Pancreatic Cancer

IHC stratification of primary tumors by HMGA2 and GATA6 status in pancreatic cancer is associated with differential outcomes, survival following chemotherapy, and tumor microenvironments. As a nuclear marker for basal disease, HMGA2 complements GATA6 to identify disease subtypes in PDAC.

Mixed NET/non-NET tumors with distinct histology and molecular profiles might be better classified as collision tumors rather than MiNENs.

We found that UMKO1 possesses a gene for the long form of cytidine deaminase, which can inactivate the standard PDAC chemotherapeutic agent gemcitabine...We found that while none of the bacterial supernatants changed the abundance of CD8 T cells, granzyme B positive CD8 T cells were the lowest in tumor explants exposed to UMKO1 , and not other isolated Klebsiella species or the non-pathogenic laboratory strain E. coli K12 . In summary, the isolated collection of bacteria and fungi from this study are a valuable toolbox to study the impact of microbiota on pancreatic cancer.

Furthermore, patients with pancreatic cancer with higher expression levels of CD3, CD8, CD56, IFN-γ and 4-1BBL exhibited longer survival, whereas those with higher expression of IL-17 had a shorter survival time. The expression levels of CD3, CD8, CD56, cytokines IL-17 and IFN-γ, and costimulatory molecule 4-1BBL were revealed to be related to the degree of differentiation, Tumour-Node-Metastasis staging and the prognosis of pancreatic cancer, and may serve as novel immunological indicators for evaluating the condition and treatment effectiveness in patients with pancreatic cancer.

Multidisciplinary consultation recommended initiation of systemic chemotherapy with cisplatin and etoposide. This case underscores the aggressive nature and poor prognosis associated with malignant insulinomas, particularly those with high proliferative indices. It highlights the complexities of managing refractory hypoglycemia in the context of widespread metastatic disease and emphasizes the urgent need for effective therapeutic strategies to improve patient outcomes.

The patient remained symptom-free for five years during follow-up post-treatment. This case highlights the importance of considering HP in young patients presenting with pseudocysts and other signs of chronic pancreatitis even during the initial acute episode.

The six-year follow-up showed that concurrent and independent orbital MALT lymphoma and axillary reactive lymphoid hyperplasia, likely due to unicentric Castleman disease, were both stable. The present case illustrates how important it is to make pathological diagnoses in different anatomical lesions after the initial diagnosis of Castleman disease.

Furthermore, PA (10:0/a-17:0) demonstrated a strong correlation with PDAC immunotherapy outcomes (Rho: 0.758; P=0.011). These findings suggest that the biliary microbiota and associated metabolites play a crucial role in the development of PDAC and may serve as potential predictive biomarkers and therapeutic targets for disease management.

The ChemoResist signature could precisely predict survival in PDAC undergoing resection and chemotherapy, and its predictive value surpassed TNM stage and other clinicopathologic factors. Moreover, the ChemoResist classifier could assist with identifying patients who would more likely benefit from adjuvant chemotherapy.

CA19-9 response to NAT alone is not enough to identify long-term post-resection PDAC survivors. The co-existence of CA19-9 and major pathologic response was predictive of the most optimal survival outcome.

The results demonstrate that this test can accurately quantitate the level of promoter methylation at the BRCA1 and RAD51C genes using FFPE samples, even when the extracted DNA is extremely degraded or the input amount is limited. This test increases the precision of diagnostic tests aimed at identifying patients who are likely and unlikely to respond to PARP inhibitor therapy.

P1/2, N=386, Active, not recruiting, Mirati Therapeutics Inc. | Recruiting --> Active, not recruiting

P2, N=78, Recruiting, Akeso | Not yet recruiting --> Recruiting | N=60 --> 78 | Trial completion date: Jun 2025 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Jun 2025

P2, N=14, Active, not recruiting, Spectrum Health Hospitals | Recruiting --> Active, not recruiting | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2026 --> Dec 2027

P1, N=66, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2024 --> Dec 2025

The responsiveness of gastrointestinal stromal tumors to imatinib requires validation via molecular testing. Patients diagnosed with pancreatic cancer may see enhanced survival rates by targeted therapy addressing microsatellite instability and BRCA mutations. In bile duct malignancies, especially intrahepatic cholangiocarcinoma of the small duct variant, the analysis of IDH1 mutations and FGFR2 fusions presents new treatment prospects.

Our results suggest that TRPS1 IHC represents a highly accurate and reliable method for differentiating metastatic BC from PAC.

Alterations in inflammatory signaling pathways occurred following KO cell exposure to CM containing sMSLN, and CM from cancer cells with intact peritoneal metastasis provoked increased KO cell secretion of IL-1α. While excess sMSLN inhibits cell clustering and peritoneal colonization, sMSLN may also promote PDAC peritoneal metastasis independent of MUC-16.

