Microscopic Omental Metastasis in Type II Endometrial Cancer Clinically Confined to the Uterus

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Boak Katelin ◽  
Fatkin Sarah ◽  
Miller Briana ◽  
Varma Shruti ◽  
Aikman Noel ◽  
...  
2022 ◽  
Vol 23 (2) ◽  
pp. 628
Author(s):  
Rahaba Marima ◽  
Rodney Hull ◽  
Mandisa Mbeje ◽  
Thulo Molefi ◽  
Kgomotso Mathabe ◽  
...  

Precision oncology can be defined as molecular profiling of tumors to identify targetable alterations. Emerging research reports the high mortality rates associated with type II endometrial cancer in black women and with prostate cancer in men of African ancestry. The lack of adequate genetic reference information from the African genome is one of the major obstacles in exploring the benefits of precision oncology in the African context. Whilst external factors such as the geography, environment, health-care access and socio-economic status may contribute greatly towards the disparities observed in type II endometrial and prostate cancers in black populations compared to Caucasians, the contribution of African ancestry to the contribution of genetics to the etiology of these cancers cannot be ignored. Non-coding RNAs (ncRNAs) continue to emerge as important regulators of gene expression and the key molecular pathways involved in tumorigenesis. Particular attention is focused on activated/repressed genes and associated pathways, while the redundant pathways (pathways that have the same outcome or activate the same downstream effectors) are often ignored. However, comprehensive evidence to understand the relationship between type II endometrial cancer, prostate cancer and African ancestry remains poorly understood. The sub-Saharan African (SSA) region has both the highest incidence and mortality of both type II endometrial and prostate cancers. Understanding how the entire transcriptomic landscape of these two reproductive cancers is regulated by ncRNAs in an African cohort may help elucidate the relationship between race and pathological disparities of these two diseases. This review focuses on global disparities in medicine, PCa and ECa. The role of precision oncology in PCa and ECa in the African population will also be discussed.


2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Raffaella Giannice ◽  
Gaetano Valenti ◽  
Yael Hants ◽  
Riccardo Garruto-Campanile ◽  
Sanjiv Manek ◽  
...  

2010 ◽  
Vol 70 (13) ◽  
pp. 5486-5496 ◽  
Author(s):  
Tao Jiang ◽  
Ning Chen ◽  
Fei Zhao ◽  
Xiao-Jun Wang ◽  
Beihua Kong ◽  
...  
Keyword(s):  

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Elisabet Aliagas ◽  
August Vidal ◽  
Laura Texidó ◽  
Jordi Ponce ◽  
Enric Condom ◽  
...  

One of the strategies used by tumors to evade immunosurveillance is the accumulation of extracellular adenosine, which has immunosupressive and tumor promoting effects. The study of the mechanisms leading to adenosine formation at the tumor interstitium are therefore of great interest in oncology. The dominant pathway generating extracellular adenosine in tumors is the dephosphorylation of ATP by ecto-nucleotidases. Two of these enzymes acting sequentially, CD39 and CD73, efficiently hydrolyze extracellular ATP to adenosine. They have been found to play a crucial role in a variety of tumors, but there were no data concerning endometrial cancer, the most frequent of the invasive tumors of the female genital tract. The aim of the present work is to study the expression of CD39 and CD73 in human endometrial cancer. We have analyzed protein and gene expression, as well as enzyme activity, in type I endometrioid adenocarcinomas and type II serous adenocarcinomas and their nonpathological endometrial counterparts. High levels of both enzymes were found in tumor samples, with significantly increased expression of CD39 in type II serous tumors, which also coincided with the higher tumor grade. Our results reinforce the involvement of the adenosinergic system in cancer, emphasizing the relevance of ecto-nucleotidases as emerging therapeutic targets in oncology.


2019 ◽  
Vol 126 ◽  
pp. 78-81
Author(s):  
Kusuma Kumari Garikapati ◽  
V.V.V. Ravi Kiran Ammu ◽  
Praveen T. Krishnamurthy ◽  
Pavan Kumar Chintamaneni ◽  
Sai kiran S.S. Pindiprolu
Keyword(s):  

2017 ◽  
Vol 129 ◽  
pp. 106S-107S
Author(s):  
Rimsha Ahmed ◽  
Stephanie Estes ◽  
Viktoriya Paroder ◽  
Marina Frimer ◽  
Joshua Kesterson ◽  
...  

2018 ◽  
Vol 19 (8) ◽  
pp. 2380 ◽  
Author(s):  
Michiel Remmerie ◽  
Veerle Janssens

Type II endometrial carcinomas (ECs) are responsible for most endometrial cancer-related deaths due to their aggressive nature, late stage detection and high tolerance for standard therapies. However, there are no targeted therapies for type II ECs, and they are still treated the same way as the clinically indolent and easily treatable type I ECs. Therefore, type II ECs are in need of new treatment options. More recently, molecular analysis of endometrial cancer revealed phosphorylation-dependent oncogenic signalling in the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways to be most frequently altered in type II ECs. Consequently, clinical trials tested pharmacologic kinase inhibitors targeting these pathways, although mostly with rather disappointing results. In this review, we highlight the most common genetic alterations in type II ECs. Additionally, we reason why most clinical trials for ECs using targeted kinase inhibitors had unsatisfying results and what should be changed in future clinical trial setups. Furthermore, we argue that, besides kinases, phosphatases should no longer be ignored in clinical trials, particularly in type II ECs, where the tumour suppressive phosphatase protein phosphatase type 2A (PP2A) is frequently mutated. Lastly, we discuss the therapeutic potential of targeting PP2A for (re)activation, possibly in combination with pharmacologic kinase inhibitors.


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