Chieko Michikawa

The University of Texas MD Anderson Cancer Center

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Jeffrey N. Myers

The University of Texas MD Anderson Cancer Center

Vlad C. Sandulache

Baylor College of Medicine

Abdullah A. Osman

The University of Texas MD Anderson Cancer Center

Jing Wang

The University of Texas MD Anderson Cancer Center

Mitchell J. Frederick

Baylor College of Medicine

Katarzyna Tomczak

The University of Texas MD Anderson Cancer Center

Mason Bartels

Baylor College of Medicine

Kunal Rai

The University of Texas MD Anderson Cancer Center

Timothy P. Heffernan

The University of Texas MD Anderson Cancer Center

Li Shen

The University of Texas MD Anderson Cancer Center

Cooperative Institutions

The University of Texas MD Anderson Cancer Center

Tokyo Medical and Dental University

Baylor College of Medicine

The University of Texas Health Science Center at Houston

Massachusetts General Hospital

Wayne State University

University of Florida

Florida College

The University of Tokyo

University of Pittsburgh

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Supplementary Figure S1 from Dysregulation and Epigenetic Reprogramming of NRF2 Signaling Axis Promote Acquisition of Cisplatin Resistance and Metastasis in Head and Neck Squamous Cell Carcinoma

Abdullah A. Osman Emre Arslan Mason Bartels Chieko Michikawa Antje Lindemann

Cisplatin resistant HNSCC cells migrate faster than their Cisplatin sensitive counterparts.

Reprogramming

10.1158/1078-0432.22490683

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Supplementary Table S1 from Dysregulation and Epigenetic Reprogramming of NRF2 Signaling Axis Promote Acquisition of Cisplatin Resistance and Metastasis in Head and Neck Squamous Cell Carcinoma

Abdullah A. Osman Emre Arslan Mason Bartels Chieko Michikawa Antje Lindemann

In vivo RNA sequencing and pair-wise comparison between 4 distinct groups in HN30-P and HN30-R8 HNSCC tumors.

Reprogramming

10.1158/1078-0432.22490653.v1

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Supplementary Table S5 from Dysregulation and Epigenetic Reprogramming of NRF2 Signaling Axis Promote Acquisition of Cisplatin Resistance and Metastasis in Head and Neck Squamous Cell Carcinoma

Abdullah A. Osman Emre Arslan Mason Bartels Chieko Michikawa Antje Lindemann

Supplementary Table S5A. Bulk-level single cell ATAC sequencing analysis showing immediate (short-term) chromatin openings (peaks) in HN30-P cells following CDDP treatment; Supplementary Table S5B. Bulk-level single cell ATAC sequencing analysis showing long-term chromatin openings (peaks) gained in cisplatin-resistant HN30-R8 cells following CDDP treatment.

Reprogramming

10.1158/1078-0432.22490641

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Supplementary Figure S6 from Dysregulation and Epigenetic Reprogramming of NRF2 Signaling Axis Promote Acquisition of Cisplatin Resistance and Metastasis in Head and Neck Squamous Cell Carcinoma

Abdullah A. Osman Emre Arslan Mason Bartels Chieko Michikawa Antje Lindemann

Cisplatin sensitivity following knockdown of NRF2 or restoration of wildtype KEAP1 in cisplatin resistant HNSCC cells is not mediated through apoptosis.

Reprogramming

10.1158/1078-0432.22490668.v1

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Data from High-Risk TP53 Mutations Are Associated with Extranodal Extension in Oral Cavity Squamous Cell Carcinoma

Vlad C. Sandulache Chieko Michikawa Pranav Kataria Frederico O. Gleber‐Netto Diana Bell

