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Biomedical subjects

Y S Shim

Publications and source records attributed to Y S Shim.

60 records · Page 4Linked to original sources

Comparison of medical v surgical treatment of major hemoptysis.

One hundred thirteen patients hospitalized with substantial hemoptysis were studied. Thirty-one patients underwent surgery and 82 were treated medically, and the two groups had similar diagnoses and bleeding patterns. There were four deaths in the surgical group and 18 deaths in the medical group. Of these, eight patients had a sudden first hemoptysis with instantaneous death. Ten patients had a terminal hemoptysis after prior bleeding, but nine of these patients had absolute contraindications for surgery. In 64 patients hemoptysis was controlled with medical treatment. Most patients showed a steady decrease of bleeding, with cessation of hemoptysis after four days. Our experience indicates that the majority of patients with serious hemoptysis can be successfully treated conservatively. Massive hemoptysis, aspiration, or recurrence of bleeding in and of themselves are not indications for surgery. Where the hemoptysis remains uncontrolled in spite of a trial of adequate medical care or where the aspiration is severe and progressive, surgery may be indicated and can be lifesaving.

Adolescent↗

Alteration of cell growth and morphology by overexpression of transforming growth factor beta type II receptor in human lung adenocarcinoma cells.

TGF-beta is a potent inhibitory regulator of cell growth, which is transduced through interaction between type I (RI) and type II (RII) receptors that form heteromeric kinase complexes. Abnormal expression of these receptors has been identified in several human epithelial cancers and has been shown to be highly associated with resistance to TGF-beta. In this study, we investigated the expression of RI and RII in 13 human non-small cell lung cancer cell lines (NSCLCs) and demonstrated decreased or loss of RII expression in five lung cancer cell lines, but not of RI. Of these cell lines, the role of RII in NCI-H358 adenocarcinoma, which lacks RII and is insensitive to TGF-beta, was investigated by transducing this cell line with a recombinant retrovirus expressing full-length TGF-beta RII. Stably transfected cells showed significant increase in RII mRNA and protein expression. These cells responded to exogenous TGF-beta1 with suppressed proliferation in a dose-dependent manner and G1 arrest accompanied by morphological change distinct from control cells. We also investigated whether overexpression of dominant-negative RII (dnRII) in NCI-H441 adenocarcinoma, which is sensitive but expresses low levels of RII, could block signaling through the receptor complex. The overexpression of this kinase-domain-truncated RII by expressing the retroviral dnRII construct led to loss of the ability to respond to TGF-beta1 and an exhibition of uncontrolled growth. These results suggest a close association between the loss of the expression of wild-type TGF-beta RII and carcinogenesis in human lung cancer cells.

Adenocarcinoma↗

Adenovirus expressing p27(Kip1) induces growth arrest of lung cancer cell lines and suppresses the growth of established lung cancer xenografts.

p27(Kip1) (p27) is a member of the universal cyclin-dependent kinase inhibitor (CDKI) family and a putative tumor suppressor gene. In several tumors including lung cancer, decreased expression of p27 is associated with poor prognosis. These observations suggest a potential role for p27 as a new gene therapy target. In this study, we constructed adenovirus expressing human p27 (ad-p27) and investigated its antitumor effects on human lung cancer cell lines. Upon transduction of several human lung cancer cells with ad-p27, a high level of p27 expression, with a decrease in cdk2 and an increase in cyclin E were observed. These changes resulted in G1/S arrest. Transduction of human lung cancer cell lines with ad-p27 showed in vitro growth inhibition and a marked suppression of colony formation upon soft agar clonogenic assay. Direct intratumoral injection of ad-p27 induced the growth suppression of established lung tumors in nude mice. From these observations, gene therapy using ad-p27 seems to offer a potential basis for the development of new cancer gene therapy modality and a useful tool to investigate the mechanisms of cell cycle control.

Adenoviridae↗

Rhabdomyosarcoma of the head and neck in adults: MR and CT findings.

PURPOSE: To evaluate imaging findings of rhabdomyosarcoma of the head and neck in adults. METHODS: We examined 11 patients (seven men and four women; 17 to 73 years old) with pathologically proved rhabdomyosarcoma of the head and neck. The tumors originated in the paranasal sinuses (n = 6), cheek (n = 3), nasal cavity (n = 1), and infratemporal fossa (n = 1). Eight of the rhabdomyosarcomas were of the embryonal type, two were pleomorphic, and one was alveolar. Necrosis was seen in four patients, but calcification or intratumoral hemorrhage was not found. Two tumors had nodal extension. Contrast-enhanced CT was performed in 10 patients, and two patients had contrast-enhanced MR imaging. RESULTS: On CT scans, the masses enhanced to the same degree as adjacent muscle. The masses showed a homogeneous pattern in six cases and a heterogeneous pattern in four cases. The tumor margins were poorly defined in eight cases. On MR images, the masses were homogeneously isointense with muscle on T1-weighted studies and were hyperintense relative to muscle on T2-weighted studies. On both CT and MR images, 10 of 11 cases showed poorly defined, homogeneous masses destroying adjacent bony structures. CONCLUSIONS: MR imaging seems to be better than CT for initial and follow-up examination of patients with rhabdomyosarcoma because of its multiplanar capability and because it more precisely defines the extent of tumor.

Adolescent↗

The inhibitory effect of adenovirus-mediated p16INK4a gene transfer on the proliferation of lung cancer cell line.

Abnormalities in the p16INK4a tumor suppressor gene are found in many lung cancer cell lines and primary lung cancer tissue. To examine its tumor suppressor function and potential adequacy in cancer gene replacement therapy, wild-type p16INK4a gene was inserted in an adenovirus derived gene delivery system and introduced into lung cancer cell lines (NCI-H441 and NCI-H157) that did not express p16INK4a. Western blot assay and immunocytochemistry demonstrated production of wild-type p16 protein in these cell lines. The biological function of exogenous p16 protein was confirmed by the inhibition of pRB phosphorylation. The expression of exogenous p16 protein via recombinant adenovirus significantly inhibited cancer cell growth and colony formation in vitro of NSCLC that can not express endogenous p16. The flow cytometric analysis showed these results correlated with G1 cell cycle arrest. These observations suggest the value of adenovirally-mediated p16INK4a gene replacement therapy for lung cancer.

Adenoviridae↗