TEST:

nCounter® PanCancer IO 360™ Panel

The worse outcomes of rectal MAC appear to be driven largely by late-stage presentation, possibly owing to later diagnosis. MAC nonetheless carries a distinct immune phenotype, detectable even in histologically normal surrounding mucosa, that likely contributes to its treatment resistance. These observations provide a basis for developing histotype-specific approaches to both early detection and treatment in this uncommon but clinically challenging tumour subtype.

RrcHSIL non-responders to imiquimod exhibited an even more immunosuppressive microenvironment than complete responders, characterized by increased infiltration of CD4 + FoxP3 + regulatory T cells and (CD14 + )CD68 + CD163 + M2-like macrophages and CD14 + HLADR- monocytic myeloid derived suppressor cells. The limited efficacy of imiquimod in rrcHSIL may be explained by a strong immunosuppressive microenvironment.

Given the small sample size and potential confounders, these results should be regarded as hypothesis-generating. Emphysema-associated immune remodeling may nevertheless represent an important biological factor worthy of validation in larger, independent cohorts.

Our results show the importance of the bone marrow microenvironment in pediatric AML and provide tools for a refined stratification of "standard-risk" patients, lacking adequate risk-oriented therapies. They also offer a promising guide for tackling immune pathways and exploiting immune-targeted therapies.

Collectively, RT sensitized BC tumors by increasing the gene signature of TIS, cytotoxicity, apoptosis, and mammary stemness. RT facilitated an immunosuppressive environment and increased RCB, suggesting that the therapeutic potential of RT is highly individualized for each patient based on their unique tumor biology, genetic makeup, and TME.

This study highlights transcriptional signatures associated with breast cancer CNS metastases, emphasizing the role of immune modulation in metastatic progression. The identified genes have potential as prognostic biomarkers and therapeutic targets, supporting the need for site-specific molecular profiling in metastatic breast cancer management.

We present here a detailed, treatment-oriented molecular comparison between two histologically distinct endometrial cancer subtypes, UPSC and UCS. Assessment of unrepaired DNA damage and, by proxy, DNA repair capacity, gives context to the immune transcriptomic landscape. Our data suggests that the immune exhausted molecular landscape of UPSC may be more amenable to IO than that of UCS, while the DNA repair-robust UCS may be more vulnerable to agents targeting DNA Damage repair such as PARP inhibitors. Further, our data suggests that estimation of DNA repair capacity via RADD may be as treatment informative as molecular sequencing.

Whole-blood gene-expression profiling enables early identification of patients at high risk for irAEs during anti-PD-1 therapy. These predictive biomarkers may guide personalized toxicity monitoring in melanoma treatment.

Our findings reveal novel fusions and validate altered replication pathways related to HPV42 in DPAC.

P1/2, N=18, Recruiting, Universitair Ziekenhuis Brussel | Phase classification: P1 --> P1/2 | Trial completion date: Dec 2020 --> Dec 2025 | Trial primary completion date: Dec 2020 --> Dec 2025 | Completed --> Recruiting

Combination therapy with poly-ICLC, especially through IT route, and anti-PD-1 provides significantly greater antitumor effects than anti-PD-1 monotherapy in syngeneic mouse models of HCC.

Conclusions Overall, these preliminary data reveal a potential crosstalk between deregulated cancer cell proliferation and MARCO+Mφs in mediating disease progression and ICI resistance of ccRCC. Mechanistic experiments will be performed to confirm this assumption and to test whether targeting cancer cell-deregulated proliferation (e.g. by FDA-approved CDK4/6-TAs) could reshape ccRCC-mediated Mφ polarization and improve ICI efficacy.