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BACKGROUND: Spontaneous regression of malignant tumors is a rare phenomenon, especially in primary lung cancer. The underlying mechanisms remain unclear, but they may often involve immunological mechanisms. CASE PRESENTATION: In January 2020, a 78-year-old female underwent examination during follow-up of interstitial pneumonia. Chest X-ray and computed tomography (CT) scan revealed a 1.2 × 1.2 cm nodule in the left lower lobe. Based on CT-guided percutaneous transthoracic needle biopsy (PTNB), it was diagnosed as small cell lung cancer (SCLC). Immunohistochemical staining showed that tumor cells were positive for CD56, synaptophysin, and chromogranin A. Twenty-three days after the CT-guided PTNB, repeat CT scan showed that the tumor size regressed to 0.6 × 0.6 cm. The tumor showed positive uptake in fluorodeoxyglucose (FDG) positron emission tomography (PET)-CT. The maximum standardized uptake value of the nodule was 2.24. PET-CT and enhanced magnetic resonance imaging of the brain showed no distant or lymph node metastasis. The patient's preoperative disease was diagnosed as cT1aN0M0, stageIA1, SCLC. In March 2020, she underwent left lower lobectomy and mediastinal lymph node dissection. Pathological examination of the resected specimen showed that the small tumor cells were dense with a high nucleus to cytoplasm ratio, and the morphological diagnosis was small cell carcinoma. The resected tumor size regressed to 0.05 × 0.02 cm, and no lymph node metastasis was observed. Because it was extremely small, immunohistochemical staining could not be conducted. Active fibrosis and inflammation were present around the tumor. Finally, the patient was pathologically diagnosed as SCLC pT1miN0M0, stage IA1. The patient is alive without recurrence 23 months after surgery with no adjuvant therapy. CONCLUSIONS: We present a rare surgical case of pathologically confirmed spontaneous regression of SCLC after CT-guided PTNB. Although spontaneous regression is extremely rare, we should recognize this phenomenon.

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BACKGROUND: There have been few reports on surgically treated primary lung cancer accompanied by contralateral partial anomalous pulmonary venous connection (PAPVC). In such cases, repair of the PAPVC might be necessary to avoid postoperative right-heart failure due to the increased flow of the left-to-right shunt. CASE PRESENTATION: We herein report a case of lung adenocarcinoma treated by left-upper lobectomy with bronchoplasty and pulmonary arterial angioplasty after induction chemoradiation therapy followed by surgical correction of the PAPVC in the right-upper lobe. The patient is alive without recurrence of lung cancer or any symptoms of heart failure 17 months after pulmonary resection. CONCLUSION: When considering performing major pulmonary resection for lung tumor, thoracic surgeons should pay close attention to the presence of a PAPVC not only on the ipsilateral side of the lung tumor, but also the contralateral side, although it is a rare phenomenon.

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OBJECTIVE: Clinical evidence comparing paravertebral (PVB) and continuous intercostal nerve (ICB) blocks for pain management post video-assisted thoracic surgery (VATS) is limited. This study confirms the analgesic effect of ICB using two catheters is not inferior to that of PVB under direct vision. METHODS: Fifty patients who underwent VATS lobectomy from July 2015 to March 2016 were prospectively recruited and randomly assigned to PVB and ICB groups. Postoperative pain was assessed using the visual analog scale (VAS). VAS score at rest at 24 h was the primary endpoint. Data on time required for catheter insertion, adverse effects, and frequency of additional analgesics as secondary endpoints were also collected. Noninferiority was assessed by adding a VAS margin of 15 mm to the PVB group. RESULTS: No significant differences were observed between the VAS scores of the two groups except at 48 h after surgery, with a margin noted for the PVB group. No significant differences were detected in the frequency of additional analgesics and occurrence of adverse effects. CONCLUSIONS: Our results could not clearly establish noninferiority of ICB to PVB. Improvements in ICB may be necessary for it to be used as an alternative method to PVB.

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Adenomatoid tumors are relatively uncommon benign tumors of mesothelial origin, usually occurring in the male or female genital tracts. Extragenital adenomatoid tumors are quite rare. Here, we report a very rare case of adenomatoid tumor of the mediastinum. A 67-year-old woman was admitted to our hospital with an abnormal shadow that appeared on a routine chest radiograph. After further radiological evaluation suggested a diagnosis of thymoma, surgical resection was performed, and histologic and immunohistochemical examination yielded a definitive diagnosis of adenomatoid tumor. The patient remained clinically free of disease at follow-up, 19 months later.

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We report a case of a 50-year-old man with multiple glomus tumors of the chest wall and buttocks. He was admitted to our hospital because of right chest pain for 10 years. The chest pain was lancinating and gradually increasing. A computed tomography (CT) showed a mass in the right 3rd intercostal space and a mass in the right buttocks. The chest tumor was enhanced with contrast medium on chest CT. Two tumors were resected completely including the 4th rib. Histological examination showed numerous vascular space lined with sheets of epithelial cells (glomus cells), so they were diagnosed as glomus tumor. The postoperative course was well, and the pain disappeared after resection. The glomus tumor of chest wall could be diagnosed as malignant tumor, based on the criteria of the size more than 2 cm and deep location. The glomus tumors which occurred in the chest wall and buttocks were very rare. We presented the case with reference to the literature.

