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Miscellaneous peritoneal malignancies
Published in Tom Cecil, John Bunni, Akash Mehta, A Practical Guide to Peritoneal Malignancy, 2019
GPM usually originates from intraperitoneal free cancer cells (IPFC), which can result from two potential sources: spontaneous exfoliation of cancer cells from the primary tumour and traumatic dissemination of cancer cells due to surgical trauma [16]. IPFC may be seen in around 25%–40% of patients with stage I and stage II/III gastric cancer respectively [17]. Tumours involving the serosal surface of the stomach have a greater predisposition to exfoliate cancer cells. During radical surgery for gastric cancer, cancer cells escape from transected lymphatic channels, tissue at the narrow margins of resection and tumour-contaminated blood lost in the surgical field from the cancer specimen [16, 18]. Though the mechanisms of subsequent peritoneal dissemination are poorly understood, there is evidence that expression of factors such as TNF-alpha, HOX-antisense intergenic RNA (HOTAIR) and Smad interacting protein 1 (SIP1) are involved [19–21].
Intrinsic and Extrinsic Factors That Influence Epigenetics
Published in Cristina Camprubí, Joan Blanco, Epigenetics and Assisted Reproduction, 2018
Ivan Nalvarte, Joëlle Rüegg, Carlos Guerrero-Bosagna
Although the exact mechanism by which EDC promote epigenetic changes is still not fully elucidated, recent research has given hints on potential mechanisms. Because EDCs mimic the action of endogenous hormones, they can, in theory, interfere with endocrine response both at the physiological and molecular levels. Such interference is reported to have reproductive effects. Well-known examples of detrimental reproductive effects are those produced by exposures to DES (54), BPA (55), and vinclozolin (56). Once EDCs bind to cytosolic receptors that belong to the nuclear hormone receptors (NHRs) superfamily, either they can trigger responses through the classical genomic pathway or through the non-genomic pathway (57). The genomic pathway involves nuclear translocation and the further binding of the ligand-activated hormone receptors to hormone-responsive elements in the genome, while the non-genomic pathway involves the rapid and transient induction of membrane-initiated signaling pathways that activate kinase cascades (57). EDCs appear to act on hormone receptors through both pathways (57). EDCs can also mimic hormonal action that takes place directly on genomic regions known as “response elements” such as the estrogen response element (ERE) (58,59). For example, Bhan et al. (60) have shown that the binding of EDCs to an ERE within the promoter of a non-coding RNA (HOTAIR) enables the binding of histones methylases that will modify the chromatin and activate gene expression (60).
Rhabdoid Tumor Predisposition Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Atypical teratoid/rhabdoid tumor has also been studied, usually in national studies. In a study of the Pediatric Oncology Group [21], 55 patients were identified as eligible participants. Of these, 34 patients were boys and 21 were girls, again indicative of a slight female predilection. The ages of the patients ranged from 2 to 60 months with an average age of presentation of 17 months [21]. Thirty-six of the study patients had tumor located in the posterior fossa. Thirteen patients with tumors in the posterior fossa demonstrated extension into the supratentorial space. Seventeen cases were primary supratentorial tumors (4 suprasellar, 3 involving the pineal gland, 3 parietal lobe, 3 temporal lobe, 2 frontal lobe, and 2 CNS site unspecified). Two cases were multifocal at the time of presentation. Cerebrospinal fluid analysis was performed in 29 patients as part of their presentation; 9 demonstrated positivity for malignant cells [21]. Twenty-five patients went on to develop craniospinal metastases [21]. The metastases are most commonly unresectable. There is now some indication that the atypical teratoid/rhabdoid tumors should be classified into subgroups that may affect treatment. Atypical teratoid/rhabdoid tumor TYR, which is characterized by location in the posterior fossa, very young age at diagnosis, typically less than 1 year, demonstrates overexpression of the genes TYR and MITF [20]. The subgroup atypical teratoid/rhabdoid tumor MYC consists of predominately supratentorial tumors, and the patients are older than average at diagnosis (4−5 years old). The genes MYC, HOX, and HOTAIR are overexpressed [20]. The third subgroup, atypical teratoid rhabdoid tumor SHH, occurs in children between 2 and 5 years old, is either supratentorial or infratentorial, and is characterized by overexpression of the sonic hedgehog genes [20].
