Breast Cancer Case Study

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3.14 Target genes

Lee et al cultured two strains of OSCC cells, SAS cells treated by AG1478 (inhibitor of EGFR) and OECM1 cells treated with EGF (activator of EGFR). While the SAS cells showed decrease in nuclear β catenin with increase in membranous β catenin, OECM1 cells showed increased amount of nuclear β catenin overtime. This showed that EGFR plays a vital role in Wnt signalling influencing the stabilisation and nuclear accumulation of β catenin. They also showed that histone markers effect the expression on target gene, cyclin D1. These ultimately lead to the progression of oral cancer. (Lee et al, 2010). c‑myc was among the first oncogenes found to be amplified in breast cancer, and it can contribute to many other forms of cancer
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Protein expression of GSK3B was significantly elevated in the cytoplasm of tumor cells. This study provides evidence that variations in Wnt genes shown to be involved in oral-facial clefting may also increase an individual’s susceptibility of developing oral squamous cell carcinoma (Filho et al, 2011).
3.16 Wnt/β catenin signaling pathway as therapeutic targets

Wnt pathway is broadly classified as canonical and non canonical, where the specific composition of Wnt/Fzd complex defines which of the two pathway is activated. The canonical Wnt pathway is better understood and was first linked to colon cancer formation. Various drugs are being identified and developed as Wnt pathway inhibitors including NSAIDS, Vitamin A, Vitamin D, monoclonal antibodies, small molecule inhibitors to disrupt Tcf - β catenin protein complex, adenoviruses engineered to express cytotoxic genes or oncolytic adenoviruses. These drugs and targeted therapies are evaluated to have indirect or direct effect on the Wnt pathway. Cancer having molecular diversity will need combination therapies. However, all the mentioned drugs are largely in its infancy with more need for clinical trials to test their safety and efficacy (Barker and Clevers, 2006).

The tightly regulated canonical Wnt pathway with a hallmark increased level of β catenin and well identified target genes like c - myc and Cyclin D can offer ample target nodal points for cancer drug development.

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