PhD student, Britta Weigelt told the meeting of the 4th European Breast Cancer Conference today (Thursday 18 March) that, contrary to what had been thought previously, any primary breast cancer cell was capable of producing secondary cancer cells, which then spread to other parts of the body. These secondary cancer cells had a strikingly similar genetic make-up to their parent cells and behaved in a similar way. Therefore, metastases were likely to have the same response to a particular treatment as their primary tumour.
The discovery has implications for the treatment of breast cancer once researchers have identified the ways that genetically different tumours respond to a variety of therapies. Based on the genetic profile of a patient's tumour, doctors could choose the best treatment for that particular type of tumour (from specific types of chemo-, radio- or hormonal therapies) and treat the patient with it from the time of diagnosis. Such early (neo-adjuvant) treatment could not only shrink the primary tumour but might also prevent the outgrowth of micrometastases, thereby saving lives, as metastases that occur in other parts of the body are notoriously difficult to treat successfully and are the main cause of death in breast cancer.
Mrs Weigelt said: "Until now it was largely unknown whether the characteristics of breast cancer that define the growth rate and therapy response of the primary tumour were alike in the metastases. Furthermore, it was unclear whether all primary breast cancer cells were capable of metastasising, or only some of them."
In the first study to do this, Mrs Weigelt and her colleagues at the Netherlands Cancer Institute in Amsterdam compared the activities of genes in samples of primary breast tumours from 15 patients and in their matching lymph node metastases, and also compared primary tumours with matching metastases that had spread to more distant parts of the body in another eight patients.
"We showed, by gene-expression profiling, that human primary breast tumours are strikingly similar to their regional lymph node metastases, as well as to more distant metastases in the same patient," said Mrs Weigelt.
"The study adds additional pieces in the puzzle of how the metastatic process in breast cancer might work. Furthermore, we showed that the metastatic outgrowths at distant organs did not result in major changes in gene expression, as had been postulated previously.
"Now, we plan to investigate more precisely when breast tumours acquire their ability to metastasise and the associated genetic causes. This could enable us to predict which tumours are more likely to metastasise so that they could be treated appropriately to prevent this happening."
Abstract no: 237 (16.00 hrs Thursday 18 March, Hall 1)