Stenzl - Figure 10
NMIBC and MIBC
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.
References
Knowles MA, Hurst CD. Molecular biology of bladder cancer: new insights into pathogenesis and clinical diversity. Nat Rev Cancer. 2015;15:25−41 https://doi.org/10.1038/nrc3817
