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Fulltext World Workshop on Oral Medicine VII: Clinical evidence of differential expression of lncRNAs in oral squamous cell carcinoma: A scoping review

Pentenero M, Bowers LM, Jayasinghe R, Yap T, Cheong SC, Kerr AR, et al.

Oral Dis, 2019 Jun;25 Suppl 1(Suppl 1):88-101.
PMID: 31140697 DOI: 10.1111/odi.13076

BACKGROUND: Long non-coding RNAs (lncRNAs) have important roles in regulating gene expression pertaining to cell proliferation, survival, migration and genomic stability. Dysregulated expression of lncRNAs is implicated in cancer initiation, progression and metastasis.
OBJECTIVES: To explore, map and summarize the extent of evidence from clinical studies investigating the differential expression of lncRNAs in oral/tongue squamous cell carcinoma.
METHODS: PubMed, Scopus and Web of Science were used as search engines. Clinical, full-length, English language studies were included. PRISMA-ScR protocol was used to evaluate and present results. The present scoping review summarizes relationships of the differential expression of lncRNAs with the presence of tumour and with clinicopathological features including survival.
RESULTS: Almost half of the investigated transcripts have been explored in more than one study, yet not always with consistent results. The collected data were also compared to the limited studies investigating oral epithelial dysplasia. Data are not easily comparable, first because of different methods used to define what differential expression is, and second because only a limited number of studies performed multivariate analyses to identify clinicopathological features associated with the differentially expressed lncRNAs.
CONCLUSIONS: Standard methods and more appropriate data analyses are needed in order to achieve reliable results from future studies.

Matched MeSH terms: Mouth Neoplasms/genetics*; Tongue Neoplasms/genetics*
Lymphocyte micronuclei frequencies in skin, haematological, prostate, colorectal and esophageal cancer cases: A systematic review and meta-analysis

Dhillon VS, Deo P, Bonassi S, Fenech M

Mutat Res Rev Mutat Res, 2021;787:108372.
PMID: 34083057 DOI: 10.1016/j.mrrev.2021.108372

Micronucleus (MN) assay has been widely used as a biomarker of DNA damage, chromosomal instability, cancer risk and accelerated aging in many epidemiological studies. In this narrative review and meta-analysis we assessed the association between lymphocyte micronuclei (MNi) and cancers of the skin, blood, digestive tract, and prostate. The review identified nineteen studies with 717 disease subjects and 782 controls. Significant increases in MRi for MNi were observed in the following groups: subjects with blood cancer (MRi = 3.98; 95 % CI: 1.98-7.99; p = 0.000) and colorectal cancer (excluding IBD) (MRi = 2.69; 95 % CI: 1.82-3.98, p

Matched MeSH terms: Esophageal Neoplasms/genetics; Colorectal Neoplasms/genetics*
Fulltext Physical activity and risks of breast and colorectal cancer: a Mendelian randomisation analysis

Papadimitriou N, Dimou N, Tsilidis KK, Banbury B, Martin RM, Lewis SJ, et al.

Nat Commun, 2020 01 30;11(1):597.
PMID: 32001714 DOI: 10.1038/s41467-020-14389-8

Physical activity has been associated with lower risks of breast and colorectal cancer in epidemiological studies; however, it is unknown if these associations are causal or confounded. In two-sample Mendelian randomisation analyses, using summary genetic data from the UK Biobank and GWA consortia, we found that a one standard deviation increment in average acceleration was associated with lower risks of breast cancer (odds ratio [OR]: 0.51, 95% confidence interval [CI]: 0.27 to 0.98, P-value = 0.04) and colorectal cancer (OR: 0.66, 95% CI: 0.48 to 0.90, P-value = 0.01). We found similar magnitude inverse associations for estrogen positive (ER+ve) breast cancer and for colon cancer. Our results support a potentially causal relationship between higher physical activity levels and lower risks of breast cancer and colorectal cancer. Based on these data, the promotion of physical activity is probably an effective strategy in the primary prevention of these commonly diagnosed cancers.

