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266 results on '"Pan, Quintin"'

5. Derivation of a comprehensive semi-empirical proton RBE model from published experimental cell survival data collected in the PIDE database.

Author

Jin, Jian-Yue, Yuan, Jiankui, Qin, Xiaohang, Li, Yinghui, Yan, Huagang, Oleinick, Nancy L., Yao, Min, Pan, Quintin, Kong, Feng-Ming, and Machtay, Mitchell

Subjects
LINEAR energy transfer, CELL survival, CURVE fitting, PROTON therapy, CELL lines
Abstract

We aimed to develop a comprehensive proton relative biological effectiveness (RBE) model based on accumulated cell survival data in the literature. Our approach includes four major components: (1) Eligible cell survival data with various linear energy transfers (LETs) in the Particle Irradiation Data Ensemble (PIDE) database (72 datasets in four cell lines); (2) a cell survival model based on Poisson equation, with α and β defined as the ability to generate and repair damage, respectively, to replace the classic linear–quadratic model for fitting the cell survival data; (3) hypothetical linear relations of α and β on LET, or α (L E T) α x = α α + b α ∗ L E T and β (L E T) β x = α β − b β ∗ L E T ; and (4) a multi-curve fitting (MCF) approach to fit all cell survival data into the survival model and derive the aα , bα , aβ , and bβ values for each cell line. Dependences of these parameters on cell type were thus determined and finally a comprehensive RBE model was derived. MCF showed that (aα , bα , aβ , bβ) = (1.09, 0.0010, 0.96, 0.033), (1.10, 0.0015, 1.03, 0.023), (1.12, 0.0025, 0.99, 0.0085), and (1.17, 0.0025, 0.99, 0.013) for the four cell lines, respectively. Thus, aα = 1.12 ± 0.04, bα = 0.0019 ± 0.0008, aβ = 0.99 ± 0.03, and bβ = 0.013 ∗ αx , and approximately α ∼ 1.12 ∗ α x and β = (0.99 − 0.013 ∗ α x ∗ L E T) ∗ β x . Consequently, a relatively reliable and comprehensive RBE model with dependence on LET, αx , βx , and dose per fraction was finally derived for potential clinical application. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Association of artificial intelligence–derived collagen disorder architecture (CoDA) features with survival outcome and objective response to immune checkpoint inhibitors in patients with head and neck squamous cell carcinoma.

Author

Nag, Reetoja, primary, Li, Haojia, additional, Corredor, Germán, additional, Fu, Pingfu, additional, Khalighi, Sirvan, additional, Steward-Tharp, Scott Michael, additional, Patel, Mihir R., additional, Schmitt, Nicole C., additional, Shi, Qiuying, additional, Toro, Paula, additional, Pathak, Tilak, additional, Pandav, Krunal, additional, Wasman, Jay, additional, Teknos, Theodoros Nicholas, additional, Trzcinska, Anna Michalina, additional, Patel, Monaliben, additional, Pan, Quintin, additional, Saba, Nabil F., additional, Lewis Jr., James, additional, and Madabhushi, Anant, additional

Published
2024
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13. Supplementary Figures S1-S22 from Integrative Analysis of a Large Real-World Cohort of Small Cell Lung Cancer Identifies Distinct Genetic Subtypes and Insights into Histologic Transformation

Author

Sivakumar, Smruthy, primary, Moore, Jay A., primary, Montesion, Meagan, primary, Sharaf, Radwa, primary, Lin, Douglas I., primary, Colón, Caterina I., primary, Fleishmann, Zoe, primary, Ebot, Ericka M., primary, Newberg, Justin Y., primary, Mills, Jennifer M., primary, Hegde, Priti S., primary, Pan, Quintin, primary, Dowlati, Afshin, primary, Frampton, Garrett M., primary, Sage, Julien, primary, and Lovly, Christine M., primary

Published
2023
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19. Integrative Analysis of a Large Real-World Cohort of Small Cell Lung Cancer Identifies Distinct Genetic Subtypes and Insights into Histologic Transformation

Author

Sivakumar, Smruthy, primary, Moore, Jay A., additional, Montesion, Meagan, additional, Sharaf, Radwa, additional, Lin, Douglas I., additional, Colón, Caterina I., additional, Fleishmann, Zoe, additional, Ebot, Ericka M., additional, Newberg, Justin Y., additional, Mills, Jennifer M., additional, Hegde, Priti S., additional, Pan, Quintin, additional, Dowlati, Afshin, additional, Frampton, Garrett M., additional, Sage, Julien, additional, and Lovly, Christine M., additional

Published
2023
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26. Image analysis reveals differences in tumor multinucleations in Black and White patients with human papillomavirus‐associated oropharyngeal squamous cell carcinoma

