Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Retinoblastoma (Rb) is the most common ocular pediatric malignancy that arises from the retina and is caused by a mutation of the two alleles of the tumor suppressor gene, RB1. Although early detection provides the opportunity of controlling the primary tumor with effective therapies, metastatic activity is fatal. Non-coding RNAs (ncRNAs) have emerged as important modifiers of a plethora of biological mechanisms including those involved in cancer. They are classified into short and long ncRNAs according to their length. Deregulation of all these molecules has also been shown to play a critical role in Rb pathogenesis and progression. It is believed that ncRNAs can provide new insights into novel regulatory mechanisms associated with clinical pathological characteristics, facilitating the development of therapeutic alternatives for the treatment of Rb. In this review, we describe a variety of ncRNAs, which capable of regulating the most likely candidate genes involved in the tumorigenesis of Rb, could prove useful in analyzing different aspects of this cancer.
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PMID:Non-Coding RNAs in Retinoblastoma. 3179 38

High-grade serous ovarian cancer (HGSOC) likely originates from the fallopian tube (FT) epithelium. Here, we established 15 organoid lines from HGSOC primary tumor deposits that closely match the mutational profile and phenotype of the parental tumor. We found that Wnt pathway activation leads to growth arrest of these cancer organoids. Moreover, active BMP signaling is almost always required for the generation of HGSOC organoids, while healthy fallopian tube organoids depend on BMP suppression by Noggin. Fallopian tube organoids modified by stable shRNA knockdown of p53, PTEN, and retinoblastoma protein (RB) also require a low-Wnt environment for long-term growth, while fallopian tube organoid medium triggers growth arrest. Thus, early changes in the stem cell niche environment are needed to support outgrowth of these genetically altered cells. Indeed, comparative analysis of gene expression pattern and phenotypes of normal vs. loss-of-function organoids confirmed that depletion of tumor suppressors triggers changes in the regulation of stemness and differentiation.
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PMID:Stable expansion of high-grade serous ovarian cancer organoids requires a low-Wnt environment. 3200 47


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