Pancreatic Ductal Adenocarcinoma

These findings suggest that therapeutic inhibition of FA synthesis may be promising for treating PDAC patients with active c-Myc/GRPEL1/FASN signaling. Overall, this study demonstrates that FA synthesis mediated by the c-Myc/GRPEL1/FASN axis is essential for PDAC growth.

Neoadjuvant SBRT achieves oncologic outcomes comparable to CFRT in BR/LA PC and is associated with greater adjuvant therapy use. A potential survival signal for SBRT in patients receiving FOLFIRINOX with CA19-9 > 1500U/mL is hypothesis-generating and warrants validation and formal interaction testing.

P1/2, N=144, Recruiting, Engeneic Pty Limited | Not yet recruiting --> Recruiting

Other immune partners might include vaccines, bispecific antibodies, and cell therapy. A major clinical opportunity eventually would be combining RAS inhibitors and immunotherapy in the adjuvant, neo-adjuvant, and interception settings, provided this new class of drugs is developed keeping its immune modulatory power in mind.

Combining cytokine mRNA immunotherapy with cytotoxic killing and immune checkpoint blockade can reactivate antitumour immunity, offering a promising strategy for treating advanced PDAC.

Single cell RNA sequencing data confirmed the elevated TIGIT expression on CD4+ T cells and increased exhausted CD4+ T cells in CLCG-low PDACs. These findings uncovered the unique underlying mechanisms of immune suppression in CLCG-deficient PDACs and identified CLCG as potential biomarkers to identify those who may benefit from TIGIT-targeting immunotherapies.

Our study demonstrates that KRT17 marks a distinct transcriptional signature in a subpopulation of epithelial cells within histologically low-grade IPMN. This population of cells likely represents a transitional state of histologically low-grade epithelial cells undergoing progression to a higher grade of dysplasia and thus may represent a higher risk of progression to carcinoma.

Targeting BCAT1 or disrupting its downstream mTOR/NF-κB signaling effectively inhibits PDAC pan-metastasis. These results uncover an unrecognized metabolic-immune crosstalk governing BCAT1+ metastasis-related tumor cells and pan-metastasis of PDAC.

YAP1 and tumor-like CAFs (tCAFs) play a pivotal role in driving desmoplasia in PDAC. YAP1 mediates the conversion of mCAFs to tCAFs and remodels the extracellular matrix (ECM), while high YAP1 activity in tCAFs regulates EMT induction to propel disease progression. Targeting the YAP1-tCAF axis can suppress desmoplasia and improve therapeutic outcomes. Magnetic resonance elastography (MRE) holds significant potential for non-invasive monitoring of stromal mechanics, offering a new perspective for stromal therapies in PDAC.

P3, N=524, Not yet recruiting, FutureGen Biopharmaceutical (Beijing) Co., Ltd

A high TSP is independently associated with improved survival in PDAC. These findings challenge traditional views of the stroma as purely tumor-promoting and suggest a potential protective role of the stromal compartment in certain contexts.