• Journal of Chest Surgery
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• v.57 no.4
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• pp.408-412
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• 2024

Fetal lung interstitial tumor (FLIT), which is characterized by immature interstitial cells resembling the fetal lung parenchyma of 20 to 24 weeks of gestation, is a rare respiratory neoplasm. This study presents the first reported FLIT in Korea. It also aims to refine the diagnostic method of FLIT and increase the accuracy of prognostic assessment by using next-generation sequencing to check for anaplastic lymphoma receptor tyrosine kinase (anaplastic lymphoma kinase) gene rearrangement. Although the initial prognosis for FLIT has been promising since its first report in 2010, certain pathological features are associated with poorer outcomes. Therefore, achieving an accurate diagnosis of FLIT is crucial for avoiding unnecessary treatments beyond surgical resection.

• Animal cells and systems
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• v.2 no.1
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• pp.1-8
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• 1998

Hepatocyte growth factor (HGF), originally discovered and cloned as a powerful mitogen for hepatocytes, is a four kringle-containing growth factor which specifically binds to membrane-spanning tyrosine kinase, c-Met/HGF receptor. HGF has mitogenic, motogenic (enhancement of cell movement), morphogenic (e.g., induction of branching tubulogenesis), and anti-apoptotic activities for a wide variety of cells. During embryogenesis, HGF supports organogenesis and morphogenesis of various tissues, including liver, kidney, lung, gut, mammary gland, and tooth. In adult tissues HGF elicits an organotrophic function which supports regeneration of organs such as liver, kidney, lung, and vascular tissues. HGF is also a novel member of neurotrophic factor in nervous systems. Together with the preferential expression of HGF in mesenchymal or stromal cells, and c-Met/HGF receptor In epithelial or endothelial cells, the HGF-Met coupling seems to orchestrate dynamic morphogenic processes through epithelial-mesenchymal (or-stromal) interactions for organogenesis and organ regeneration. HGF or HGF gene may well become unique therapeutic tools for treatment of patients with various organ failure, through its actions to reconstruct organized tissue architectures. This review focuses on recently characterized biological and physiological functions integrated by HGF-Met coupling during organogenesis and organ regeneration.

• Tuberculosis and Respiratory Diseases
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• v.76 no.1
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• pp.8-14
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• 2014

Non-small cell lung cancer harboring epidermal growth factor receptor (EGFR) sensitizing mutations has a distinct disease entity. Patients with this cancer have better prognosis, and frequently achieve long-term survival. EGFR-tyrosine kinase inhibitor (TKI) is the drug of choice for this cancer; but the disease inevitably progresses, after durable response. The tumor is a mixture of EGFR-TKI sensitive clones and resistant clones, regardless of their molecular mechanisms. EGFR-TKI sensitive clones are very susceptible to this drug, but rarely eradicated; so, withdrawal of the drug permits rapid regrowth of drug sensitive clones, possibly causing "disease flare." Re-administration or continuation of EGFR-TKI can effectively suppress the expansion of drug sensitive clones, even when the total tumor volume continuously increases. Chemotherapy can definitely prolong the survival of patients experiencing EGFR-TKI failure. Prospective clinical trials are warranted to compare efficacies of chemotherapeutic agents. A few retrospective studies suggested that a taxanebased regimen may be superior to others. Here, we reviewed therapeutic options and clinical evidence about this unique disease entity.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.1
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• pp.233-237
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• 2015

Background: Lung cancer is the leading cause of cancer death in Brunei Darussalam, accounting for almost 20% of the total. The epidermal growth factor receptor (EGFR) is a member of the erbB family of tyrosine kinase receptor proteins, which includes c-erbb2(HER2/neu), erb-B3, and erb-B4. EGFR overexpression is found in a third of all epithelial cancers, often associated with a poor prognosis. Materials and Methods: Protein expression of EGFR in 27 cases of lung cancer tissue samples and 9 cases of normal lung tissue samples was evaluated using an immunohistochemical approach. Results: The results demonstrated significant increase and overexpression of EGFR in Bruneian lung cancer tissue samples in comparison to normal lung tissue. However, there was no significant relationship between clinicopathologic variables (age and sex) of patients and EGFR protein expression. Conclusions: EGFR is overexpressed in Bruneian lung cancer patient tissue samples in comparison to normal lung tissue samples. This may indicate that EGFR protein over expression plays an important role in the genesis of this type of cancer in Brunei Darussalam.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4485-4494
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• 2013

Epidermal growth factor receptor (EGFR) is considered to be one of the key driver genes in non-small cell lung cancer (NSCLC). Several clinical trials have shown great promise of EGFR tyrosine kinase inhibitors (TKIs) in the first-line treatment of NSCLC. Many advances have been made in the understanding of EGFR signal transduction network and the interaction between EGFR and tumor microenvironment in mediating cancer survival and development. The concomitant targeted therapy and radiation is a new strategy in the treatment of NSCLC. A number of preclinical studies have demonstrated synergistic anti-tumor activity in the combination of EGFR inhibitors and radiotherapy in vitro and in vivo. In the present review, we discuss the rationale of the combination of EGFR inhibitors and radiotherapy in the treatment of NSCLC.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.4
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• pp.1609-1615
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• 2016

