Intratumoral Heterogeneity of RPL22 Frameshift Mutation in Colorectal Cancers

Intratumoral Heterogeneity of RPL22 Frameshift Mutation in Colorectal Cancers Pathology & Oncology Research https://doi.org/10.1007/s12253-018-0438-0 LETTER TO THE EDITOR Intratumoral Heterogeneity of RPL22 Frameshift Mutation in Colorectal Cancers 1 2 1 1 1 Ju Hwa Lee & Chang Hyeok An & Min Sung Kim & Nam Jin Yoo & Sug Hyung Lee Received: 1 December 2017 /Accepted: 30 May 2018 Arányi Lajos Foundation 2018 Dear Editor, After SSCP, Sanger DNA sequencing reactions were per- RPL22 gene encodes a cytoplasmic ribosomal protein that formed in the cancers with mobility shifts in the SSCP [5]. is a component of the large 60S subunit of ribosome. An We found RPL22 somatic frameshift mutations in 16 CRCs earlier study identified that RPL22 protein functions as a (16/79, 20.3%) and 9 GCs (9/34, 26.5%) with MSI-H, but not haploinsufficient tumor suppressor [1]. RPL22 inactivation in CRCs (0/45) and GCs (0/45) with MSS (Fisher’s exact test, promotes transformation by inducing expression of Lin28B p < 0.001). These mutations were not detected in their normal [1]. A recent study discovered that RPL22 was frequently tissues. The mutations consisted of ‘A’ deletion (c.44delA mutated in colorectal cancer (CRC) and endometrial cancers (p.Lys16Serfsx4)), ‘A’ duplication (c.44dupA by frameshift mutations in A8 repeat, especially those in mi- (p.Lys16Glufsx9)) and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pathology & Oncology Research Springer Journals

Intratumoral Heterogeneity of RPL22 Frameshift Mutation in Colorectal Cancers

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Publisher
Springer Netherlands
Copyright
Copyright © 2018 by Arányi Lajos Foundation
Subject
Biomedicine; Cancer Research; Oncology; Pathology; Immunology; Biomedicine, general
ISSN
1219-4956
eISSN
1532-2807
D.O.I.
10.1007/s12253-018-0438-0
Publisher site
See Article on Publisher Site

Abstract

Pathology & Oncology Research https://doi.org/10.1007/s12253-018-0438-0 LETTER TO THE EDITOR Intratumoral Heterogeneity of RPL22 Frameshift Mutation in Colorectal Cancers 1 2 1 1 1 Ju Hwa Lee & Chang Hyeok An & Min Sung Kim & Nam Jin Yoo & Sug Hyung Lee Received: 1 December 2017 /Accepted: 30 May 2018 Arányi Lajos Foundation 2018 Dear Editor, After SSCP, Sanger DNA sequencing reactions were per- RPL22 gene encodes a cytoplasmic ribosomal protein that formed in the cancers with mobility shifts in the SSCP [5]. is a component of the large 60S subunit of ribosome. An We found RPL22 somatic frameshift mutations in 16 CRCs earlier study identified that RPL22 protein functions as a (16/79, 20.3%) and 9 GCs (9/34, 26.5%) with MSI-H, but not haploinsufficient tumor suppressor [1]. RPL22 inactivation in CRCs (0/45) and GCs (0/45) with MSS (Fisher’s exact test, promotes transformation by inducing expression of Lin28B p < 0.001). These mutations were not detected in their normal [1]. A recent study discovered that RPL22 was frequently tissues. The mutations consisted of ‘A’ deletion (c.44delA mutated in colorectal cancer (CRC) and endometrial cancers (p.Lys16Serfsx4)), ‘A’ duplication (c.44dupA by frameshift mutations in A8 repeat, especially those in mi- (p.Lys16Glufsx9)) and

Journal

Pathology & Oncology ResearchSpringer Journals

Published: Jun 2, 2018

References

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