FIG. 10:  We know that both muscle-invasive and non-muscle-invasive (NMI) bladder cancer have distinct features, and it has been known for years that NMI bladder cancer may have different outcomes, depending on a few genomic arrangements, eg, diploid karyotype, which we knew about (or aneuploidy in muscle-invasive bladder cancer), and other alterations, as well as the presence or absence of carcinoma in situ. 

It is possible that deletions or alterations on chromosome 9 are responsible for a large percentage of changes that occur in the tumor and the patient.  If so, then we must ask whether some the important drivers are on chromosome 9 and look at these molecular changes as potentially enabling us to predict how a patient’s bladder cancer will develop.  For example, we may learn whether a tumor will remain pTa low grade or develop infiltration or become a high-grade tumor with a flat lesion with carcinoma in situ that, in itself, has a high chance of progression and eventually metastasis.  Alternatively, even without carcinoma in situ, a tumor may already have reached the muscularis of the bladder wall or even gone beyond the organ and infiltrated some of the neighboring organs.