Survival Outcome and Clinicopathologicl analysis of Homeobox gene cluster-embedded LncRNAs in Human Cancers: A Systematic Review and Meta-analysis
Published in Expert Review of Molecular Diagnostics, 2021
Min Gao, Zhigang Cui, Sixuan Li, Na Li, Lianwei Tong, Ying Wang, Mingyang Song, Baosen Zhou, Zhihua Yin
HOTAIR is the mainly LncRNA located on HOXC cluster, which is a well-known focus and has been widely explored oncogene in a substantial number of cancers [51–53]. The biological mechanisms of performing in massive neoplasms can be induced as follows: First, at transcriptional level: HOTAIR acts as a kind of trans-acting element, which specifically binds to cis-regulatory elements of target genes. For instance, HOTAIR influenced tumor expression and development by competing with several miRNAs for binding to specific target genes [54–57], it also induced the promoter activity and subsequently regulated the expression of cancer-related proteins [58–60]. Second, HOTAIR affected DNA methylation through H3 lysine 27 trimethylation (H3K27me3), DNMT1 and DNMT3b expression and promoted cancer metastasis by regulating polycomb complex chromatin modification [61–63]. Third, ectopic expression of HOTAIR also inclined to mediate the drug-resistance in part of malignant tumors, and enhanced the processing of the proliferation and invasion [64–67]. HOXC-AS, another LncRNA located in HOXC cluster, has been reported to be accelerated cell proliferation, migration, and EMT process in oral squamous cell carcinoma, nasopharyngeal carcinoma, and glioma [68–70], also played as a candidate hallmark of prognosis in neck squamous cell carcinoma and hepatocellular carcinoma [71,72]. In summary, LncRNA HOTAIR and HOXC13-AS can be regarded as promising biomarkers of diagnosis and prognosis in malignant tumors.
Emerging circulating MiRNAs and LncRNAs in upper gastrointestinal cancers
Published in Expert Review of Molecular Diagnostics, 2020
Esmat Abdi, Saeid Latifi-Navid, Fatemeh Abdi, Zahra Taherian-Esfahani
Liu et al. proved that three lncRNAs, AC100830.4, CTC-501O10.1, and RP11-210K20.5, were up-regulated in GC patients’ plasma with the AUCs of 0.724, 0.730, and 0.737, respectively. The AUC resulted from the combination of the three lncRNAs was 0.764 [110]. Recently, a study showed that the expression of serum exosomal lnc-GNAQ-6:1 was significantly lower in the GC patients. AUC was 0.732, which was higher than the diagnostic accuracy of CA72–4, CA 19–9, and CEA. Therefore, GNAQ-6:1 might be assessed in larger studies as a new diagnostic GC biomarker [111]. Yörüker et al. assessed the prognostic and diagnostic values of circulating H19 in GC. The higher circulating H19 levels were detected in patients with GC compared to control ones. H19 was identified as a potential diagnostic marker in GC [112]. The HOTAIR plasma level was significantly greater in patients with GC compared to healthy participants. The plasma HOTAIR was able to detect GC with sensitivity of 88% and specificity of 84%. Moreover, the increased expression of HOTAIR was correlated with higher grades, advanced stages of tumor, and metastasis. Thus, the plasma HOTAIR can act as a potential noninvasive biomarker for GC diagnosis [113].
Rs145204276 and rs4759314 affect the prognosis of prostate cancer by modulating the GAS5/miR-1284/HMGB1 and HOTAIR/miR-22/HMGB1 signalling pathways
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2020
Zhi-Hai Deng, Gan-Shen Yu, Bin Pan, Zhen-Hua Feng, Qiang Huang, Jian-Zhong Deng, Bo Chen, Shi-Kun Yang
Growing evidence has shown that HOTAIR can regulate key signalling pathways involved in cancer metastasis and invasion. For example, HOTAIR was shown to increase the metastasis and invasiveness of breast cancer by enhancing the expression of LAMC2, LAMB3 and ABL2 SNAIL, all of which were reported to enhance cancer metastasis [15]. On the other hand, upregulated expression of HOTAIR in HCC may be used as a prognostic factor for post-hepatectomy recurrence of HCC by regulating the expression of VEGF and MMP9 [26]. The above results suggest that HOTAIR plays an essential role in the progression of PC. Moreover, the rs4759314 polymorphism located in the promoter of HOXC11can affect the expression of HOXC11 by regulating its transcription efficiency [26]. In fact, compared with the A allele of the rs4759314 polymorphism, the G allele was shown to increase the expression of HOTAIR, suggesting that the G allele is associated with a higher risk of carcinogenesis.