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2. Segmentation and quantitation pipeline for image analysis from Targeting RNA-Polymerase I in Both Chemosensitive and Chemoresistant Populations in Epithelial Ovarian Cancer

Author

Cornelison, Robert, primary, Dobbin, Zachary C., primary, Katre, Ashwini A., primary, Jeong, Dae Hoon, primary, Zhang, Yinfeng, primary, Chen, Dongquan, primary, Petrova, Yuliya, primary, Llaneza, Danielle C., primary, Steg, Adam D., primary, Parsons, Laura, primary, Schneider, David A., primary, and Landen, Charles N., primary

Published
2023
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3. Supplementary Figure 1 from Targeting Aldehyde Dehydrogenase Cancer Stem Cells in Ovarian Cancer

Author

Landen, Charles N., primary, Goodman, Blake, primary, Katre, Ashwini A., primary, Steg, Adam D., primary, Nick, Alpa M., primary, Stone, Rebecca L., primary, Miller, Lance D., primary, Mejia, Pablo Vivas, primary, Jennings, Nicolas B., primary, Gershenson, David M., primary, Bast, Robert C., primary, Coleman, Robert L., primary, Lopez-Berestein, Gabriel, primary, and Sood, Anil K., primary

Published
2023
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5. Supplementary Table 1 from Endoglin (CD105) Contributes to Platinum Resistance and Is A Target for Tumor-Specific Therapy in Epithelial Ovarian Cancer

Author

Ziebarth, Angela J., primary, Nowsheen, Somaira, primary, Steg, Adam D., primary, Shah, Monjri M., primary, Katre, Ashwini A., primary, Dobbin, Zachary C., primary, Han, Hee-Dong, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Conner, Michael, primary, Yang, Eddy S., primary, and Landen, Charles N., primary

Published
2023
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7. Supplementary Figure 2 from Targeting Aldehyde Dehydrogenase Cancer Stem Cells in Ovarian Cancer

Author

Landen, Charles N., primary, Goodman, Blake, primary, Katre, Ashwini A., primary, Steg, Adam D., primary, Nick, Alpa M., primary, Stone, Rebecca L., primary, Miller, Lance D., primary, Mejia, Pablo Vivas, primary, Jennings, Nicolas B., primary, Gershenson, David M., primary, Bast, Robert C., primary, Coleman, Robert L., primary, Lopez-Berestein, Gabriel, primary, and Sood, Anil K., primary

Published
2023
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8. Supplementary Figure Legends from Targeting Aldehyde Dehydrogenase Cancer Stem Cells in Ovarian Cancer

Author

Landen, Charles N., primary, Goodman, Blake, primary, Katre, Ashwini A., primary, Steg, Adam D., primary, Nick, Alpa M., primary, Stone, Rebecca L., primary, Miller, Lance D., primary, Mejia, Pablo Vivas, primary, Jennings, Nicolas B., primary, Gershenson, David M., primary, Bast, Robert C., primary, Coleman, Robert L., primary, Lopez-Berestein, Gabriel, primary, and Sood, Anil K., primary

Published
2023
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18. Differential expression of breast cancer-associated genes between stage- and age-matched tumor specimens from African- and Caucasian-American Women diagnosed with breast cancer

Author

Grunda Jessica M, Steg Adam D, He Qinghua, Steciuk Mark R, Byan-Parker Suzanne, Johnson Martin R, and Grizzle William E

Subjects
Breast cancer, Gene expression, Race, Estrogen signaling, Cell cycle, Cell migration, Medicine, Biology (General), QH301-705.5, Science (General), Q1-390
Abstract

Abstract Background Recent studies suggest that the poorer breast cancer outcome observed in African-American women (AAW) may, in part, result from underlying molecular factors. The purpose of this study was to investigate gene expression differences between Caucasian-American women (CAW) and AAW that may contribute to this poorer prognosis. Methods The expression of 84 genes involved in breast carcinoma prognosis, response to therapy, estrogen signaling, and tumor aggressiveness was assessed in age- and stage-matched CAW and AAW paraffin-embedded breast cancer specimens. The Wilcoxon–Mann–Whitney Test was used to identify genes with a significant difference in expression between CAW and AAW. To determine if the differentially expressed genes could segregate between the CAW and AAW, we performed semi-supervised principal component analysis (SSPCA). Results Twenty genes were differentially expressed between AAW and CAW. SSPCA incorporating these 20 genes segregated AAW and CAW into two distinct groups. AAW were significantly (p < 0.05) more likely to display aberrations in G1/S cell-cycle regulatory genes, decreased expression of cell-adhesion genes, and low to no expression of ESR1, PGR, ERBB2 and estrogen pathway targets. Conclusions The gene expression differences identified between AAW and CAW may contribute to more aggressive disease, resistance to therapy, enhanced metastatic potential and poor clinical outcome. These findings support the hypothesis that breast cancer specimens collected from AAW display distinct gene expression differences compared to similar tissues obtained from CAW. Additional population-based studies are necessary to determine if these gene expression variations contribute to the highly aggressive and treatment-resistant breast cancer phenotype frequently observed in AAW.

