Editorial - Journal of Molecular Oncology Research (2020) Volume 4, Issue 4

The Genetic Modifications in Wilms Tumour

Ming Luo^*

University of Michigan Medical School, USA

Corresponding Author:

Ming Luo
University of Michigan Medical School
USA
E-mail: mingluoresearch.22@gmail.com

Accepted date: July 14, 2020

Citation: Luo M. The genetic modifications in wilm’s tumour. J Mol Oncol Res. 2020;4(4):6-7.

Abstract

The most common renal cancers of childhood is Wilms tumour .However, majority of the cases can be treated and curable. The genetic changes related Wilms tumour have been illustrated from the various studies of clinical case studies and undifferentiated dna sequencing of tumour genomes all these approaches together defined the overview of the genes that are active in Wilms tumour, in which many of the genes are indirectly linked to the fetal neophrogenesis. Improvement in the understanding of germ line and somatic genetic changes that are linked to the Wilms tumour may help in better patient outcomes. Recognizing the favoured mutations that led to the potential new targets with some new compounds undergoing testing in early phase trials.

Keywords

HBV; Intra hepatic cholangio carcinoma; Molecular; Cancer

Introduction

Based on the histological history of stages in neophrogenesis and age of onset, wilms tumour is considered to be embryonic childhood tumour. 90% of childhood renal tumours and constitutes 7% of all childhood cancers account for wilms tumour. In this review article we give brief information in epidemiology, stages of wilms tumour, management and risk stratification, relapse, bilateral tumours, anaplasia, wilms tumorigenesis and nephrogenesis, germ line mutations, syndromic and familial wilms tumour, non-syndromic wilms tumour, novel therapeutic targets [1].

Epidemiology

Out of 10,000 children, one child is affected by wilms tumour world wide before the age of 15 years. Incidence rates appear to be slightly elevated for US and African blacks when compared to whites, but are only half as great among Asians [2,3].

Management and Risk Stratification

With modern surgery, chemotherapy, and radiation therapy procedures, the overall survival rate for patients with wilms tumour has reached 90%. Extraordinarily, the increase in survival has been accomplished with a reduction in therapy for most patient subgroups, leading not only to more survivors, but also to healthier survivors. A key contributor to upgraded outcomes has been the development of clinical and biologic prognostic markers that have entitled risk- directed therapy [4,5].

Conclusion

The journal will publish original articles, reviews, technical notes, editorials, news and views and letters to the editor. Our editorial board members are instrumental providing a rapid and efficient editorial process and maintaining high standards within our publication we would like to take this opportunity to thank you for the effort and expertise that you contribute to reviewing, without which it would be impossible to maintain the high standards of double peer-reviewed journals. For the success of any journal, reviewers are an essential part and therefore the reviewers merit appreciation. The journal of molecular oncology research relies on the efforts and benevolence of the reviewers on assessing the suitability of a manuscript for publication the journal of molecular oncology research. The inputs of reviewers are frequently used in improving the quality of a submitted manuscript. The reviewing of a manuscript is very essential to assure the quality of the manuscript published in any journal. I thank all reviewers for their excellent contributions. At this stage we are calling for submissions of articles, commentaries, and letters to the editor for the upcoming issues. Reviews are by invitation only. We glance forward to receiving your exciting contribution. Finally I would like to thank you, the contributors and readers for your interest in the journal and I encourage you to continue to send us your valuable feedback and ideas for further improvement of our journal.

References

1. Breslow N, Olshan A, Beckwith JB Green DM. Epidemiology of Wilms tumour. Med Pediatr Oncol. 1993;10(21):172-181.
2. Rivera MN, Haber DA. Wilms’ tumour: connecting tumorigenesis and organ development in the kidney. Nat. Rev. Cancer. 2005;5(2):699-712.
3. Lee SB, Haber DA. Wilms Tumor and the WT1 gene. Exp cell res. 2001;264(21):74-99.
4. Koesters R. Mutational activation of the β-catenin proto- oncogene is a common event in the development of wilms’ tumors. Cancer Res. 1999;59(1):3880-3882.
5. Torrezan GT. Recurrent somatic mutation in DROSHA induces micro RNA profile changes in Wilms tumour. Nat Commun. 2014;5(11):4039.