Why TROP-2?


Advanced UC is a very heterogeneous disease, and the identification of molecular pathways potentially implicated in carcinogenesis has been an area of research focus within recent years1

The advent of molecular profiling has allowed comprehensive characterisation of advanced urothelial tumours and further understanding of specific molecular pathways that may be implicated in carcinogenesis, such as TROP-2, NECTIN-4, PD-L1, HER2, and FGFRalt1

The identification of highly ubiquitously expressed antigens may help circumvent these limitations

High expression of TROP-26

A recent study by Bahlinger, et al. ASCO GU 2023 (N=200 cases) found that TROP-2 is:

  • Highly expressed in advanced UC tumours (>93%)
  • Not associated with the expression of other antigens like PD-L1, NECTIN-4 or FGFR3

Molecular pathways of interest in advanced UC*

Other pathways of interest:7 PIK3CA (17%), FGFR3 (15%), AKT3 (12%), ERBB2 (8%), TSC1 (6%), EGFR (6%), ERBB3 (6%),
NF1 (4%), HRAS (3%), NRAS (2%), PIK3R1 (2%), PTEN (2%), TSC2 (1%)

TROP-2 is a cell-surface antigen associated with oncogenic processes8,9

  • Trophoblast cell-surface antigen 2 (TROP-2) is a transmembrane glycoprotein, calcium signal transducer, involved in oncogenic processes such as cell migration and anchorage-independent growth8,9​​

TROP-2 is highly expressed in patients with multiple solid tumour types, including:8–11

BLADDER

BREAST

GASTRIC

COLORECTAL

LUNG

CERVICAL/
OVARIAN

Exploring the science of antigens like TROP-2 could bring new possibilities for patients with advanced UC, without the potential need to select patient populations based on molecular screening

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