Nigerian scientists to study stubborn bladder cancer gene

Researchers want to study a gene called “OTX1” because it seems to allow bladder cancer to escape the effects of anticancer drugs.

Since the cancer often recurs despite treatment, understanding how the gene works may be important for developing better cancer therapies.

Researchers say that cancer stem cells (CSC) might be the reason for cancer returning after treatments (recurrence), because they can form a tumour able to resist or fight off cancer drugs. In bladder cancer specifically, researchers have shown that a gene called OTX1 might be responsible for this effect.

In 2020 researchers proposed to study the exact mechanism of this gene, in other words how it is able to protect bladder tumours from current medicines. 

They planned to collect samples from Nigerian bladder cancer patients to see how common the OTX1 gene is. They want to see what happens in the cell when the gene is switched on or off, and if it changes the features of bladder cancer. 

This would have been the first investigation into the OTX1 gene in bladder cancer at the time, and having this information could help improve treatments that would lead to bladder cancer remission. (Cancer remission is when cancer signs and symptoms disappear partially or completely.)

The researchers who proposed this study are from Nigeria.

Abstract

Bladder cancer has the highest cost per patient among all cancers due to the high risk of 

recurrence and the need for life-long routine monitoring as well as therapy. Cancer stem cells. (CSCs) are hypothesised to be linked to long-term recurrence risk due to its ability to repopulate the entire tumour population in a small number of cells. In addition, CSC as according to the stem cell model, has the property of self-renewal. Thus, only CSC has sufficient time to accumulate adequate genetic mutations that drive the acquisition of resistance against chemo- and radiation-therapy leading to initiation of recurrence. Recently, OTX1 has been shown to be involved in the differentiation of breast CSCs into differentiated cancer cells. The gene is also reported to be involved in other cancers such as subset of B cells in aggressive non-Hodgkin lymphomas, lung cancer and most recently in bladder cancer.  Although the involvement of OTX1 in cancers is demonstrated by limited number of studies, the gene remains to be an interesting candidate for further investigation. We propose that OTX1 may be responsible for the differentiation of CSC and also promote tumour aggressiveness. We plan to establish the expression and localisation patterns of OTX1 gene for Nigerian bladder cancer patients and correlate with clinical characteristics such as stage and grade; risk of recurrence; disease progression and age. To understand the role of OTX1 in bladder cancer stem cells, the gene will be overexpressed/knockdown in non OTX1 expressing and OTX1 expressing CSCs, respectively, and the resulting phenotypic effects will be compared.

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