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nCounter® PanCancer Pathways Panel

Our initial findings distinguish recurrent chordomas from their primary counterparts based on cancer gene expression changes that encourage growth and proliferation, remodel the bone matrix environment, and evade the immune system. Continued investigation is needed to assemble a broader patient sample. Examining the pathways and genetic mutations across the chordoma disease progression may reveal novel therapeutic avenues for recurrent chordomas.

P=N/A; Trial completion date: Jan 2024 --> Jan 2025

PIK3CA is also prevalent in MpBC and potentially targetable. Our findings may inform the development of novel targeted therapeutic regimens and improve outcomes for this rare but aggressive breast cancer subtype.

The majority of recurrent SCLC retained their pre-treatment subtype, by both RNA expression and IHC evaluation. It suggests subtype is an intrinsic characteristic of SCLC regardless of treatment. IHC subtyping demonstrated high concordance with RNA expression thus can be utilized effectively in pathology practice.

In summary, the study demonstrated the anti-tumor effects of compounds c1 and c2 associated with the induction of oxidative stress and senescence-dependent mechanisms. These compounds can be further evaluated as potential anti-cancer agents for HCC.

Like HIV associated DLBCL, these results show that PTLD is more genomically stable than IC-DLBCL, and that genomic stability is further enhanced in EBV(+)PTLD which have increased expression of UPS related genes. In contrast, EBV(-)PTLD have increased expression of DNA damage repair genes, including RAD51. In summary, monomorphic DLBCL PTLD tumors have enhanced genomic stability that appears to be mediated by two distinct mechanisms stratified by EBV status.

P=N/A; Trial completion date: Jun 2023 --> Jan 2024

Mechanically, FGF11 was regulated by hypoxia-inducible factor-1α (HIF-1α) to modulate the DDP sensitivity. FGF11 was highly expressed in platinum-resistant OCCC tissues, promoting progression and resistance to DDP through the HIF-1α/FGF11 signaling axis.

We identified a 78-gene signature that might help define a more accurate diagnosis for lung adenocarcinoma.; Cell and molecular biology; Endoscopy and interventional pulmonology; Pulmonary function testing; Epidemiology; Surgery; Public health; General respiratory patient care; Imaging

Among these DEGs, the expression of CHEK2 and BRCA1 genes might be promising predictive biomarkers.ConclusionWe identified potential gene signatures with diagnostic, prognostic and predictive value for LUAD patients. These findings may contribute to a tailored management for lung cancer patients, although further studies are needed.

Further, in silico data revealed that loss of RKIP was associated with worse overall survival in adenocarcinoma patients.ConclusionAltogether, these data show that RKIP's loss of expression induces lung adenocarcinoma aggressiveness. Importantly, this work pointed to the importance of exploring the role of RKIP, together with the tumor microenvironment and the immune system, to fully understand the consequences of RKIP's loss in tumorigenesis.

The dysregulated genes in the PI3K, MAPK, and Cell Cycle-Apoptosis pathways identified and postulated mechanisms could help to probe biomarkers of OCCC platinum sensitivity, providing a research basis for further exploration of targeted therapy.

Our data evoke a negative prognostic role of STIM2 in AML. We highlight a role of STIM2 in cell proliferation and survival via protection against genotoxic stress and p53-dependent control of apoptosis and cell cycle in leukemic and myeloid cells. STIM2 acts as a Ca 2+ censor, detecting reticular calcium depletion and opening of ORAI channels at cell membrane.

"The research was funded by: Servier Laboratoires Introduction: The Nordic Lymphoma Group (NLG) performed a dose-finding/expansion trial evaluating pixantrone, etoposide, bendamustine and, in CD20+ lymphomas, rituximab (P[R]EBEN) in patients (pts) with relapsed diffuse large B-cell (DLBCL) or peripheral T-cell (PTCL) lymphomas. The P[R]EBEN regimen is feasible on an out-pt basis and shows encouraging response rates and DoR. In PTCL, we observed an overrepresentation of AML/MDS, possibly related to the use of etoposide in multiple treatment lines. Gene expression analysis identified signatures and single genes predictive of long-term response."

P=N/A; N=47; Active, not recruiting; Sponsor:National Cancer Institute, Naples

A gene expression profile that may be helpful in the identification of patients with CIN2+ was identified. This approach could be used together with currently used LBC in a clinical setting, allowing the identification of patients with high risk of CIN2+.

In vivo efficacy was assessed in cell-line derived and patient-derived xenograft models. When administered in combination with doxorubicin, epirubicin, and etoposide, peposertib exhibited synergistic antiproliferative activity in TNBC cell lines in vitro. Our findings suggest that cotreatment with the DNA-PK inhibitor peposertib can enhance the efficacy of anthracycline/TOPO II-based chemotherapies.

Background: RXC004 is a potent and selective inhibitor of the Wnt pathway regulator Porcupine, and is currently being investigated in phase 2 studies in patients with advanced cancers, including Biliary Tract Cancers (BTCs) +/- Pembrolizumab (NCT04907851 and NCT04907539). These data demonstrate that (1) RXC004 is efficacious in pre-clinical PDX models of BTC, (2) RXC004 induces multiple PD effects in BTC models at the level of gene expression, cell proliferation and cell differentiation, and (3) PDX models of BTC can be clustered based on baseline transcriptomic profiles of Wnt signalling genes and predict RXC004 sensitivity.

We found that HG EMM has an IHC and gene expression profile deviated from LG EMM and positioned between LG EMM and BMM. SMM, BMM, and HG EMM have higher EZH2 and PD-L1 expression. Pathway dysregulation was observed in those subtypes, indicating potential therapeutic strategies.

High ATM expression is an important poor prognostic marker which is independent of conventional risk parameters and can be a potential therapeutic target with or without secondary DDS repair protein inhibitors (synthetic lethality) among AML-CN patients.

GEP and IHC showed that GZMB expression is highly heterogeneous in ENKTLs and associated with activation of JAK-STAT3 signaling and higher MYC expression. GZMB-negative ENKTL has distinct GEP and advanced clinical stage, although not prognostically significant in our dataset. These findings imply that GZMB is a potential biomarker mirroring a certain molecular subtype of ENKTL.