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J Cancer Metastasis Treat 2020;6:5 I http://dx.doi.org/10.20517/2394-4722.2020.13 Page 9 of 38

I am a radiation oncologist at MD Anderson Cancer Center with a large proportion of my practice
dedicated to prostate cancer. I would like to update the audience with the basic algorithms of radiation,
hormonal, and systemic therapy for low, intermediate, and high risk. This talk would include information
on active surveillance, definitive radiation treatment, brachytherapy as single modality and boost treatment,
adjuvant and salvage (post-operative) radiation therapy, and hypofractionation and stereotactic body
radiation therapy. I understand the audience is a variety of clinicians in the medical field. I would tailor the
talk to provide an overview so all can understand what is available to all prostate cancer patients and the
updated studies to support these recommendations.

12. Novel DNA modification in cancer

2
1,#
1
4
4
Tao P. Wu 2,6,# , Qi Xie , Ryan C. Gimple 1,3,# , Zheng Li , Qiulian Wu , Yang Yu , Yinsheng Wang ,
Shideng Bao , Andrew Z. Xiao , Jeremy N. Rich 1
5
2
1 Department of Medicine, Division of Regenerative Medicine, University of California, San Diego, La Jolla, CA
92037, USA.
2 Department of Genetics and Yale Stem Cell Center, Yale School of Medicine, New Haven, CT 06520, USA.
3 Department of Pathology, Case Western Reserve University, Cleveland, OH 44120, USA.
4 Department of Chemistry, University of California, Riverside, Riverside, CA 92521, USA.
5 Department of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic,
Cleveland, OH 44195, USA.
6 Present address: Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor
Plaza, Houston, TX 77030, USA.
# Co-equal first authors.

Genetic drivers of cancer can be dysregulated through epigenetic modifications of DNA. Although the
critical role of DNA 5-methylcytosine (5mC) in the regulation of transcription is recognized, the functions
of other non-canonical DNA modifications remain obscure.

We report the identification of novel DNA N6-methyladenine (N6-mA) modifications in human tissues
and implicate this epigenetic mark in human disease, specifically the highly malignant brain cancer
glioblastoma. Glioblastoma markedly upregulated N6-mA levels, which co-localized with heterochromatic
histone modifications, predominantly H3K9me3. N6-mA levels were dynamically regulated by the DNA
demethylase ALKBH1, depletion of which led to transcriptional silencing of oncogenic pathways through
decreasing chromatin accessibility. Targeting the N6-mA regulator ALKBH1 in patient-derived human
glioblastoma models inhibited tumor cell proliferation and extended the survival of tumor-bearing mice,
supporting this novel DNA modification as a potential therapeutic target for glioblastoma.

Furthermore, ALKBH1 controls the hypoxia responding genes in glioblastoma. Collectively, our results
uncover a novel epigenetic node in cancer through the DNA modification N6-mA. The regulators of this
new modification could serve as novel therapeutic targets in cancer therapy.

13. Evaluation of undiagnosed liver masses that do not exhibit typical imaging features,
including even Stage C HCC

Metin Basaranoglu

Bezmialem Vakif University, İstanbul 34093, Turkey.