TSPYL1 (Testis-Specific Y-Encoded-Like Protein 1)

Our findings provide novel diagnostic and prognostic biomarker candidates and insights into mechanisms driving EOC progression with histotype- and stage-specificity. This may aid the development of improved clinical tools for detection, patient stratification, and targeted therapies in EOC.

Importantly these immune responses diminished and TSPY could exacerbate oncogenic growth at late stage. These findings suggest that as a male-specific cancer-testis antigen, TSPY is extremely immunogenic capable of eliciting robust immune and inflammatory responses at the early stage and is a significant candidate for development of immunotherapeutics, such as therapeutic cancer vaccine and antibody-drug conjugates, in treatments of hepatocellular carcinoma in men.

In vivo PDT experiments showcased that TSPy-SS-P had excellent tumor retention capability, effective tumor ablation ability and good biocompatibility. This work provided a two-pronged strategy to design organelles targeted photosensitizers for H2S detection and effective PDT of tumors.

The data demonstrates the prime role of TSPYL2 in causing the dramatic defects in TSPYL1 deficiency. An intricate counter-balancing role of TSPYL1 and TSPYL2 in regulating TGFβ signaling is also unraveled.

Western blot results suggested that knockdown of TSPYL2 enhanced the phosphorylation level of AKT, while TSPYL2 overexpression reversed it. Taken together, our study suggested TSPYL2 could be a tumor suppressor in thyroid cancer by regulating SIRT1/AKT pathway.

In conclusion, RNA sequencing identified a subgroup of patients with clear expression of ESR1 and its downstream targets, probably still benefiting from ER-targeting agents. The lower ER expression in the other subgroup might be partially explained by ER activity still being blocked by recently administered endocrine treatment, indicating that biopsy timing relative to endocrine treatment needs to be considered when interpreting transcriptomic data.

Undetectable serum AMH and inhibin B cannot reliably predict the absence of germ cells and germ cell tumours in individuals with 45,X/46,XY or 46,XY gonadal dysgenesis. This information should help in counselling about prophylactic gonadectomy, taking into account both the germ cell cancer risk and potential for gonadal function.

With specific antibodies for DDX3Y, TSPY, and UTY we analyzed their putative Gonadoblastoma Y (GBY) tumour susceptibility function in the same specimen. We conclude GBY expression is only diagnostic for GCT development in the aberrant germ cells of these DSD individuals when strong OCT3/4 expression has marked their pluripotency.

Using WGCNA analysis and text mining, pre-existing gene expression data were used to provide novel insight into potential AAA-related protein targets. For two of these targets, compounds could be predicted.

This research project was supported by a grant (01GM0627) from the BMBF (Bundesministerium für Bildung und Forschung), Germany to P.H.V. and B.B. The authors have no competing interests.