CEA may rise in more than half of postoperative PDAC patients without recurrence. CEA alone is not a robust postoperative marker.

Under optimal conditions, it displays good linear relationship within the range of 0.01 U mL-1 to 100 U mL-1, the detection limit being 0.0012 U mL-1. Additionally, the immunosensor prepared in this work is characterized by superior interference immunity, reproducibility and storage stability, and has yielded satisfactory recovery rate in testing the serum samples of patients.

MDM2/p53/CXCL5 is the key pathway of TAX inhibiting the proliferation of PC cells.

P=N/A, N=48, Not yet recruiting, Allegheny Singer Research Institute (also known as Allegheny Health Network Research Institute)

P1, N=177, Recruiting, BeiGene | Not yet recruiting --> Recruiting

P1/2, N=30, Not yet recruiting, Lisata Therapeutics, Inc. | Trial completion date: Jun 2027 --> Sep 2027 | Initiation date: Dec 2024 --> Mar 2025 | Trial primary completion date: Jun 2027 --> Sep 2027

P1/2, N=200, Recruiting, Linnaeus Therapeutics, Inc. | Trial completion date: Dec 2024 --> Dec 2027 | Trial primary completion date: Mar 2024 --> Dec 2026

P2, N=10, Completed, Liverpool Hospital | Active, not recruiting --> Completed

P=N/A, N=261, Completed, University of Pittsburgh | Phase classification: P3 --> P=N/A

P=N/A, N=50, Active, not recruiting, H. Lee Moffitt Cancer Center and Research Institute | Trial completion date: Nov 2024 --> Nov 2025

An immune/metabolism score integrating the features of six genes was developed as a predictive biomarker for immunotherapy response in multiple cohorts, allowing for the selection of patients most likely to experience positive outcomes from this therapy regimen. In conclusion, our study provides proof-of-concept data supporting the potential of SHR-1701 plus famitinib as an effective and safe subsequent-line therapy for refractory BTC and PDAC, highlighting the promise of targeting PD-L1, TGF-β, and angiogenesis pathways simultaneously.

No abstract available

Sunitinib for c-KIT mutations did not meet the primary end point, but in this small sample size, a potential signal cannot be ruled out. Rate of eligible c-KIT mutations was low, affecting accrual to this arm.

Strikingly, MAP3K1, MAPK11, PPP2R1A, and α2 integrin expression were higher in chemotherapy-resistant tumours in breast cancer patients. Our results identified the α2β1 integrin/p38 signalling axis as a novel regulator of ECM endocytosis, which drives invasive migration and tumour progression, demonstrating that our high-content screening approach has the capability of identifying novel regulators of cancer cell invasion.

Consequently, the tumor cells highly expressing NCF-1 obtained coincident accumulation of ROS and reduced glutathione (GSH) with expression of glutathione peroxidase 4 (GPX4), a quencher involved in ferroptosis. Unlike the conventional role of ROS as a representative cytotoxic factor, these findings suggest that NCF-1-mediated ROS generation may be required for expansive growth of PDAC and gastric cancers.

In IPMN-derived PDAC, the optimal cutoff for early recurrence is 10.5 months. Both CA19-9 and N stage predict early recurrence. Adjuvant chemotherapy is associated with survival benefit only for high-risk patients.

Overall, this study identified several proteins, metabolites and lipids involved in various pathways including cholesterol and lipid metabolism to be changing in patients. In addition, we discovered a multi-analyte signature that could be further tested for detection of PDAC.

P1/2, N=42, Recruiting, Medigen Biotechnology Corporation

P2, N=4, Active, not recruiting, H. Lee Moffitt Cancer Center and Research Institute | Recruiting --> Active, not recruiting | N=212 --> 4

P=N/A, N=40, Not yet recruiting, Fred Hutchinson Cancer Center | Trial completion date: Jan 2025 --> Jan 2026 | Trial primary completion date: Jan 2025 --> Jan 2026

P1/2, N=6, Terminated, ImmunityBio, Inc. | N=80 --> 6 | Unknown status --> Terminated; Study halted prematurely and will not resume; participants are no longer being examined or receiving intervention

In conclusion, our study introduces a robust in vitro assay for fibrosis and identifies ORAI1 as being engaged in PSC-driven fibrosis.

LLMs, especially GPT-4, are proficient in deriving oncologic insights from radiology reports. Their performance is enhanced by effective summarization strategies, demonstrating their potential in clinical support and health care analytics. This study also underscores the possibility of zero-shot open model utility in environments where proprietary models are restricted. Finally, by providing a set of annotated radiology reports, this paper presents a valuable data set for further LLM research in oncology.

SRC inhibitors (DGY-06-116, dasatinib, and bosutinib) also exhibit synergistic effects with MRTX849 in eliminating various tumor cell lines carrying KRAS-G12C mutations. Thus, SRC inhibitors amplify the therapeutic utility of G12Ci.