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Non-small cell lung cancer frequently shows loss of heterozygosity of the chromosome 3p21.3 region and several genes such as RASSF1A, BLU, and SEMA3B have been identified as candidate tumor suppressor genes at this region since their downregulation and hypermethylation at their promoter regions were frequently detected in lung cancer. To determine whether these three genes are simultaneously inactivated during lung cancer development, we studied 138 primary non-small cell lung cancers for the promoter methylation status of these genes and allelic loss of the chromosome 3p21.3 region. We found promoter hypermethylation at 32% in RASSF1A, 30% in BLU, and 47% in SEMA3B. Allelic loss of 3p21.3 was detected in 54 (58%) of 93 informative tumors. Despite the weak association of methylation status among these three genes, there was no correlation between the methylation status of each gene and loss of heterozygosity. We also studied possible genes downstream of RASSF1A in 16 primary non-small cell lung cancers and found that the expressions of SM22 and SPARC were significantly downregulated in RASSF1A-hypermethylated tumors. Our results showed that, while candidate tumor suppressor genes at this locus can be simultaneously inactivated by epigenetic alterations, loss of heterozygosity without any hypermethylation of the three genes can also occur in some cases, suggesting that just one allelic loss might also be sufficient for the inactivation of any of these genes for lung cancer development.

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Krüppel-like factor 6 (KLF6) is a ubiquitously expressed zinc finger transcriptional factor, which has been suggested to be a candidate tumor suppressor gene in prostate cancer and astrocytic glioma. Because KLF6 is located at chromosome 10p15, where non-small cell lung cancers (NSCLCs) also exhibit frequent allelic loss, we hypothesized that the inactivation of KLF6 is also involved in the development of NSCLC. To determine this, we performed mutational analysis for 105 NSCLCs, including 9 cell lines and 96 primary tumors, and Northern blot analysis for 74 NSCLCs, including the 9 cell lines and 65 primary tumors. Although somatic mutations were not detected in the coding sequence of KLF6, expression of KLF6 mRNA was down-regulated in the 9 cell lines and in 55 (85%) of the 65 primary tumors compared with normal lung tissue. Treatment of two cell lines expressing KLF6 at low levels with 5-azacytidine did not induce KLF6 expression, suggesting that KLF6 down-regulation is not due to promoter hypermethylation. We also performed loss of heterozygosity (LOH) analysis using the laser capture microdissection technique, and found that 21 of 62 (34%) informative samples had LOH in the KLF6 gene locus. Comparing the LOH status with mRNA expression of KLF6, we found that 14 of the 14 (100%) samples with LOH showed KLF6 down-regulation, and that even 23 of 31 (74%) samples without LOH also showed this down-regulation. We also studied the expression of the WAF1 gene, a possible downstream gene of KLF6, and detected simultaneous down-regulation of WAF1 and KLF6 mRNA in 6 of 9 (67%) cell lines and 48 of the 55 (87%) primary tumors, although there was not a significant association between loss of KLF6 and WAF1 expression. Furthermore, colony formation assay of two NSCLC cell lines (NCI-H1299 and NCI-H2009) induced a markedly reduced colony formation by KLF6 transfection, and Annexin V staining and terminal deoxynucleotidyl transferase-mediated nick end labeling assays revealed that KLF6 induced apoptosis. Our present studies demonstrated that KLF6 is frequently down-regulated in NSCLC and suppresses tumor growth via induction of apoptosis in NSCLC, which may suggest that KLF6 is a tumor suppressor for NSCLC.

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Activating mutations of RAS gene families have been found in a variety of human malignancies, including lung cancer, suggesting their dominant role in tumorigenesis. However, several studies have shown a frequent loss of the wild-type KRAS allele in the tumors of murine models and an inhibition of oncogenic phenotype in tumor cell lines by transfection of wild-type RAS, indicating that wild-type RAS may have oncosuppressive properties. To determine whether loss of wild-type KRAS is involved in the development of human lung cancer, we investigated the mutations of KRAS, NRAS and BRAF in 154 primary non-small cell lung cancers (NSCLCs) as well as 10 NSCLC cell lines that have been shown to have KRAS mutations. We also determined the loss of heterozygosity status of KRAS alleles in these tumors. We detected point mutations of KRAS in 11 (7%) of 154 NSCLCs, with 10 cases at codon 12 and 1 at codon 61, but no mutations of NRAS or BRAF were found. Using the laser capture microdissection technique, we confirmed that 9 of the 11 tumors and 7 of the 10 NSCLC cell lines retained the wild-type KRAS allele. Among the cell lines with heterozygosity of mutant and wild-type KRAS, all of the cell lines tested for expression were shown to express more mutated KRAS than wild-type mRNA, with higher amounts of KRAS protein also being expressed compared to the cell lines with a loss of wild-type KRAS allele. In addition, among 148 specimens available for immunohistochemical analysis, 113 (76%) showed positive staining of KRAS, indicating that the vast majority of NSCLCs continue to express wild-type KRAS. Our findings indicate that the wild-type KRAS allele is occasionally lost in human lung cancer, and that the oncogenic activation of mutant KRAS is more frequently associated with an overexpression of the mutant allele than with a loss of the wild-type allele in human NSCLC development.

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