Matched MeSH terms: Breast Neoplasms/genetics*; Colorectal Neoplasms/genetics*
Fulltext Genome-Wide Meta-Analyses of Breast, Ovarian, and Prostate Cancer Association Studies Identify Multiple New Susceptibility Loci Shared by at Least Two Cancer Types

Kar SP, Beesley J, Amin Al Olama A, Michailidou K, Tyrer J, Kote-Jarai Z, et al.

Cancer Discov, 2016 Sep;6(9):1052-67.
PMID: 27432226 DOI: 10.1158/2159-8290.CD-15-1227

Breast, ovarian, and prostate cancers are hormone-related and may have a shared genetic basis, but this has not been investigated systematically by genome-wide association (GWA) studies. Meta-analyses combining the largest GWA meta-analysis data sets for these cancers totaling 112,349 cases and 116,421 controls of European ancestry, all together and in pairs, identified at P < 10(-8) seven new cross-cancer loci: three associated with susceptibility to all three cancers (rs17041869/2q13/BCL2L11; rs7937840/11q12/INCENP; rs1469713/19p13/GATAD2A), two breast and ovarian cancer risk loci (rs200182588/9q31/SMC2; rs8037137/15q26/RCCD1), and two breast and prostate cancer risk loci (rs5013329/1p34/NSUN4; rs9375701/6q23/L3MBTL3). Index variants in five additional regions previously associated with only one cancer also showed clear association with a second cancer type. Cell-type-specific expression quantitative trait locus and enhancer-gene interaction annotations suggested target genes with potential cross-cancer roles at the new loci. Pathway analysis revealed significant enrichment of death receptor signaling genes near loci with P < 10(-5) in the three-cancer meta-analysis.
SIGNIFICANCE: We demonstrate that combining large-scale GWA meta-analysis findings across cancer types can identify completely new risk loci common to breast, ovarian, and prostate cancers. We show that the identification of such cross-cancer risk loci has the potential to shed new light on the shared biology underlying these hormone-related cancers. Cancer Discov; 6(9); 1052-67. ©2016 AACR.This article is highlighted in the In This Issue feature, p. 932.

Matched MeSH terms: Breast Neoplasms/genetics*; Ovarian Neoplasms/genetics*; Prostatic Neoplasms/genetics*
Relationships between PTEN gene mutations and prognosis in glioma: a meta-analysis

Xiao WZ, Han DH, Wang F, Wang YQ, Zhu YH, Wu YF, et al.

Tumour Biol., 2014 Jul;35(7):6687-93.
PMID: 24705863 DOI: 10.1007/s13277-014-1885-1

We conducted a meta-analysis in order to investigate the relationships between PTEN gene mutations and the prognosis in glioma. The following electronic databases were searched for relevant articles without any language restrictions: Web of Science (1945 ~ 2013), the Cochrane Library Database (Issue 12, 2013), PubMed (1966 ~ 2013), EMBASE (1980 ~ 2013), CINAHL (1982 ~ 2013), and the Chinese Biomedical Database (CBM) (1982 ~ 2013). Meta-analyses were conducted using the STATA software (Version 12.0, Stata Corporation, College Station, Texas USA). Hazard ratio (HR) with its corresponding 95 % confidence interval (95%CI) was calculated. Six independent cohort studies with a total of 357 glioma patients met our inclusion criteria. Our meta-analysis results indicated that glioma patients with PTEN gene mutations exhibited a significantly shorter overall survival (OS) than those without PTEN gene mutations (HR = 3.66, 95%CI = 2.02 ~ 5.30, P < 0.001). Ethnicity-stratified subgroup analysis demonstrated that PTEN gene mutations were closely linked to poor prognosis in glioma among Americans (HR = 3.72, 95%CI = 1.72 ~ 5.73, P < 0.001), while similar correlations were not observed among populations in Sweden, Italy, and Malaysia (all P > 0.05). Our meta-analysis provides direct and strong evidences for the speculation of PTEN gene mutations' correlation with poor prognosis of glioma patients.

