Comparison of the immunotherapy efficacy between invasive mucinous and non-mucinous adenocarcinoma in advanced lung cancer patients with KRAS mutation: a retrospective study

Inhibition of the Alternative Complement Pathway May Cause Secretion of Factor B, Enabling an Early Detection of Pancreatic Cancer

“…It is well-known that KRAS mutation is the primary driver in the progression of pancreatic cancer and other cancers like lung and colorectal cancers, starting from their early stages of development. − In fact, the majority of PDAC patients (>85%) harbor KRAS mutation. − Specifically, PDAC cell lines harboring KRAS mutation have been found to exhibit higher expression levels of CFB, shedding light on the oncogenic activity of CFB within the context of KRAS mutation. , Furthermore, it is known that KRAS mutation positively regulates the expression levels of complement factors and their regulator (s), including C3b, CFB, CFH, and AM (Figures and ). For the AM’s role in carcinogenesis, previous studies have indicated that tumor-associated macrophages (TAMs) induce AM synthesis, which, in turn, promotes cancer cell growth, suggesting a synergistic role of AM and TAMs in the malignant development of cancer. , Indeed, elevated levels of AM expression are often observed in PDAC patients and are associated with a poor prognosis. , Furthermore, the interaction between AM and CFH within cancer cells can prolong the malignant stage of pancreatic cancer within TME. , In addition, the strong interaction between AM and CFH (Figure D), facilitated by CFH’s binding motifs, is likely to reinforce CFH-mediated disruption of the ACP cascade (Figure ). …”

“…64,66 Furthermore, the interaction between AM and CFH within cancer cells can prolong the malignant stage of pancreatic cancer within TME. 66,67 In addition, the strong interaction between AM and CFH (Figure 5D), facilitated by CFH's binding motifs, is likely to reinforce CFH-mediated disruption of the ACP cascade (Figure 6). 65 Considering these intricate features of ACP regulatory factors, it seems plausible to propose a hypothetical axis of KRAS mutation−AM−CFH, playing a crucial role in both the ACP cascade and PDAC development (Figure 7C).…”

Pulmonary mucinous adenocarcinoma: An overview of pathophysiology and advancements in treatment

“… Immunotherapy: the role of immunotherapy in PMA, particularly in patients with KRAS mutations, is under investigation. Xu et al [ 28 ] reported differing responses to immunotherapy between IMA and NMA in advanced stages. …”