Published
2012
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19. Targeting RNA-Polymerase I in Both Chemosensitive and Chemoresistant Populations in Epithelial Ovarian Cancer

Author

Cornelison, Robert, primary, Dobbin, Zachary C., additional, Katre, Ashwini A., additional, Jeong, Dae Hoon, additional, Zhang, Yinfeng, additional, Chen, Dongquan, additional, Petrova, Yuliya, additional, Llaneza, Danielle C., additional, Steg, Adam D., additional, Parsons, Laura, additional, Schneider, David A., additional, and Landen, Charles N., additional

Published
2017
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21. Simple regression for correcting ΔCt bias in RT-qPCR low-density array data normalization

Author

Cui, Xiangqin, primary, Yu, Shaohua, additional, Tamhane, Ashutosh, additional, Causey, Zenoria L, additional, Steg, Adam, additional, Danila, Maria I, additional, Reynolds, Richard J, additional, Wang, Jinyi, additional, Wanzeck, Keith C, additional, Tang, Qi, additional, Ledbetter, Stephanie S, additional, Redden, David T, additional, Johnson, Martin R, additional, and Bridges, S Louis, additional

Published
2015
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28. Endoglin (CD105) Contributes to Platinum Resistance and Is A Target for Tumor-Specific Therapy in Epithelial Ovarian Cancer

Author

Ziebarth, Angela J., primary, Nowsheen, Somaira, additional, Steg, Adam D., additional, Shah, Monjri M., additional, Katre, Ashwini A., additional, Dobbin, Zachary C., additional, Han, Hee-Dong, additional, Lopez-Berestein, Gabriel, additional, Sood, Anil K., additional, Conner, Michael, additional, Yang, Eddy S., additional, and Landen, Charles N., additional

Published
2013
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35. Targeting Aldehyde Dehydrogenase Cancer Stem Cells in Ovarian Cancer

Author

Landen, Charles N., primary, Goodman, Blake, additional, Katre, Ashwini A., additional, Steg, Adam D., additional, Nick, Alpa M., additional, Stone, Rebecca L., additional, Miller, Lance D., additional, Mejia, Pablo Vivas, additional, Jennings, Nicolas B., additional, Gershenson, David M., additional, Bast, Robert C., additional, Coleman, Robert L., additional, Lopez-Berestein, Gabriel, additional, and Sood, Anil K., additional

Published
2010
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40. Phase II Study of Capecitabine With Concomitant Radiotherapy for Patients With Locally Advanced Pancreatic Cancer: Up-Regulation of Thymidine Phosphorylase

Author

Saif, Muhammad Wasif, primary, Black, Glenda, additional, Roy, Shalija, additional, Bell, Diana, additional, Russo, Suzanne, additional, Eloubeidi, Mohamed A, additional, Steg, Adam, additional, Johnson, Martin R., additional, Zelterman, Daniel, additional, and Diasio, Robert B., additional

Published
2007
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41. Hedgehog signaling and response to cyclopamine differs in epithelial and stromal cells in benign breast and breast cancer

Author

Mukherjee, Shibani, primary, Frolova, Natalya, additional, Sadlonova, Andrea, additional, Novak, Zdenek, additional, Steg, Adam, additional, Page, Grier, additional, Welch, Danny R., additional, Lobo-Ruppert, Susan M., additional, Ruppert, J. Michael, additional, Johnson, Martin R., additional, and Frost, Andra R., additional

Published
2006
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42. Simple regression for correcting ΔCt bias in RT-qPCR low-density array data normalization.

Author

Xiangqin Cui, Shaohua Yu, Tamhane, Ashutosh, Causey, Zenoria L., Steg, Adam, Danila, Maria I., Reynolds, Richard J., Jinyi Wang, Wanzeck, Keith C., Qi Tang, Ledbetter, Stephanie S., Redden, David T., Johnson, Martin R., and Bridges Jr., S. Louis

Subjects
GENE expression, REGRESSION analysis, RHEUMATOID arthritis, GENOMICS, QUANTITATIVE research
Abstract

Background: Reverse transcription quantitative PCR (RT-qPCR) is considered the gold standard for quantifying relative gene expression. Normalization of RT-qPCR data is commonly achieved by subtracting the Ct values of the internal reference genes from the Ct values of the target genes to obtain ΔCt. ΔCt values are then used to derive ΔΔCt when compared to a control group or to conduct further statistical analysis. Results: We examined two rheumatoid arthritis RT-qPCR low density array datasets and found that this normalization method introduces substantial bias due to differences in PCR amplification efficiency among genes. This bias results in undesirable correlations between target genes and reference genes, which affect the estimation of fold changes and the tests for differentially expressed genes. Similar biases were also found in multiple public mRNA and miRNA RT-qPCR array datasets we analysed. We propose to regress the Ct values of the target genes onto those of the reference genes to obtain regression coefficients, which are then used to adjust the reference gene Ct values before calculating ΔCt. Conclusions: The per-gene regression method effectively removes the ΔCt bias. This method can be applied to both low density RT-qPCR arrays and individual RT-qPCR assays. [ABSTRACT FROM AUTHOR]

Published
2015
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44. Phase II Study of Capecitabine With Concomitant Radiotherapy for Patients With Locally Advanced Pancreatic Cancer: Up-Regulation of Thymidine Phosphorylase.