Matched MeSH terms: Brain Neoplasms/genetics*
Dietary non-nutritive factors in targeting of regulatory molecules in colorectal cancer: an update

Pandurangan AK, Esa NM

Asian Pac J Cancer Prev, 2013;14(10):5543-52.
PMID: 24289544

Colorectal cancer (CRC), a complex multi-step process involving progressive disruption of homeostatic mechanisms controlling intestinal epithelial proliferation/inflammation, differentiation, and programmed cell death, is the third most common malignant neoplasm worldwide. A number of promising targets such as inducible nitric acid (iNOS), cyclooxygenase (COX)-2, NF-E2-related factor 2 (Nrf2), Wnt/β-catenin, Notch and apoptotic signaling have been identified by researchers as useful targets to prevent or therapeutically inhibit colon cancer development. In this review article, we aimed to explore the current targets available to eliminate colon cancer with an update of dietary and non-nutritional compounds that could be of potential use for interaction with regulatory molecules to prevent CRC.

Matched MeSH terms: Colorectal Neoplasms/genetics*
Gene expression profiling and cancer-related pathways in type I endometrial carcinoma

Saghir FS, Rose IM, Dali AZ, Shamsuddin Z, Jamal AR, Mokhtar NM

Int. J. Gynecol. Cancer, 2010 Jul;20(5):724-31.
PMID: 20973258

INTRODUCTION: Malignant transformation of type I endometrium involves alteration in gene expression with subsequent uncontrolled proliferation of altered cells.
OBJECTIVE: The main objective of the present study was to identify the cancer-related genes and gene pathways in the endometrium of healthy and cancer patients.
MATERIALS AND METHODS: Thirty endometrial tissues from healthy and type I EC patients were subjected to total RNA isolation. The RNA samples with good integrity number were hybridized to a new version of Affymetrix Human Genome GeneChip 1.0 ST array. We analyzed the results using the GeneSpring 9.0 GX and the Pathway Studio 6.1 software. For validation assay, quantitative real-time polymerase chain reaction was used to analyze 4 selected genes in normal and EC tissue.
RESULTS: Of the 28,869 genes profiled, we identified 621 differentially expressed genes (2-fold) in the normal tissue and the tumor. Among these genes, 146 were up-regulated and 476 were down-regulated in the tumor as compared with the normal tissue (P < 0.001). Up-regulated genes included the v-erb-a erythroblastic leukemia viral oncogene homolog 3 (ErbB3), ErbB4, E74-like factor 3 (ELF3), and chemokine ligand 17 (CXCL17). The down-regulated genes included signal transducer and activator transcription 5B (STAT5b), transforming growth factor A receptor III (TGFA3), caveolin 1 (CAV1), and protein kinase C alpha (PKCA). The gene set enrichment analysis showed 10 significant gene sets with related genes (P < 0.05). The quantitative polymerase chain reaction of 4 selected genes using similar RNA confirmed the microarray results (P < 0.05).
CONCLUSIONS: Identification of molecular pathways with their genes related to type I EC contribute to the understanding of pathophysiology of this cancer, probably leading to identifying potential biomarkers of the cancer.

Matched MeSH terms: Endometrial Neoplasms/genetics*
Fulltext The prevalence and assessment of ErbB2-positive breast cancer in Asia: a literature survey

Tan YO, Han S, Lu YS, Yip CH, Sunpaweravong P, Jeong J, et al.

