China
Africa
Explore chapters and articles related to this topic
Mosaic Variegated Aneuploidy Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
TRIP13 helps sustain mitotic SAC by converting the mitotic checkpoint protein MAD2 from a closed (active) to an open (inactive) conformation in prometaphase, silences the mitotic checkpoint in metaphase through inactivation of MAD2 when all kinetochores are attached, and triggers anaphase onset. In addition, TRIP13 promotes early steps of DNA double-strand breaks (DSBs) repair process.
Role of High-Risk Human Papillomaviruses in Breast Carcinogenesis
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
It is well established that high-risk human papillomavirus (HPV) infections are associated with the development of anogenital cancers including those of the cervix (Castellsagué et al. 2006; Smith et al. 2007), while infections by the low-risk HPVs induce only benign genital warts (de Villiers et al. 2004; Bernard 2005). HPV is mainly a sexually transmitted infection (Rylander et al. 1994). The lifetime risk of HPV infection is greater than 50% for sexually active men and women (Sawaya and Smith-McCune 2007), and approximately 5%–30% of those infected carry multiple subtypes (Revzina and Diclemente 2005). In parallel, it has been reported that high-risk HPV infection alone, produced by only one type of these viruses, is not sufficient to induce neoplastic transformation of human normal cervical epithelial cells; the high-risk HPV-infected cells must undergo additional genetic changes. High-risk HPVs are also important risk factors for other human cancers such as colorectal and head and neck (HN) cancer; roughly 80% and 30% of these cancers are positive for high-risk HPVs, respectively (Daling et al. 2004; Venuti et al. 2004; Ragin and Taioli 2007). Moreover, it was observed that the presence of high-risk HPVs serves as a prognostic factor in early-stage cervical, colorectal, and HN cancers and is associated with vascular invasion, lymph node metastases, and tumor size (Begum et al. 2003; Graflund et al. 2004; Zuna et al. 2004; Umudum et al. 2005; Varnai et al. 2006). Nevertheless, during high-risk HPVs infection, E6/E7 oncoproteins are expressed and, as a result, the restraint on cell cycle progression is abolished and normal terminal differentiation is retarded (Sherman et al. 2007). Meanwhile, it was recently reported that E5 oncoprotein deregulates cell cycle progression and therefore cell differentiation through its interaction with epidermal growth factor-receptor 1 (EGF-R1) signaling as well as with other genes, such as Bub1 and Mad2 (Pedroza-Saavedra et al. 2010; Liao et al. 2013).
Proteogenomic examination of esophageal squamous cell carcinoma (ESCC): new lines of inquiry
Published in Expert Review of Proteomics, 2020
Shobha Dagamajalu, Manavalan Vijayakumar, Rohan Shetty, D. A. B. Rex, Chinmaya Narayana Kotimoole, T. S. Keshava Prasad
Feng et al. have reported that proteins such as Annexin A2 and Cdc42 were upregulated in several cancers and validated in ESCC [46]. The reduced expression of Annexin II is correlated to the progression of carcinogenesis, which may be a candidate biomarker for early diagnosis of ESCC [47]. Singhal et al. have observed the alteration of cancer-associated lipids and low molecular weight proteins in upper GI tract cancers and proposed that these molecules can be used to detect upper GI-tract cancers [48]. Antibody-based proteomic investigation by Uemura et al. has identified BubR1, Mad2, NF-kappaB-activating kinase (NAK), caspase 10, and activator protein-1 (AP-1) in ESCC [14]. The same group also reported Transglutaminase 3 as a prognostic marker for ESCC [49]. The progressive increase of candidate biomarkers such as alpha-actinin 4 (ACTN4) and 67 kDa laminin receptor (67LR) was identified in the ESCC stage I to III tissues [50]. The downregulated expression of a specific novel protein, beta tropomyosin (TMbeta) was detected in Iranian ESCC patients [51].
Olaparib for the treatment of breast cancer
Published in Expert Review of Anticancer Therapy, 2018
Gaia Griguolo, Maria Vittoria Dieci, Valentina Guarneri, PierFranco Conte
As the use of PARP inhibitors in BC will expand in the next few years, the understanding of the mechanisms of resistance to these agents will be of extreme importance in order to accurately design therapeutic sequences in homologous recombination repair deficient BC. The acquisition of secondary BRCA mutations that result in restoration of BRCA function has been described [73]; in these cases, the subsequent activity of alternative treatments based on the alteration of the homologous recombination repair, such as platinum salts or other DNA-crosslinking agents, might be limited. However, other mechanisms of resistance have also been described, such as drug efflux by P-glycoprotein [37] or BRCA-independent restoration of homologous recombination (e.g. somatic mutations of tumor protein p53 binding protein 1 or loss of MAD2 mitotic arrest deficient-like 2) [74,75]. In these cases, the patients might still benefit from treatment with DNA crosslinkers.
Gene expression microarray analysis reveals prognostic markers of survival in high grade astrocytomas
Published in Neurological Research, 2018
Jun Yang, Ziming Hou, Changjiang Wang, Hao Wang, Hongbing Zhang
The STRING tool was used to obtain the PPIs of 598 prognostic risk genes. PPI network with 1253 edges connecting 381 nodes were showed in Figure 3(a), Furthermore, there were 8 hub genes with connective degree ≥40, including CDC6 (cell division cycle 6) (degree = 48), POLD1 (polymerase (DNA directed), delta 1, catalytic subunit) (degree = 46), KNTC1 (kinetochore associated 1) (degree = 42), AURKB (aurora kinase B) (degree = 41), AURKA (aurora kinase A) (degree = 41), RRM2 (ribonucleotide reductase M2) (degree = 40), MAD2L1 (MAD2 mitotic arrest deficient-like 1 (yeast) (degree = 40), and CDC20 (cell division cycle 20) (degree = 40).