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Mark Long

As seen in: Nature, BMJ Oncology, MDPI, The BMJ, The Motley Fool (U.S.), BioRxiv, Cell Reports, GIGAZINE, KRIV-TV (Houston, TX), Jackson Hole Daily and
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Articles

M1C is a druggable target for NSCLC KRAS G12C mutant tumors resistant to KRAS inhibitors

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By Shinkichi Takamori, Naoki Haratake, Hiroki Ozawa, Keisuke Shigeta, Kentaro Nonaka, Takefumi Komiya, Hiroki Komatsuda, Tomoyoshi Takenaka, Tomoharu Yoshizumi, Chendi Li, Jiehui Deng, Aaron N. Hata, Kwok Wong, Mark Long, Atrayee Bhattacharya, Mai Onishi, Donald Kufe
| Nature Verified
Abstract Treatment of NSCLC KRAS G12C mutant tumors with the allele-selective sotorasib and adagrasib inhibitors is invariably associated with acquired resistance. The MUC1-encoded oncogenic M1C protein is necessary for self-renewal of NSCLC KRAS mutant cells. We report that treatment of NSCLC KRAS G12C cells with sotorasib induces M1C expression by a STAT1-dependent pathway.
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MUC1-C auto-regulatory complex with EBNA1 is responsible for latent Epstein-Barr virus-associated gastric cancer progression - Oncogene

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By Hiroki Ozawa, Henry Withers, Keyi Wang, Mark Long
| Nature Verified
Abstract Latent Epstein-Barr Virus (EBV) infection promotes cancers derived from B-lymphocytes and epithelial cells by mechanisms that largely remain unclear. EBV-encoded nuclear antigen 1 (EBNA1) is uniformly expressed in EBV-associated cancers; however, how EBNA1 contributes to cancer progression is not known. The MUC1 gene evolved in mammals to protect barrier tissues from viral infections. We report that MUC1 is upregulated in EBV-associated gastric cancers (EBVaGCs).
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Associations of DNA methylation in breast tumour subtypes with parity and breastfeeding in a cohort of 1459 Black women: implications for public health

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By Christine B. Ambrosone, Song T. Yao, Mark Long, Chunyu Liu
| BMJ Oncology Verified
Except for suggestive evidence from one small pilot study, it is unknown why women who have children and do not breastfeed are more likely to develop oestrogen receptor (ER) negative (ER−) breast cancer. We formed a consortium and conducted the largest genome-wide study of DNA methylation to date (n=1459 Black women with breast cancer) to determine if methylation is the contributing mechanism and to identify the pathways involved, which could have implications for prevention.
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