Cancer, 2010 Dec 1;116(23):5348-57.
PMID: 20715159 DOI: 10.1002/cncr.25476

Overexpression of the epidermal growth factor receptor-related gene ErbB2 occurs in 18% to 25% of patients with breast cancer in Western countries and is associated with a poor prognosis. The prevalence of ErbB2-positive tumors in Asia is unclear, partly because data are limited. The objective of this review was to summarize the reported prevalence of ErbB2-positive tumors from a large sample of Asian patients and to examine ErbB2 assessment methods in Asia. From searches of MEDLINE, local language journals, and local and international conference proceedings as well as locoregional breast cancer experts' recommendations, the authors selected up to 5 studies each from India, Korea, Malaysia, the Philippines, Singapore, Taiwan, and Thailand that reported ErbB2 results based on assessment with immunohistochemistry (IHC) and/or fluorescence in situ hybridization (FISH). The reported prevalence of ErbB2-positive tumors in 22 studies on 24,671 patients, of whom 14,398 patients were assessed for ErbB2 status, varied widely (range, 6%-65%) as did the assessment methods used. Most studies (n=21) used IHC to assess ErbB2 status, but definitions for positivity varied. When robust assessment methods were used, the median prevalence was 19% based on strong IHC staining (IHC3+; n=9812 patients) and 25% based on FISH (n=681 patients). Data on the prevalence of ErbB2-positive breast cancer in Asia are limited. The current survey indicated that the prevalence in Asia may be similar to that in Western countries; thus, up to 1 in 4 Asian patients with breast cancer potentially could benefit from ErbB2-targeted treatment. A standard, reliable ErbB2 assessment method available to patients across Asia is urgently required.

Matched MeSH terms: Breast Neoplasms/genetics*
Letter regarding "CD95 rs1800682 polymorphism and cervical cancer risk: evidence from a meta-analysis" by Zhang et al

Tan SC

Tumour Biol., 2015 Nov;36(11):8275-6.
PMID: 26515334 DOI: 10.1007/s13277-015-4330-1
Matched MeSH terms: Uterine Cervical Neoplasms/genetics*
Molecular genetic analysis of anaplastic pleomorphic xanthoastrocytoma

Nasuha NA, Daud AH, Ghazali MM, Yusoff AA, Zainuddin N, Abdullah JM, et al.

Asian J Surg, 2003 Apr;26(2):120-5.
PMID: 12732498

A case of pleomorphic xanthoastrocytoma in a 10-year-old Malay boy is reported. The patient presented with headache and epilepsy. On computed tomography, a ring-enhancing low-density lesion was observed in the left fronto-temporal area. During surgery, a cystic tumour containing serous fluid was found and almost totally removed. Histologically, the tumour exhibited marked pleomorphism of oval and spindle-shaped cells intermixed with uni- and multinucleated giant cells, and xanthomatous cells with foamy cytoplasm. The tumour displayed pericellular reticulin and periodic acid-Schiff positive granules. Focally, six mitotic characters per 10 high-power fields were seen, and necrosis was confined only to the inner lining of the cyst. Mutational analysis showed that a frameshift mutation (a 4-bp deletion) in the p53 gene had occurred in codons 273 and 274 of exon 8. No mutation was detected in the p16 gene. No allelic loss and/or loss of heterozygosity were observed on chromosome 10 using microsatellite marker D105532. The patient was treated with postoperative radiotherapy because of histological anaplasia and the presence of residual tumour. The patient showed marked neurological recovery after a follow-up period of 2 years.

Matched MeSH terms: Brain Neoplasms/genetics*
Fulltext Bilateral pure gonadoblastoma in a 46 XY individual--a case report

Siti Aishah MA, Chandran R, Tahir H

Med J Malaysia, 1991 Dec;46(4):384-7.
PMID: 1840451

We report here a rare case of bilateral pure gonadoblastoma which accounts for only 0.2% of all ovarian tumours seen at Universiti Kebangsaan Malaysia from 1980 to 1987. This tumour occurred in an 18 year old Chinese "female" who presented with primary amenorrhoea. Examination showed a phenotypic female with poorly developed external gentalia. Exploratory laparotomy revealed a hypoplastic uterus, rudimentary fallopian tubes and streak gonads. Histological examination of the gonads showed a mixed tumour comprising large germ cells and smaller sex cord derivatives arranged in characteristic nests or islands containing hyaline material.

