Sunday, December 19, 2021

Research & Publications

Cancer Development Model

Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease.” This research describes a series of mouse cell lines developed sequentially to mimic this type of progression.

Durwood Barber Ray, Ph.D., Gerald A Merrill, Ph.D., Frederic J Brenner, Ph.D., Laurie S Lytle, Tan Lam, et al “T24 HRAS Transformed NIH/3T3 Mouse Cells (GhrasT-NIH/3T3) in Serial Tumorigenic Passages Give Rise to Increasingly Aggressive Tumorigenic Cell Lines T1-A and T2-A and Metastatic Cell Lines T3-HA and T4-PA.” Experimental Cell Research 340, 1-11, 2016.



Publication:

Ray, D. B., Lam, T. M. and Jones, D. H. "Lactate Formation and Mitochondrial DNA Structure in Mouse Cells Progressing to Malignancy." Federation Proceedings, 48 (1990) 763A.



Medical Genetics
After undergraduate, I worked full-time at Children Medical Center in Tulsa studied fragile X syndrome. Our lab used six polymorphic loci, DXS369, DXS297, DXS296, DXS304, IDS and DXS374 to map the fragile X FRAXA chromosome. We report the results of genetic linkage analysis of 32 fragile X [fra(X)] families using 12 polymorphic loci including these new markers. Cytogenetic and molecular data were combined in two-point linkage analysis for the estimation of lod scores and carrier probabilities in potential carriers. Use of these six new marker loci substantially changed the carrier risk estimates for members of 7 of the 32 families from the risk estimates previously calculated on the basis of less closely linked probes available prior to 1989. I was co-author of a publication in this work, appeared in the Amer. J. Medical Genetics 43, 312-319, 1992.

Publication:

Carpenter, Nancy J., Swart-Boyd, Jennifer, Prichard, Jane K., Lam, Tan M.  "Linkage and risk assessment in fragile X families using new DNA probes at Xq27."  American Journal of Medical Genetics 43, 312-319, 1992.  






Immunology and Virology
As a graduate student, I had three laboratory rotations involved in the studying viral enhancer in leukemia specificity, cholesterol acyltransferase (ACAT), and gamma interferon MHC class I gene expression. I was a co-author for the study of gamma interferon (Cellular Immunology 150, 90-100, 1993).  Finally, my thesis examined the epitope variation in CTL-resistant and identifying of minor and major epitopes in murine leukemia viruses. My research these required my independent analyze experimental results, design follow up experiments, modify techniques, and troubleshoot technical problems. I have two publications derived from my research (Viral Immunology 7:51-59, 1994 and J. of General Virology, 76, 635-641, 1995)

Publications:

Hillary D. White, Douglas A. Roeder, Tan M. Lam, and William R. Green.  "Major and Minor Kb-Restricted Epitopes Encoded by the Endogenous Ecotropic Murine Leukemia Virus AKR623 That Are Recognized by Anti-AKR/Gross Virus CTL."  Viral Immunology 7, 51-59, 1994.





Publications:

Tan M. Lam, Michael A. Coppola, Rendall R. Strawbridge and William R. Green.  "Recognition of Endogenous Ecotropic Murine Leukemia Viruses by Anti-AKR/Gross Virus CTL."  J. of General Virology 76, 635-641, 1995.



Diabetes
After Dartmouth, I went to work for BetaGene, Dallas, Texas for two years involved in deriving several insulin-secreting cell lines, working extensively with molecular genetics, such as cloning, rat-insulin gene knockout, transfecting human insulin gene into rat cell lines, and designing techniques to optimize human insulin excretion in rat cell lines.

Contact
Email is the preferred method for initial contact.  Thank you.

Tan Lam
P.O. Box 48031
Burien, WA 98148
tanlam@tanlam.com