Author

Wasif Saif, Muhammad, Black, Glenda, Roy, Shalija, Bell, Diana, Russo, Suzanne, Eloubeidi, Mohamed A., Steg, Adam, Johnson, Martin R., Zelterman, Daniel, and Diasio, Robert B.

Subjects
RADIATION, THYMIDINE, TUMOR necrosis factors, PANCREATIC cancer, CANCER patients
Abstract

Purpose: The objectives of this phase 11 study were to evaluate the effect of radiation (XRT) on thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD), and tumor necrosis factor-α (TNF-α) and the efficacy of capecitabine-XRT in patients with locally advanced pancreatic cancer. Patients and Methods: Twenty patients received 50.4 Gy XRT with capecitabine 1,600 mg/m² on Monday through Friday for 6 weeks determined from our phase I study (Saif MW, Eloubeidi MA, Russo S, et al. J Clin Oncol. 2005:23:8679-8687). After capecitabine- XRT, stable and responding patients received capecitabine 2,000 mg/m² for 14 days every 3 weeks till progression. Restaging was performed every 9 weeks. Tumor specimens were procured with endoscopic ultrasound-fine needle aspiration before and at week 2 after capecitabine-XRT was started to evaluate the effect of XRT on TP, DPD, and TNF-α mRNA levels, determined by reverse transcriptase- polymerase chain reaction. Results: Among 20 patients, 4 (20%) had a partial response and 13 (65%) had stable disease. Two patients underwent surgical resection (10%). The 6-month survival rate was 84%, and the 1-year survival was 58%. Grade ≥3 toxicities included nausea/vomiting (5%), thrombosis (5%), hyperbilirubinemia (5%), and grade 3 gastrointestinal bleeding (5%). TP was elevated during week 2 when compared with the pre-XRT TP (P = 0.01). However, no such effect of XRT was found either on DPD {P = 0.22) or on TNF-α (P = 0.6). No correlation between TP and TNF-α was noticed. Also, no association between TP/DPD ratio and efficacy of capecitabine was identified. Conclusions: This phase II study further confirms our phase I results and suggests that capecitabine-XRT is an effective, tolerable, and convenient alternative to an infusional 5-fluorouracil regimen for patients with pancreatic cancer. Although results support the use of capecitabine-XRT and TP was up-regulated, [ABSTRACT FROM AUTHOR]

Published
2007
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45. Long-term survival on capecitabine in two gemcitabine refractory pancreatic cancer patients. Is there a pharmacogenetic explanation?

Author

Saif MW, Kang SP, Ledbetter L, Steg A, Diasio R, and Johnson M

Subjects
Adenocarcinoma metabolism, Biomarkers metabolism, Capecitabine, Deoxycytidine therapeutic use, Dihydrouracil Dehydrogenase (NADP) metabolism, Female, Fluorouracil therapeutic use, Humans, Male, Middle Aged, Pancreatic Neoplasms metabolism, Pharmacogenetics, Survival Analysis, Thymidine Phosphorylase metabolism, Treatment Outcome, Gemcitabine, Adenocarcinoma drug therapy, Antimetabolites, Antineoplastic therapeutic use, Deoxycytidine analogs & derivatives, Fluorouracil analogs & derivatives, Pancreatic Neoplasms drug therapy
Abstract

Context: Capecitabine has shown efficacy in treatment of metastatic pancreatic cancer. Several researchers have identified thymidine phosphorylase, dihydropyrimidine dehydrogenase, or their ratio as indicators of response to capecitabine in various cancers., Case Report: We report two patients with metastatic pancreatic carcinoma who had long-term survivals on capecitabine after gemcitabine failure. These two cases prompted us to measure thymidine phosphorylase and dihydropyrimidine dehydrogenase levels to facilitate discourses regarding their relationship with efficacy of capecitabine. We also describe a novel method of measuring thymidine phosphorylase level from serum without an invasive tissue biopsy. One patient is alive as of today, with improved performance status, 50 months after capecitabine was started. CA 19-9 and CT scans remained stable during 57 cycles. Her thymidine phosphorylase level was 1.77 compared to a control level of 1.00. Dihydropyrimidine dehydrogenase level was 4.14 compared to a control level of 1.00. Their ratio was 0.43. The other patient was alive on capecitabine for 24 months. His performance status, bilirubin, AST, and ALT improved on capecitabine. CT scans and CA 19-9 remained stable during this period. He had thymidine phosphorylase level of 5.56, dihydropyrimidine dehydrogenase level of 2.74, and their ratio of 2.03., Conclusion: Capecitabine resulted in long term survivals in two patients with metastatic pancreatic cancer after gemcitabine failure. The use of capecitabine as second-line treatment in metastatic pancreatic cancer should be further explored along with the role of thymidine phosphorylase and dihydropyrimidine dehydrogenase levels in its activity. A non-invasive method of thymidine phosphorylase measurement we described should be validated in larger trials.

Published
2007

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