Matched MeSH terms: Ovarian Neoplasms/genetics
Fulltext Mutations of the p53 gene in gliomas from Malay patients

Jafri A, Aziz MY, Ros S, Nizam I

Med J Malaysia, 2003 Jun;58(2):236-42.
PMID: 14569744

This is the first investigation performed to detect the presence of the p53 mutation in Malay patients with gliomas. The p53 gene was amplified using polymerase chain reaction (PCR) from 33 fresh-frozen tumour tissues from patients histologically confirmed as glioma. Four hot spot areas that lie between exon 5 to 8 were screened for mutation by mean of non-isotopic "cold" single strand conformation polymorphism (SSCP) analysis and direct sequencing. The frequency of p53 gene mutation in gliomas examined was 33% (11 of 33). Five (45.5%) cases had mutation in exon 7, four (36.4%) had mutation in exon 8 and two (18.1%) had mutation in exon 6. Seven (63.6%) of 11 mutations were single nucleotide point mutations of which 5 were missense mutations, 1 was nonsense mutation and 1 was, silent mutation. Three (27.3%) showed insertion mutation and 1 (9.1%) showed deletion mutation. Of the point mutations, 57.1% were transitions and 42.9% were transversions. These results suggested that p53 mutations frequently occur in gliomas and this gene does play an important role in the tumourigenesis process of Malay patients with brain tumours.

Matched MeSH terms: Brain Neoplasms/genetics*
Identification of a recurrent BRCA1 exon 21-22 genomic rearrangement in Malay breast cancer patients

Hasmad HN, Sivanandan K, Lee V, Yip CH, Mohd Taib NA, Teo SH

Clin Genet, 2015 Apr;87(4):392-4.
PMID: 25066186 DOI: 10.1111/cge.12451
Matched MeSH terms: Breast Neoplasms/genetics*
Global Disparities in Breast Cancer Genetics Testing, Counselling and Management

Yip CH, Evans DG, Agarwal G, Buccimazza I, Kwong A, Morant R, et al.

World J Surg, 2019 05;43(5):1264-1270.
PMID: 30610270 DOI: 10.1007/s00268-018-04897-6

Hereditary breast cancers, mainly due to BRCA1 and BRCA2 mutations, account for only 5-10% of this disease. The threshold for genetic testing is a 10% likelihood of detecting a mutation, as determined by validated models such as BOADICEA and Manchester Scoring System. A 90-95% reduction in breast cancer risk can be achieved with bilateral risk-reducing mastectomy in unaffected BRCA mutation carriers. In patients with BRCA-associated breast cancer, there is a 40% risk of contralateral breast cancer and hence risk-reducing contralateral mastectomy is recommended, which can be performed simultaneously with surgery for unilateral breast cancer. Other options for risk management include surveillance by mammogram and breast magnetic resonance imaging, and chemoprevention with hormonal agents. With the advent of next-generation sequencing and development of multigene panel testing, the cost and time taken for genetic testing have reduced, making it possible for treatment-focused genetic testing. There are also drugs such as the PARP inhibitors that specifically target the BRCA mutation. Risk management multidisciplinary clinics are designed to quantify risk, and offer advice on preventative strategies. However, such services are only possible in high-income settings. In low-resource settings, the prohibitive cost of testing and the lack of genetic counsellors are major barriers to setting up a breast cancer genetics service. Family history is often not well documented because of the stigma associated with cancer. Breast cancer genetics services remain an unmet need in low- and middle-income countries, where the priority is to optimise access to quality treatment.

