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Chemistry Seminars

Chemistry Seminar
April 17, 2014
Room 114 Smith Hall 11:00 a.m.

Mr. Ayman Huzair

Islet cell replacement: a treatment option for diabetes mellitus

The administration of oral hypoglycemic agents and intravenous insulin injections are currently the most predominant means of treating individuals suffering from type II diabetes. A substantial percentage of these cases are believed to be caused by beta cell dysfunction, but many of the current treatment options seek to mitigate insulin resistance, not beta cell dysfunction. Recently, , there has been a significant breakthrough in stem cell research aimed at ameliorating beta cell dysfunction rather than mitigating insulin resistance. Specifically, human eyelid adipose tissue-derived stem cells (hEA) were differentiated to form insulin-secreting cells (hEA-ISCs) for transplantation into a type II diabetes mouse model. Measurements of insulin, c-peptide, blood glucose levels, gene expression, and levels of inflammation were analyzed in three separate groups of type II diabetes mice that received undifferentiated hEAs (UDC group), differentiated hEA-ISCs (DC group), or no hEA-ISCs (sham group). The DC group presented higher levels of insulin and c-peptide than the UDC group, along with lowered blood glucose levels. Compared with the UDC group, reverse transcriptase polymerase chain reaction (RT-PCR) revealed the DC group to express substantially more human beta-cell related genes. A future goal of this study aims to assess endogenous hEA-ISC transplantation as a viable treatment option for type II diabetes.

Mr. Syed Samad

Ado-trastuzumab Emtansine (T-DM1): An Antibody–Drug Conjugate (ADC)
for HER2-Positive Breast Cancer

The anti-body drug conjugate known as Ado-trastuzumab emtansine (T-DM1) combines the antitumor properties of the anti-human epidermal growth factor receptor 2 (HER2) antibodies (trastuzumab) with the maytansinoid, a potent microtubule-disrupting agent. After the anti-body drug conjugate is bound to HER2, the drug is internalized by receptor-mediated endocytosis and an active derivative of DM1 is then released by proteolytic degradation of the moiety within the lysosome. Further clinical evaluation led to phase III clinical trials in advanced HER2-positive breast cancer patients who had previously relapsed with treatment from trastuzumab and a taxane.T-DM1 was shown to prolong the progression of HER2-positive metastatic breast cancer in patients and provided higher survival rates with less toxicity than lapatinib plus capecitabine. T-DM1 received FDA approval in 2013 for treatment of patients with HER2-positive metastatic breast cancer who had previously received trastuzumab and a taxane. It is the first ADC to receive full approval based on a randomized study.