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Tumor markers
Published in J. Richard Smith, Giuseppe Del Priore, Robert L. Coleman, John M. Monaghan, An Atlas of Gynecologic Oncology, 2018
CA-19-9 is an monosialoganglioside secreted by mucinous tumors of the gastrointestinal tract, including the pancreas and biliary tree (Pavai and Yap 2003). It is more frequently elevated in mucinous (76%) than serous (27%) EOC (Gocze et al. 1988, Terracciano et al. 2005). Markedly elevated serum levels (>1000 U/mL) may be found in benign mucinous neoplasms as well as in borderline and malignant tumors. Elevated levels cannot be used to predict whether an ovarian mucinous tumor is benign, borderline, or malignant (Kelly et al. 2010).
Improvement of hyperandrogenism, oligo-ovulation, and ovarian morphology in a patient with polycystic ovary syndrome: possible role of ovarian wedge resection
Published in Gynecological Endocrinology, 2018
YuanYuan Zhang, SuiYu Luo, ZhiQuan Gong, XiaoYa Feng, ZiYi Wang, HaoHui Zhu, Yu Wang
Taking into consideration the history of ovarian mucinous tumor and abnormal ultrasound imaging indicating recurrence of ovarian tumor, an exploratory laparotomy was scheduled. The procedural exploration revealed neoplasm in the ovary with clear margin and smooth surface and independent from surrounding organs. Interestingly, we also found normal morphology of right ovarian without multiple cystic-like follicles which indicated PCOS was healed. A salpingo-oophor-ectomy of the lesion adnexa was performed as scheduled and frozen sections examination revealed benign, which confirmed the diagnosis of the recurrence of ovarian mucinous tumor, there was no need for complete surgery staging of ovary tumor (Figure 4).
A transcriptional regulatory network of HNF4α and HNF1α involved in human diseases and drug metabolism
Published in Drug Metabolism Reviews, 2022
Jianxin Yang, Xue Bai, Guiqin Liu, Xiangyang Li
HNF4α participates in the proliferation, invasion, migration, and apoptosis of tumor cells and has the dual properties of oncogenicity and anti-tumor effects. This makes it a novel biomarker for tumor diagnosis and prognosis and an effective target for cancer treatment (Lv et al. 2021). HNF4α, a regulator of hepatic sulfur-containing amino acid metabolism, modulates liver cancer sensitivity to methionine-restricted dietary therapy (Xu et al. 2020), thereby possibly inhibiting liver cancer cell proliferation and development (Gao et al. 2019). Overexpression of HNF4α inhibited liver cancer cell proliferation by regulating miR-122 and downregulating the ADAM17 pathway (Yang et al. 2020). Downregulation of HNF4α in prostate cancer inhibited the malignant proliferation of prostate cancer cells via regulating the senescence-regulating gene CDKN1A (p21WAF1/CIP1) (Wang et al. 2020). HNF4α was downregulated in renal cell carcinoma, which was related to tumor stage and grade, recurrence, metastasis, and poor prognosis in renal cell carcinoma patients (Gao et al. 2019). HNF4α was specifically overexpressed in gastric cancer cells and was a biomarker to distinguish primary and metastatic gastric cancer from breast cancer (van der Post et al. 2014). It participated in the occurrence and development of gastric cancer by regulating the isocitrate dehydrogenase 1 metabolic pathway in vivo (Xu et al. 2020). HNF4α also acted as a marker for the diagnosis of lung invasive mucinous adenocarcinoma and ovarian mucinous tumor (Sugai et al. 2008; Sugano et al. 2013). HNF4α induced the formation of Barrett’s esophagus, which might lead to the occurrence of esophageal adenocarcinoma (Colleypriest et al. 2017). In addition, it promoted pancreatic cancer cell proliferation, and its overexpression is related to poor prognosis in pancreatic cancer patients (Sun et al. 2019). Different isoforms of HNF4α perform different functions and regulate different genes; specifically, P1 isoforms mainly participate in cell differentiation and metabolism, whereas P2 isoforms regulate cell proliferation and carcinogenesis (Lambert et al. 2020). Unlike HNF4α8, HNF4α2 inhibits Tet-On-inducible colon cancer cells; this may be due to different interactions between AP-1 and Wnt/β-catenin/TCF4 pathways (Vuong et al. 2015). Moreover, HNF4α is associated with other epithelial tumors (Lazarevich et al. 2010). Therefore, HNF4α is generally regarded as a major antitumor factor inhibiting epithelial-mesenchymal transition, progression, and metastasis of hepatocellular carcinoma, renal cell carcinoma, prostate cancer, colorectal cancer, and cholangiocarcinoma; conversely, it is a carcinogenic factor in lung cancer, gastric cancer, pancreatic cancer, and neuroblastoma (Wang et al. 2021).