Matched MeSH terms: Breast Neoplasms/genetics*
Recent trends in cancer therapy: A review on the current state of gene delivery

Yahya EB, Alqadhi AM

Life Sci, 2021 Mar 15;269:119087.
PMID: 33476633 DOI: 10.1016/j.lfs.2021.119087

Cancer treatment has been always considered one of the most critical and vital themes of clinical issues. Many approaches have been developed, depending on the type and the stage of tumor. Gene therapy has the potential to revolutionize different cancer therapy. With the advent of recent bioinformatics technologies and genetic science, it become possible to identify, diagnose and determine the potential treatment using the technology of gene delivery. Several approaches have been developed and experimented in vitro and vivo for cancer therapy including: naked nucleic acids based therapy, targeting micro RNAs, oncolytic virotherapy, suicide gene based therapy, targeting telomerase, cell mediated gene therapy, and CRISPR/Cas9 based therapy. In this review, we present a straightforward introduction to cancer biology and occurrence, highlighting different viral and non-viral gene delivery systems for gene therapy and critically discussed the current and various strategies for cancer gene therapy.

Matched MeSH terms: Neoplasms/genetics
Gene symbol: APC. Disease: colorectal cancer

Tan LP, Ng BK, Balraj P, Poh BH, Lim PK, Peh SC

Hum Genet, 2005 Dec;118(3-4):539-40.
PMID: 16521263
Matched MeSH terms: Colorectal Neoplasms/genetics*
Reviewing the molecular mechanisms which increase endometrial cancer (EC) risk in women with polycystic ovarian syndrome (PCOS): time for paradigm shift?

Shafiee MN, Chapman C, Barrett D, Abu J, Atiomo W

Gynecol Oncol, 2013 Nov;131(2):489-92.
PMID: 23822891 DOI: 10.1016/j.ygyno.2013.06.032

Endometrial cancer (EC) is the commonest gynaecological cancer in North American and European women. Even though it has been shown that women with polycystic ovary syndrome (PCOS) have a three-fold increase in the risk of developing EC compared to women without PCOS, the precise molecular mechanisms which increase EC risk in women with PCOS remain unclear. Clinical strategies to prevent EC in PCOS are therefore not well researched and understood. Although raised estrogen levels, hyperinsulinaemia and, reduced apoptosis have been suggested as potential mechanisms, there is a lack of clarity about how these factors and other factors may interact to increase EC risk in PCOS. This article reviews the literature, on the potential molecular links between PCOS and EC but argues for a paradigm shift, to a systems biology-based approach in future research into the molecular links between PCOS and EC. The potential challenges of a systems biology-based approach are outlined but not considered insurmountable.

Matched MeSH terms: Endometrial Neoplasms/genetics*
Integrated analysis of copy number and loss of heterozygosity in primary breast carcinomas using high-density SNP array

Ching HC, Naidu R, Seong MK, Har YC, Taib NA

Int J Oncol, 2011 Sep;39(3):621-33.
PMID: 21687935 DOI: 10.3892/ijo.2011.1081

Breast cancer is a heterogeneous disease, marked by extensive chromosomal aberrations. In this study, we aimed to explicate the underlying chromosomal copy number (CN) alterations and loss of heterozygosity (LOH) implicated in a cohort of Malaysian hospital-based primary breast carcinoma samples using a single nucleotide polymorphism (SNP) array platform. The analysis was conducted by hybridizing the extracted DNA of 70 primary breast carcinomas and 37 normal peripheral blood samples to the Affymetrix 250K Sty SNP arrays. Locus-specific CN aberrations and LOH were statistically summarized using the binary segmentation algorithm and hidden Markov model. Selected genes from the SNP array analysis were also validated using quantitative real-time PCR. The merging of CN and LOH data fabricated distinctive integrated alteration profiles, which were comprised of finely demarcated minimal sites of aberrations. The most prevalent gains (≥ 30%) were detected at the 8q arm: 8q23.1, 8q23.3, 8q24.11, 8q24.13, 8q24.21, 8q24.22, 8q24.23 and 8q24.3, whilst the most ubiquitous losses (≥ 20%) were noted at the 8p12, 8p21.1, 8p21.2, 8p21.1-p21.2, 8p21.3, 8p22, 8p23.1, 8p23.1‑p23.2, 8p23.3, 17p11.2, 17p12, 17p11.2-p12, 17p13.1 and 17p13.2 regions. Copy-neutral LOH was characterized as the most prevailing LOH event, in which the most frequent distributions (≥ 30%) were revealed at 3p21.31, 5q33.2, 12q24.12, 12q24.12‑q24.13 and 14q23.1. These findings offer compre-hensive genome-wide views on breast cancer genomic changes, where the most recurrent gain, loss and copy-neutral LOH events were harboured within the 8q24.21, 8p21.1 and 14q23.1 loci, respectively. This will facilitate the uncovering of true driver genes pertinent to breast cancer biology and the develop-ment of prospective therapeutics.

