Altered cytokine levels and increased CD4+CD57+ T cells in the peripheral blood of hepatitis C virus-related hepatocellular carcinoma patients

Abstract

+ αβtcr + cells (cD57 + t cells), showed a significant inverse correlation with pB-IFn-γ-producing capability. the present results suggest that an increase in cD4 + cD57 + t cells controls the capability of pB to produce the antitumor cytokine IFn-γ and that pB-IFn-γ production is impaired with Hcc tumor progression. IntroductionHepatocellular carcinoma (HCC) is the fifth most common cancer in men and the eighth most common cancer in women worldwide. Hcc is highly prevalent in patients with chronic liver diseases resulting mainly from hepatitis B virus (HBV) or hepatitis c virus (HcV) infection, and its incidence is now increasing. In Japan, Hcc is the third most common cause of mortality, and the most frequent cause of Hcc is chronic infection with HcV (1,2 A b b re vi a t i o n s:A lt, a la n i n e t r a n s a m i n a s e; A F p, α

Producing Capabilities of Interferon-gamma and Interleukin-10 in Peripheral Blood from Oral Squamous Cell Carcinoma Patients

“…These studies comparing the Th1/Th2 balance of cancer patients demonstrated that there was a Th1 deficit in cancer patients, while Th2 cytokine was found to be increased. In line with these observations, we have also demonstrated that the IFN-γ producing capability from LPS-stimulated PB is significantly reduced in gastric cancer [ 10 ] and hepatocellular carcinoma patients [ 11 ].…”

Impact of Interleukin-18 Polymorphisms -607A/C and -137G/C on Oral Cancer Occurrence and Clinical Progression

“…We suggest that IL-18 can act against the occurrence of oral cancer and induce angiogenesis and metastasis, which, in part, play a role in the advanced progression of oral cancer. Our study also demonstrates that patients with G/C alleles of IL-18 -137 G/C polymorphism can express lower levels of IL-18 compared with patients with G/G homozygotes, which benefits the inhibition of angiogenesis and tumor growth and consequently protects patients from the progression of oral cancer [5,9,37]. …”

“…However, the higher concentrations of IL-18 in serum and culture supernatants of PMN from patients with oral cancer in Stages III and IV as compared with patients in Stages I and II could be the host’s response against the growth and progression of oral cancer. Furthermore, it is probable that IL-18 acts as both a suppressor and promoter in the regulation of oral cancer development [5,35-37]. One of the possible explanations for the controversial effect of IL-18 -137 G/C polymorphism in oral cancer susceptibility and clinical progression is that IL-18 has dual effects on cancer development and progression [5,37-39].…”

“…Furthermore, it is probable that IL-18 acts as both a suppressor and promoter in the regulation of oral cancer development [5,35-37]. One of the possible explanations for the controversial effect of IL-18 -137 G/C polymorphism in oral cancer susceptibility and clinical progression is that IL-18 has dual effects on cancer development and progression [5,37-39]. Studies have suggested that IL-18 plays a major role in angiogenesis.…”

“…Specifically, it has been reported that malignant cancer cells increase their adherence to microvascular wall and even promote production of angiogenic and tumor growth-stimulating factor through the IL-18 -dependendent pathway [38,39]. Over-expression of IL-18 was found among cancer patients with malignant prognosis, including oral cancer, lung cancer, gastric cancer, pancreatic cancer, and hepatocellular carcinoma [5,37,40-42]. We suggest that IL-18 can act against the occurrence of oral cancer and induce angiogenesis and metastasis, which, in part, play a role in the advanced progression of oral cancer.…”