{"id":6,"date":"2020-01-19T11:03:23","date_gmt":"2020-01-19T03:03:23","guid":{"rendered":"http:\/\/wp.kmu.edu.tw\/jackhsu\/?page_id=6"},"modified":"2022-07-25T11:18:29","modified_gmt":"2022-07-25T03:18:29","slug":"jack-hsu-blog","status":"publish","type":"page","link":"https:\/\/wp.kmu.edu.tw\/jackhsu\/","title":{"rendered":"Jack Hsu Lab."},"content":{"rendered":"

\u00a0\u00a0\u00a0<\/b> <\/b>Cancer<\/span><\/strong><\/em>,\u00a0 medically known as a malignant<\/a> neoplasm<\/a>, is a broad group of various diseases<\/a>\u00a0and directly affects at least one-third of the human population, all involving unregulated cell growth. In cancer, cells<\/a> divide and grow uncontrollably, forming malignant tumors, and invade nearby parts of the bodyby EMT. The cancer may also spread<\/a> to more distant parts of the body through the lymphatic system<\/a> or bloodstream<\/a>. Not all tumors are cancerous. Benign tumors<\/a> do not grow uncontrollably, do not invade neighboring tissues, and do not spread throughout the body. There are over 200 different known cancers that afflict humans.[1]<\/a><\/sup><\/p>\n

\u00a0\u00a0 Despite<\/strong><\/em> this extensive research prevalence, the genetic determinants of cancer risk remain largely unknown. Highly potent mutations of proto- oncogenes <\/span><\/strong><\/em>as well as tumor suppressor genes, and more subtle and complex genetic interactions within each individual are currently thought to influence susceptibility to cancer<\/p>\n

\"Tumor-Ganas-Pada-Hati\"\"3003854-poster-20121210leukemia\"<\/a><\/p>\n

Hepatocellular Carcinoma and leukemia<\/p>\n

In our laboratory<\/span>, <\/b>our long-term goal is to define the relationship between genes, development, and cancers through molecular and cell biology coupling clinical evidences application. From 2005 to 2012, several novel genes were cloned for further characterization through the molecular cloning approach. The pathogenic functions in cancer development were identified to ensure whether it was a proto-oncogene, including GPR177(WLS)<\/span><\/strong><\/em>, <\/span><\/b>SPZ1<\/span><\/strong><\/em>, <\/span><\/b>and <\/span>ISX<\/span><\/strong><\/em>. <\/b>In the secondary exploration stage from 2012\u20132017, extension studies were addressed on the molecular regulation mechanism, spectrums of downstream target, and potential oncogenic activities of these proto-oncogenes in cancer cells transcriptionally. Currently (2017\u20132022), our study aimed to clarify the pathogenic crosstalk effects of these proto-oncogenes on tumor microenvironment editing in both immune<\/span><\/strong> and cancer cells<\/span><\/strong> when cancer metastasis<\/span><\/strong> occurs. <\/b>During the past 5 years, the underlying proto-oncogenes regulatory mechanism in the enhancement of tumor epithelial-to-mesenchymal transition (EMT)<\/span><\/strong> were characterized and verified. The regulatory roles of immune cells<\/span><\/strong>, such as dendritic cells (DCs)<\/span><\/strong> and macrophages<\/span> (M\u03a6)<\/span><\/strong>, <\/b>in tumor EMT and microenvironment editing were addressed and verified. These proto-oncogenes, like a double sword, showed differential regulatory effects on both immune and cancer cells contributing different effects on cancer metastasis. The relevant regulatory effects of WLS, SPZ1,<\/span><\/strong><\/em> and <\/span>ISX <\/span><\/strong>in vitro<\/em> and in vivo<\/em> were characterized in our laboratory. Some have been published in several important cell biology and oncology journals (Autophagy, Cancer Letters, Oncogene and Cancer Research<\/span><\/strong><\/em>). <\/b><\/p>\n

Shih-Hsien, Hsu Ph. D.\/Professor <\/span><\/span><\/em><\/h1>\n

(\u8a31\u4e16\u8ce2 \u535a\u58eb\/\u6559\u6388)<\/span><\/em><\/h1>\n

No100, Shi-Chuan 1st Road, San Ming District,807 Kaohsiung , Taiwan, R.O.C.
\nTel:886-7-23121101 Ext 2136#28 Fax:886-7-3118902
\nE-mail\uff1a jackhsu@kmu.edu.tw<\/span><\/p>\n

Position:<\/span> <\/em><\/span>\u00a0Professor, Graduate Institute of Medicine, Kaohsiung Medical University (KMU)<\/span><\/strong><\/p>\n

Present Job:<\/span><\/span><\/strong><\/em><\/span><\/p>\n