Matched MeSH terms: Breast Neoplasms/genetics*
E-cadherin: Its dysregulation in carcinogenesis and clinical implications

Wong SHM, Fang CM, Chuah LH, Leong CO, Ngai SC

Crit Rev Oncol Hematol, 2018 Jan;121:11-22.
PMID: 29279096 DOI: 10.1016/j.critrevonc.2017.11.010

E-cadherin is a transmembrane glycoprotein which connects epithelial cells together at adherens junctions. In normal cells, E-cadherin exerts its tumour suppressing role mainly by sequestering β-catenin from its binding to LEF (Lymphoid enhancer factor)/TCF (T cell factor) which serves the function of transcribing genes of the proliferative Wnt signaling pathway. Despite the ongoing debate on whether the loss of E-cadherin is the cause or effect of epithelial-mesenchymal transition (EMT), E-cadherin functional loss has frequently been associated with poor prognosis and survival in patients of various cancers. The dysregulation of E-cadherin expression that leads to carcinogenesis happens mostly at the epigenetic level but there are cases of genetic alterations as well. E-cadherin expression has been linked to the cellular functions of invasiveness reduction, growth inhibition, apoptosis, cell cycle arrest and differentiation. Studies on various cancers have shown that these different cellular functions are also interdependent. Recent studies have reported a rapid expansion of E-cadherin clinical relevance in various cancers. This review article summarises the multifaceted effect E-cadherin expression has on cellular functions in the context of carcinogenesis as well as its clinical implications in diagnosis, prognosis and therapeutics.

Matched MeSH terms: Neoplasms/genetics
Role of the Tristetraprolin (Zinc Finger Protein 36 Homolog) Gene in Cancer

Gupta G, Bebawy M, Pinto TJA, Chellappan DK, Mishra A, Dua K

Crit Rev Eukaryot Gene Expr, 2018;28(3):217-221.
PMID: 30311568 DOI: 10.1615/CritRevEukaryotGeneExpr.2018021188

Cancer is a complicated transformational progression that fiercely changes the appearance of cell physiology as well as cells' relations with adjacent tissues. Developing an oncogenic characteristic requires a wide range of modifications in a gene expression at a cellular level. This can be achieved by activation or suppression of the gene regulation pathway in a cell. Tristetraprolin (TTP or ZFP36) associated with the initiation and development of tumors are regulated at the level of mRNA decay, frequently through the activity of AU-rich mRNA-destabilizing elements (AREs) located in their 3'-untranslated regions. TTP is an attractive target for therapeutic use and diagnostic tools due to its characteristic appearance in cancer tissue alone. Thus, the illumination of TTP in diverse types of cancer might deliver additional effective remedies in the coming era for cancer patients. The objective of this review is to familiarize the reader with the TTP proteins, focus on efficient properties that endow them with their effective oncogenic potential, describe their physiological role in cancer cells, and review the unique properties of TT, and of TTP-driven cancer.

Matched MeSH terms: Neoplasms/genetics*

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