Breast cancer is one of among all cancers with increased incidence, high mortality rate, and high economic and social costs. The the most common type of cancer among females worldwide, breast cancer is actually the uncontrolled proliferation of cells which attain malignancy. Recently it has shown that breast cancer contributes 11% among all types of cancer diagnosed globally on an annual basis and it is one of the leading causes of death among women. The human epidermal growth factor receptor 2 (HER-2) is a receptor tyrosine-protein kinase erbB-2 normally involved in the proliferation and division of breast cells. In some abnormal cases the HER2 gene does not work correctly and makes too many copies of itself. HER2-positive (HER2+) breast cancers constitute an aggressive type of breast cancer and tend to grow faster and are more likely to spread. However, therapies that specifically target HER2, such as Herceptin$^{(R)}$ (traztuzumab), are very effective. HER2 targeted therapies, has significantly improved the therapeutic outcome for patients with HER2 positive breast cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.695-700
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• 2013

Background: Mutations affecting the epidermal growth factor receptor (EGFR) are good predictors of clinical efficacy of EGFR tyrosine kinase inhibitors (TKI) in patients with non-small cell lung cancer. Serum carcinoembryonic antigen (CEA) levels are also regarded as predictive for the efficacy of EGFR-TKI and EGFR gene mutations. This study analyzed the association between EGFR gene mutations and clinical features, including serum tumor marker levels in lung adenocarcinomas patients. Patients and Methods: A total of 70 lung adenocarcinoma patients with complete clinical data and pathological specimens were investigated. EGFR gene mutations at exons 19 and 21 were assessed. Serum tumor markers were detected by protein chip-chemiluminescence at the corresponding time, and correlations were analyzed. Results: Mutations of the EGFR gene were detected in 27 of the 70 patients and the serum CEA and CA242 concentrations were found to be significantly associated with the incidence of EGFR gene mutations (P<0.05). The AUCs for CEA and CA242 were 0.724 (95% CI: 0.598~0.850, P<0.05) and 0.769 (95% CI: 0.523~0.800, P<0.05) respectively. Conclusions: Serum CEA and CA242 levels are associated with mutations of the EGFR gene in patients with lung adenocarcinomas.

• The Journal of Korean Medicine
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• v.31 no.3
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• pp.66-78
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• 2010

Background: Peripheral nerve injuries are a commonly-encountered clinical problem and often result in a chronic pain and severe functional deficits. Objectives: The aim of this study was to evaluate the effects of acupuncture on the descending pain and the recovery of the locomotor function that follows sciatic crushed nerve injury in rats. Method: In order to assess the effects of acupuncture on the descending pain and functional recovery, we investigated the walking track analysis, brain-derived neurotrophic factor (BDNF) and its receptor tyrosine receptor kinase B (TrkB) expression in the sciatic nerve, and on the expressions of c-Fos and nitric oxide synthase in the paraventricular nucleus (PVN) of the hypothalamus and in the ventrolateral periaqueductal gray (vlPAG) region resulting from sciatic crushed nerve injury in rats. Results: Acupuncture treatment at Huantiao (GB30), Yanglingquan (GB34), and Weizhong (BL40) facilitated functional recovery. C-Fos and nitric oxide synthase expressions in the brain and BDNF and TrkB expressions in the sciatic nerve were decreased by acupuncture treatment. The most potent effects of acupuncture were observed at the GB30 acupoint. Conclusion: It is possible that acupuncture can be used for pain control and functional recovery from sciatic nerve injury.

• Animal cells and systems
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• v.5 no.2
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• pp.145-151
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• 2001

p62 is a phosphotyrosine-independent ligand of the SH2 domain of $p56^{Ick}$, a T-cell specific Src family tyrosine kinase. Recently p62 has been shown to interact with a number of proteins, such as $PKC\varsigma$ and ubiquitin, and implicated in important cellular functions such as cell proliferation. Since the two p62 interacting proteins, $p56^{Ick}$ and $PKC\varsigma$, have been reported to play roles in cell death, 1 have addressed the potential role of p62 during apoptosis in Jurkat cells in this study. Herein 1 show that p62 was specifically cleaved into two peptides by a caspase-3-like activity during Fas-receptor mediated apoptosis in Jurkat cells. This cleavage generated two fragments with molecular weights of about 35 kDa that differed in subcellular localizations. The N-terminal cleaved fragment was present in the detergent-insoluble fraction whereas the C-terminal fragment was found in the detergent-soluble fraction. In addition, the C-terminal fragment appeared to be subjected to further degradation as apoptosis prolonged. Moreover, overexpression of p62 in Jurkat cells attenuated the Fas receptor mediated apoptosis, suggesting that p62 is involved in apoptotic signal transduction pathway in lymphocytes.

• Journal of Life Science
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• v.17 no.3 s.83
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• pp.356-361
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• 2007

To investigate the region of ErbB2 for the $ErbB2-{\beta}-catenin$ interaction, a proteasome $resistant-{\beta}-catenin$ and various ErbB2 constructs were transfected in COS7 cells. ErbB2 proteins were immunoprecipitated, and coimmunoprecipitated ${\beta}-catenin$ was examined by Western blotting. ${\beta}-catenin$ coimmunoprecipitated with full length ErbB2. Of the truncated ErbB2 proteins DT (1-1123), DHC (1-1031) and DK (1-750), the ErbB2 constructs containing the kinase domain, DT and DHC, precipitated together with ${\beta}-catenin$ but DK containing no kinase domain did not. To further test the requirement of the kinase domain for ${\beta}-catenin-ErbB2$ interaction, the presence of ${\beta}-catenin$ in the immunocomplex was examined following transfection with an ErbB2 mutant (${\triangle}750-971$) whose kinase domain is internally deleted and subsequent immunoprecipitation of the ErbB2 mutant. ${\beta}-catenin$ was not detected in the immunocomplex. These results suggest that the ErbB2 kinase domain comprises a potential site for ${\beta}-catenin$ binding to the receptor tyrosine kinase.