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Noonan Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Besides the above-mentioned genes, several other genes (e.g., SOS2, RASA2, RRAS, SYNGAP1, A2ML1, LZTR1, MYST4, SPRY1, MAP3K8) have been recently implicated in the development of Noonan syndrome. It should be noted that while germline mutations in these genes are responsible for Noonan syndrome and its phenotypic variants, somatic nucleotide variants in PTPN11, KRAS, NRAS, BRAF, or MAP2K1 are sometimes detected in sporadic tumors (including leukemia and solid tumors) that tend to occur as single tumors without any other findings of Noonan syndrome. In the latter cases, predisposition to these tumors is not heritable. Furthermore, these somatic mutations appear to be more strongly activating than germline counterparts, as activating oncogenic mutations are not tolerated in the germline or in early development.
MicroRNAs in Human Cancers
Published in II-Jin Kim, Cancer Genetics and Genomics for Personalized Medicine, 2017
A role for this miRNA in early leukemogenesis was proven in a transgenic mouse model with a B cell–targeted overexpression of miR-155, which underwent a polyclonal preleukemic pre–B-cell proliferation followed by full-blown B-cell malignancy [58]. More recently, it was reported in lymphoma study with miR-155 overexpressing mice that tumor cell survival can be addicted to the expression of miR-155 [59]. This addiction theory can be a huge benefit to cancer therapies, since targeting one specific oncogenic miRNA may be sufficient to inhibit entire tumor progression [59]. The addiction of cancer cells to a certain miRNA expression was first reported in miR-21. Overexpression of miR-21 in spleen of mice has shown to develop lethal B-cell lymphoma, and more importantly the malignancy was addicted to the expression level of miR-21 [60]. MiR-21 is the most frequently upregulated miRNA in almost every type of human cancers including both hematopoietic and solid tumors, such as AML, CLL, glioblastoma, and cancers of the pancreas, prostate, stomach, colon, lung, breast, and liver [61]. Transgenic mice that are overexpressing miR-21 throughout whole body showed no tumor formation. When the miR-21 transgenic mice were crossed to activated k-Ras mutant mice, miR-21 over-expression increased tumor incidents in lung cancer by negatively regulated multiple tumor suppressors (Spry1, Spry2, Btg2 and Pdcd4) through activated Ras/Mek/Erk pathway [62] consistent with the previous report [63].
SPRY1 promotes cell proliferation and inhibits apoptosis by activating Hedgehog pathway in acute myeloid leukemia
Published in Hematology, 2022
Guiyang Lv, Yuanyuan Wang, ChunXiao Ji, Chunlei Shi, Ying Li
Sprouty (SPRY) family consists of four members (SPRY1, SPRY2, SPRY3 and SPRY4), which differs in tissue distribution, activity and interaction partners [4]. Growing evidence has demonstrated that SPRY1 plays an important role in cell proliferation, differentiation, migration and apoptosis [5]. SPRY1 is reported to be involved in the development of different types of cancers, such as ovarian cancer [6,7], gastric cancer [8], glioma [9] and breast cancer [5]. Additionally, the analysis of the Cancer Genome Atlas (TCGA) confirms that SPRY1 expression is significantly upregulated in patients with AML. However, none of the studies report on the effects of SPRY1 in AML to date.