Teaching Courses:

Clinical Microbiology 1 (MT500.01)

Clinical Microbiology 1 (MT500.02)

Clinical Correlation of Microbial Infections (MT602)

Molecular Investigation of Infectious disease Outbreaks (MT 600.01)

Professional Activities:

            Membership

                American Association of Cancer Research (AACR)

                American Society of Clinical     Pathology (ASCP)

            National Credentialing Agency (NCA) for Clinical Personnels

            National Certification:

Medical Technologist (MT).   Certified by American Society of Clinical  Pathology (ASCP)

Clinical Laboratory Specialist in Molecular Biology (CLSpMB).   Certified by National Credentialing Agency (NCA)            

            Research Interest:

Resistance to programmed cell death (apoptosis) is one of the most common molecular defects accounts for malignancy in multiple human cancers.   My research work focus on examining the impair apoptotic machinery that might confer the chemotherapy drug resistance and relapse outcomes in breast and cervical woman cancers.   Particularly, the phosphoinositol 3-OH-kinase (PI3-K), 3-  phosphoinositide-dependent protein kinase-1 (PDK-1) and protein kinase B (AKT) signaling  pathways are currently under investigation.   The ultimate goals are to develop specific therapeutic drugs which specifically re-install apoptotic machinery and re-sensitize cancer cells in response to treatment.

             United States Patent:

United States Patent #5604113.  Cells having oncogene suppressed p53-mediated apoptosis and methods of use to identify  anti-oncogenic compounds.

            Publications:

1.      Lin H-J, Hsieh, F.-C., Song, H., and Lin, J. (2005)   Elevated activation of PDK1/AKT/mTOR pathway in human breast carcinoma.  (2005, Submitted).

2. Bian X, Giordano TD, Lin H-J, Solomon G, Castle VP, Opipari AW Jr.  Chemotherapy-induced apoptosis of S-type neuroblastoma cells requires caspase-9 and is augmented by CD95/Fas stimulation. Journal of Biological Chemistry. 279:4663-4669 (2004).
3. Lin J., Jin X., Rothman K., Lin H-J, Tang H., and Burke W. Modulation of signal transducer and activator of transcription 3 activates by p53 tumor suppressor in breast cancer cells.   Cancer Research.  62: 376-380 (2002).
4. Burke W., Jin X., Lin H-J, Huang M., Liu R., Reynolds R. K. and Lin J.  Inhibition of constitutively active Stat3 suppresses growth of human ovarian and breast cancer cells.  Oncogene. 20:7925-7934 (2001).
5. Jasty R, van Golen C, Lin H-J, Solomon G, Heidelberger K, Polverini P, Opipari A., Feldman E, Castle VP.   Bcl-2 and N-Myc coexpression increases IGF-IR and features of malignant growth in neuroblastoma cell lines.  Neoplasia.  3:304-313 (2001).
6. Lin H-J, Holman P, Lu J, Finniss S, Dickinson C and Castle VP. Functional activity of chimeric molecules containing a death signal against neuroblastoma.  Clin. Cancer Res. 5 (11/99 suppl. #427).
7. Lin H-J, Flint SJ.  Identification of a cellular repressor of transcription of the adenoviral late Iva₂ gene that is unaltered in activity in infected cells.  Virology. 277:397-410 (2000).
8. Page C, Lin H-J*, Jing Y, Castle VP, Nuñez G, Lin J.  Overexpression of Akt/AKT can modulate chemotherapy-induced apoptosis.  Anticancer Res. 20:407-16, (2000).  *First two authors contributed equally to this work.
9. Lin H-J, Eviner V, Prendergast GC, White E.  Activated H-ras rescues E1A-induced apoptosis and cooperates with E1A to overcome p53-dependent growth arrest.  Mol Cell Biol.  15:4536-4544 (1995).
10. White E, Chiou S-K, Rao L, Sabbatini P, Lin H-J.  Control of p53-dependent apoptosis by E1B, Bcl-2, and H-ras proteins.  Cold Spring Harbor Symp Quant Biol.  59:395-402 (1994).
11. Lin H-J, Upson RH, Simmons DT.  Nonspecific DNA binding activity of simian virus 40 large T antigen:  evidence for the cooperation of two regions for full activity.  J. Virology  66:5443-5452 (1992).
12. Wang F-F, Wang Y-J, Lee H-J, Fong J-C.  Identification of erythropoietin receptors of erythroleukemic cells.  Biochem International.  18:163-171 (1989).