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Articles by A. Y Kim
Total Records ( 2 ) for A. Y Kim
  S. H Park , S. Y Kim , S. S Lee , L Bogoni , A. Y Kim , S. K Yang , S. J Myung , J. S Byeon , B. D Ye and H. K. Ha

OBJECTIVE. The purpose of our study was to determine the sensitivity of CT colonography (CTC) interpreted by human readers and with computer-aided detection (CAD) for genuinely nonpolypoid colorectal lesions, defined as 2 mm or less in lesion height at colonoscopy.

MATERIALS AND METHODS. A computerized database search for a 33-month period found 21 patients who had undergone both colonoscopy and CTC and who had a total of 23 genuinely nonpolypoid colorectal lesions: eight adenomas (9-30 mm in width), 10 stage Tis or T1 adenocarcinomas (10-25 mm), and five nonadenomatous lesions (8-20 mm). CTC was performed using a cathartic preparation and fecal tagging and was interpreted by experienced readers in a blinded manner using a primary 3D method and with CAD.

RESULTS. The sensitivities of human readers for nonpolypoid adenomatous lesions (i.e., both adenomas and adenocarcinomas), adenocarcinomas, and nonadenomatous lesions were 66.7% (12/18), 90% (9/10), and 0% (0/5), respectively. Sensitivities were 55.6% (10/18), 90% (9/10), and 0% (0/5) for CAD. A 10-mm stage T1 adenocarcinoma was missed by a human reader on blinded review but was detected with CAD. Both human readers and CAD yielded significantly higher sensitivity for adenomatous lesions than for nonadenomatous lesions (p = 0.014 and 0.046, respectively) and for adenocarcinomas than for noncancerous lesions (p = 0.003 and 0.0001, respectively).

CONCLUSION. CTC showed a high sensitivity for nonpolypoid stage Tis and T1 adenocarcinomas 10 mm or greater in width despite the limited overall sensitivity for nonpolypoid adenomatous lesions, when performed using cathartic preparation and fecal tagging.

  A. Y Kim , Y. S Lee , K. H Kim , J. H Lee , H. K Lee , S. H Jang , S. E Kim , G. Y Lee , J. W Lee , S. A Jung , H. Y Chung , S Jeong and J. B. Kim

In obesity, dysregulation of adipocytokines is involved in several pathological conditions including diabetes and certain cancers. As a member of the adipocytokines, adiponectin plays crucial roles in whole-body energy homeostasis. Recently, it has been reported that the level of plasma adiponectin is reduced in several types of cancer patients. However, it is largely unknown whether and how adiponectin affects colon cancer cell growth. Here, we show that adiponectin suppresses the proliferation of colon cancer cells including HCT116, HT29, and LoVo. In colon cancer cells, adiponectin attenuated cell cycle progression at the G1/S boundary and concurrently increased expression of cyclin-dependent kinase inhibitors such as p21 and p27. Adiponectin stimulated AMP-activated protein kinase (AMPK) phosphorylation whereas inhibition of AMPK activity blunted the effect of adiponectin on the proliferation of colon cancer cells. Furthermore, knockdown of adiponectin receptors such as AdipoR1 and AdipoR2 relieved the suppressive effect of adiponectin on the growth of colon cancer cells. In addition, adiponectin repressed the expression of sterol regulatory element binding protein-1c, which is a key lipogenic transcription factor associated with colon cancers. These results suggest that adiponectin could inhibit the growth of colon cancer cells through stimulating AMPK activity.

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