The Role of Myeloid Cells on the Development of Hepatic Metastases in Gastrointestinal Cancer.

The development of hepatic metastases is the leading cause of mortality in gastrointestinal (GI) cancers and substantial research efforts have been focused on elucidating the intricate mechanisms by which tumor cells successfully migrate to, invade, and ultimately colonize the liver parenchyma. Recent evidence has shown that perturbations in myeloid biology occur early in cancer development, characterized by the initial expansion of specific innate immune populations that promote tumor growth and facilitate metastases. This review summarizes the pathophysiology underlying the proliferation of myeloid cells that occurs with incipient neoplasia and explores the role of innate immune-host interactions, specifically granulocytes and neutrophil extracellular traps, in promoting hepatic colonization by tumor cells through the formation of the "premetastatic niche".

IL-23R is a senescence-linked circulating and tissue biomarker of aging.

Cellular senescence is an aging mechanism characterized by cell cycle arrest and a senescence-associated secretory phenotype (SASP). Preclinical studies demonstrate that senolytic drugs, which target survival pathways in senescent cells, can counteract age-associated conditions that span several organs. The comparative efficacy of distinct senolytic drugs for modifying aging and senescence biomarkers in vivo has not been demonstrated.

CREB activation drives acinar to ductal reprogramming and promote pancreatic cancer progression in animal models of alcoholic chronic pancreatitis.

Background And Aims: induction of alcoholic chronic pancreatitis (ACP) causes significant acinar damage, increased fibroinflammatory response, and heightened activation of cyclic response element binding protein 1 (CREB) when compared with alcohol (A) or chronic pancreatitis (CP) mediated pancreatic damage. However, the study elucidating the cooperative interaction between CREB and the oncogenic (*) in promoting pancreatic cancer progression with ACP remains unexplored.

Methods: Experimental ACP induction was established in multiple mouse models, followed by euthanization of the animals at various time intervals during the recovery periods.

Tumor Cell-Intrinsic p38 MAPK Signaling Promotes IL1α-Mediated Stromal Inflammation and Therapeutic Resistance in Pancreatic Cancer.

Unlabelled: Pancreatic ductal adenocarcinoma (PDAC) is characterized by a KRAS-driven inflammatory program and a desmoplastic stroma, which contribute to the profoundly chemoresistant phenotype. The tumor stroma contains an abundance of cancer-associated fibroblasts (CAF), which engage in extensive paracrine cross-talk with tumor cells to perpetuate protumorigenic inflammation. IL1α, a pleiotropic, tumor cell-derived cytokine, plays a critical role in shaping the stromal landscape.

Nationwide Outcomes After Neoadjuvant Chemotherapy for Locally Advanced Sigmoid Colon Cancer-A Propensity Score-Matched Analysis.

Background: The role of neoadjuvant chemotherapy (NAC) in advanced sigmoid colon carcinoma remains to be further characterized. Rationale for NAC includes downstaging on final pathology and optimization of microscopically negative margins (R0 resection). We investigated rates of neoadjuvant chemotherapy use in advanced sigmoid colon cancer at academic cancer centers and assessed factors associated with likelihood of NAC administration.