 (50.0) BMS345541 nmr III 5 (100) 2 (40.0) 2 (40.0) 1 (20.0) IV 3 (100) 1 (33.3) 1 (33.3) 1 (33.3) learn more Histology AIS 16 (100) 8 (50.0) 5 (31.3) 1 (6.3) 1 (6.3) 1 (6.3) Invasive Adc 5 (100) 3 (60.0) 2 (40.0) LCC 1 (100) 1 (100) K: k-ras codon 12; P: p53 exons 4-8; E: EGFR exons 19-21. Discussion Somatic genetic changes have been believed to play important roles in human tumorigenesis, but the cancer type in which
somatic rearrangement occurs is limited to leukemias, lymphomas and soft tissue tumors [2]. Overexpression of Notch3 was found to be associated with chromosome 19 translocation in lung cancer [27]. EML4-ALK fusion gene [28] and ETS fusion genes [29, 30] exist in NSCLC and prostate cancer, respectively. It is still unclear whether chromosome aberrations are important in the initiation of epithelial Astemizole tumorigenesis. AIS (formerly named BAC) is a subset of adenocarcinoma characterized by non-invasive growth along alveolar septae [19, 25]. It is more prevalent in women, non-smokers, and
Asians [25]. Despite the lack of stromal, vascular, or pleural invasion, AIS is malignant and surgical resection is currently the mainstay of curative treatment. We previously discussed about a multi-step model of lung cancer development, especially AIS as carcinoma in situ [31]. Genetic changes can sequentially accumulate and cause bronchioalveolar stem cells to transform, leading to development of invasive phenotype in human cancers. However, it is unclear what is the cause for transformation of atypical bronchioloalveolar cells into invasive adenocarcinoma or maintenance for the growth characterization in AIS. Several important players such as K-ras, p53, and survivin, etc.