The Role of Mucin Expression in the Diagnosis of Oesophago-Gastric Cancer: A Systematic Literature Review

Patel, Nikhil Manish; Geropoulos, Georgios; Patel, Pranav Harshad; Bhogal, Ricky Harminder; Harrington, Kevin Joseph; Singanayagam, Aran; Kumar, Sacheen

doi:10.3390/cancers15215252

Cited by 1 publication

(2 citation statements)

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“…Among the five genes with de novo variants in the most cell lines were the mucin genes MUC6 (15 cell lines), MUC2 (14 cell lines), MUC4 (13 cell lines), and MUC16 (9 cell lines) (Fig.3A, SupFile.4). These are large genes that are known to be commonly mutated and have been reported to be involved in cancer cell drug resistance 28–32 . De novo mutations in CDC27, which has also been linked to drug resistance in cancer, were also found in 9 resistant sublines 33,34 (Fig.3A, SupFile.4).…”

Section: Resultsmentioning

confidence: 99%

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Resistance patterns in drug-adapted cancer cell lines reflect complex evolution in clinical tumors

Grimsley,

Antczak,

McLaughlin

et al. 2024

Preprint

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Here, we introduce a novel set of drug-adapted triple-negative breast cancer (TNBC) cell lines consisting of the parental cell lines MDA-MB-468, HCC38, and HCC1806 and their sublines adapted to cisplatin, doxorubicin, eribulin, paclitaxel, gemcitabine, or 5-fluorouracil. Whole exome sequencing in combination with the analysis of TCGA-derived patient data resulted in the identification of 135 biomarker candidates for the guidance of personalized TNBC therapies for further investigation, including 58 novel ones that had not been associated with drug resistance before. The analysis of exome sequencing data showed remarkably few overlaps among the resistant sublines, suggesting that each resistance formation process follows an individual, unpredictable route. This complexity was confirmed by cancer cell line drug sensitivity profiles to cytotoxic anti-cancer drugs and DNA damage repair inhibitors. Drug-adapted sublines of the same parental cell line and sublines adapted to the same drug substantially differed in their drug response patterns. Cross-resistance levels were lowest for the CHK2 inhibitor CCT241533, the PLK1 inhibitor SBE13, and the RAD51 recombinase inhibitor B02, making CHK2, PLK1, and RAD51 promising drug targets for therapy-refractory TNBC. In conclusion, we present novel preclinical models of acquired drug resistance in TNBC and 58 novel candidate biomarkers for further investigation. Whole exome data and drug sensitivity profiles showed that each cancer cell line adaptation process follows an unpredictable route, which reflects recent findings on cancer cell evolution in patients, supporting the relevance of drug-adapted cancer cell lines as preclinical models of acquired resistance.

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Section: Resultsmentioning

confidence: 99%

“…3A, SupFile.4). These are large genes that are known to be commonly mutated and have been reported to be involved in cancer cell drug resistance [28][29][30][31][32] . De novo mutations in CDC27, which has also been linked to drug resistance in cancer, were also found in 9 resistant sublines 33,34 (Fig.…”

Section: Analysis Of the Distribution Of De Novo Variantsmentioning

confidence: 99%