The Garnis Lab welcomes Becki Towle, from UBC, as a co-op student. She will be trained in several molecular biology and cell culture techniques over the coming months and it will be exciting to see what she is able to learn while she is with the lab.

CNN has picked up on the Esquire article and also details some of the basics of head and neck cancers and other high profile individuals who have been afflicted by this condition. It is heartening that people might become more educated about head and neck cancers as a consequence of this publicity. Perhaps more profiles like this will lead at-risk individuals to go in for screening.

Large genomic, epigenomic, and gene expression datasets are now mainstays of molecular research. Analytical approaches to integrating these data are steadily improving. This review describes the state of work in this area and also delves into the high throughput functional tools that are available for validating results from integrated analysis.

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(from L to R: Razan Sheta, Shevaun Hughes, Cathie Garnis)

This picture was taken during a Garnis Lab outing to the GE Ice Plaza at Robson Square.

(more info on the venue here)

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For more information about the graduate studies program associated with Dr. Garnis, please visit:

Interdisciplinary Oncology Program

UBC Experimental Medicine

Canadians and permanent residents of Canada will be given priority.

Vestibular Schwannomas (VS) are tumours arising from the vestibular portion of the eighth cranial nerve. Although VS are benign tumours and they usually present with hearing loss only in one ear, disease symptoms secondary to uncontrolled growth or secondary to treatment can be quite severe; larger tumors can cause compression of the brainstem, leading to symptoms associated with increased cranial pressure and death. Existing treatments, while effective in controlling tumour growth (radiotherapy) or in removing tumours (microsurgery), place a heavy burden on the patient and may cause additional nerve damage. Hearing cannot be restored. New targeted therapies that are able to eliminate the tumor in a less morbid manner may also be able to restore hearing upon tumor shrinkage. Molecular analysis of VS represents the best approach for identifying these new potential targets. My research focuses on identifying the molecular mechanism of VS growth.

Earlier this month Adam “MCA” Yauch was treated for a tumor on his salivary gland. Here is Mr. Yauch speaking a bit about it himself:

We’re posting this to remind everyone of the fact that head and neck cancer remains one of the most commonly diagnosed cancer types in the world – and that the incidence of this disease is continuing to rise (important facts and statistics can be found in many locations online, including here, here, and here).

We are all hoping for a speedy recovery for Mr. Yauch and looking forward to a tour in support of the new Beastie Boys album.

Oral cancer is mainly caused by smoking or chewing tobacco or by alcohol consumption. Since these activities can be found around the world, oral tumors represent the most frequently occurring subtype of head and neck malignancies and one of the most common global causes of cancer death. Survival rates for oral cancer are particularly low because tumors are often diagnosed at late, advanced stages and because these tumors have a high rate of recurrence. A better understanding of the molecular changes that make oral cancer cells behave differently is needed in order to find new ways to treat this disease and predict patient outcomes, thus improving our treatment strategies for this disease.

For many cancer types, early detection is a key to an improved clinical outcome. While the oral cavity is easily investigated for precancerous disease, there are currently no tools that allow clinicians to determine whether a given low grade oral lesion is likely to progress to an invasive tumor. “Watchful waiting” is the standard clinical approach in these cases since only a small fraction will progress; intervention for all premalignant disease would be impractical and result in over-treatment for a majority of patients. Unfortunately, waiting means that the opportunity for early intervention in cases that will progress is lost. Tools that will allow us to determine the progression risk for each low grade precancerous lesion are urgently needed.

In order to address this clinical challenge, I have begun to investigate the molecular alterations that underlie the earliest stages of oral cancer. By doing this, I will uncover the specific gene changes that drive the initiation and progression of this disease. When we are able to associate these changes with specific clinical outcomes (for example, finding gene changes associated only with premalignant lesions that progress to tumors), we will have a biomarker we can use to identify early stage patients that require aggressive intervention. An additional benefit from this analysis is that cancer associated genes I uncover will also be useful as targets for the next generation of therapies being developed for oral cancer.