<div>AbstractPurpose: Development of extranodal extension (ENE) has been associated with poor survival in patients with oral cavity squamous cell carcinoma (OSCC). Here, we sought to confirm the role of ENE as a poor prognostic factor, and identify genomic and epigenetic markers of ENE in order to develop a predictive model and improve treatment selection.Experimental Design: An institutional cohort (The University of Texas MD Anderson Cancer Center) was utilized to confirm the impact of ENE on clinical outcomes and evaluate the genomic signature of primary and ENE containing tissue. OSCC data from The Cancer Genome Atlas (TCGA) were analyzed for the presence of molecular events associated with nodal and ENE status.Results: ENE was associated with decreased overall and disease-free survival. Mutation of the TP53 gene was the most common event in ENE+ OSCC. The frequency of TP53 mutation in ENE+ tumors was higher compared with ENE− tumors and wild-type (WT) TP53 was highly represented in pN0 tumors. pN+ENE+ patients had the highest proportion of high-risk TP53 mutations. Both primary tumors (PT) and lymph nodes with ENE (LN) exhibited a high rate of TP53 mutations (58.8% and 58.8%, respectively) with no significant change in allele frequency between the two tissue sites.Conclusions: ENE is one of the most significant markers of OSCC OS and DFS. There is a shift toward a more aggressive biological phenotype associated with high-risk mutations of the TP53 gene. Prospective clinical trials are required to determine whether TP53 mutational status can be used for personalized treatment decisions. Clin Cancer Res; 24(7); 1727–33. ©2018 AACR.</div>

10.1158/1078-0432.c.6525755

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Table S5 from High-Risk TP53 Mutations Are Associated with Extranodal Extension in Oral Cavity Squamous Cell Carcinoma

Vlad C. Sandulache Chieko Michikawa Pranav Kataria Frederico O. Gleber‐Netto Diana Bell

Table S5 from High-Risk TP53 Mutations Are Associated with Extranodal Extension in Oral Cavity Squamous Cell Carcinoma

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10.1158/1078-0432.22464605.v1

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Table S9 from High-Risk TP53 Mutations Are Associated with Extranodal Extension in Oral Cavity Squamous Cell Carcinoma

Vlad C. Sandulache Chieko Michikawa Pranav Kataria Frederico O. Gleber‐Netto Diana Bell

Table S9 from High-Risk TP53 Mutations Are Associated with Extranodal Extension in Oral Cavity Squamous Cell Carcinoma

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10.1158/1078-0432.22464587.v1

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Table S3 from High-Risk TP53 Mutations Are Associated with Extranodal Extension in Oral Cavity Squamous Cell Carcinoma

Vlad C. Sandulache Chieko Michikawa Pranav Kataria Frederico O. Gleber‐Netto Diana Bell

Supp Table 3

Table (database)

10.1158/1078-0432.22464611.v1

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Supplementary Table S5 from Dysregulation and Epigenetic Reprogramming of NRF2 Signaling Axis Promote Acquisition of Cisplatin Resistance and Metastasis in Head and Neck Squamous Cell Carcinoma

Abdullah A. Osman Emre Arslan Mason Bartels Chieko Michikawa Antje Lindemann

Reprogramming

Single-Cell Analysis

10.1158/1078-0432.22494738.v1

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Gene expression changes in initiation and progression of oral squamous cell carcinomas revealed by laser microdissection and oligonucleotide microarray analysis

International Journal of Cancer (2012)

Jun Sumino Narikazu Uzawa Norihiko Okada Ken Miyaguchi Kaoru Mogushi

Abstract Oral carcinogenesis is a complex process involving multiple genes. However, the genetic changes involved in this process are not apparent in identical oral squamous cell carcinomas (OSCCs). According to pathological characteristics, samples of normal tissue, oral dysplastic lesions (ODLs), and invasive cancers were obtained from identical OSCCs using laser microdissection (LMD). Large‐scale gene expression profiling was carried out on 33 samples derived from 11 OSCCs. We analyzed genes differentially expressed in normal tissues vs . ODLs and in ODLs vs . invasive tumors and identified 15 candidate genes with continuously increasing or decreasing expression during oral carcinogenesis. One of these genes, ISG15 , was chosen for further characterization. Real‐time quantitative reverse transcription‐polymerase chain reaction and immunohistochemical analysis confirmed that ISG15 expression consistently increased during oral tumorigenesis. An ISG15 high‐expression level was significantly associated with poor prognosis ( p = 0.027). In addition, patients with high‐expression tumors had a poorer 5‐year survival rate than patients with low expression levels ( p = 0.019). In conclusion, we identified 15 genes with continuously increasing or decreasing expression during oral carcinogenesis. One of these, ISG15 , is likely to be associated with both dysgenesis and tumorigenesis and may be a potential prognostic marker for oral cancer.

Laser capture microdissection

Microdissection

10.1002/ijc.27702

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