Author

Koyuncu, Can F., primary, Nag, Reetoja, additional, Lu, Cheng, additional, Corredor, Germán, additional, Viswanathan, Vidya S., additional, Sandulache, Vlad C., additional, Fu, Pingfu, additional, Yang, Kailin, additional, Pan, Quintin, additional, Zhang, Zelin, additional, Xu, Jun, additional, Chute, Deborah J., additional, Thorstad, Wade L., additional, Faraji, Farhoud, additional, Bishop, Justin A., additional, Mehrad, Mitra, additional, Castro, Patricia D., additional, Sikora, Andrew G., additional, Thompson, Lester D.R., additional, Chernock, Rebecca D., additional, Lang Kuhs, Krystle A., additional, Wasman, Jay K., additional, Luo, Jingqin R., additional, Adelstein, David J., additional, Koyfman, Shlomo A., additional, Lewis Jr, James S., additional, and Madabhushi, Anant, additional

Published
2022
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30. Treatment failure patterns are similar between p16− and p16+ oropharyngeal squamous cell carcinomas

Author

Hamill, Chelsea S., primary, Muller, Richard Grant, additional, Clancy, Kate, additional, Vu, Brandon, additional, Gui, Shanying, additional, Thuener, Jason Eric, additional, Wasman, Jay, additional, Li, Shawn, additional, Fowler, Nicole, additional, Rezaee, Rod, additional, Lavertu, Pierre, additional, Teknos, Theodoros N., additional, Pan, Quintin, additional, and O'Neill, Wendi Quinn, additional

Published
2022
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33. Repositioning Fenofibrate to Reactivate p53 and Reprogram the Tumor-Immune Microenvironment in HPV+ Head and Neck Squamous Cell Carcinoma

Author

O’Neill, W. Quinn, primary, Xie, Xiujie, additional, Gui, Shanying, additional, Yu, Heping, additional, Davenport, Jacqueline, additional, Cartwright, Thomas, additional, Storl-Desmond, Marta, additional, Ryu, Esther, additional, Chan, Ernest R., additional, Cao, Shufen, additional, Fu, Pingfu, additional, Teknos, Theodoros N., additional, and Pan, Quintin, additional

Published
2022
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35. Impact of p16 Status and Anatomical Site in Anti-PD-1 Immunotherapy-Treated Recurrent/Metastatic Head and Neck Squamous Cell Carcinoma Patients

Author

Clancy, Kate, primary, Hamill, Chelsea S., additional, O’Neill, Wendi Q., additional, Vu, Brandon, additional, Thuener, Jason, additional, Gui, Shanying, additional, Li, Shawn, additional, Fowler, Nicole, additional, Rezaee, Rod, additional, Lavertu, Pierre, additional, Wasman, Jay, additional, Patel, Monaliben, additional, Shaikh, Hira, additional, Vick, Eric, additional, Madabhushi, Anant, additional, Wise-Draper, Trisha M., additional, Burkitt, Kyunghee, additional, Teknos, Theodoros N., additional, and Pan, Quintin, additional

Published
2021
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39. African Americans With p16+ and p16− Oropharyngeal Squamous Cell Carcinomas Have Distinctly Poor Treatment Outcomes Independent of Medical Care Access

Author

O'Neill, W. Quinn, primary, Wasman, Jay, additional, Thuener, Jason, additional, Chatfield-Reed, Kate, additional, Lukesic, Lizabeth, additional, Kyasram, Ravi, additional, Shanahan, John, additional, Szelesety, Blake, additional, Vu, Brandon, additional, Lavertu, Pierre, additional, Rezaee, Rod, additional, Li, Shawn, additional, Fowler, Nicole, additional, Teknos, Theodoros N., additional, and Pan, Quintin, additional

Published
2021
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44. Current and future management of recurrent respiratory papillomatosis

Author

Ivancic, Ryan, Iqbal, Hassan, deSilva, Brad, Pan, Quintin, and Matrka, Laura

Subjects
microdebrider, vaccine, General Otolaryngology, Recurrent respiratory papillomatosis (RRP), laryngeal papillomatosis, Review, human papillomavirus (HPV)
Abstract

Objectives Recurrent respiratory papillomatosis (RRP) is a chronic disease of the respiratory tract that occurs in both children and adults. It is caused by the human papillomavirus (HPV), in particular low‐risk HPV6 and HPV11, and aggressiveness varies among patients. RRP remains a chronic disease that is difficult to manage. This review provides perspectives on current and future management of RRP. Results The current standard of care is surgical excision, with adjuvant therapies as needed. Surgical management of RRP has evolved with the introduction of microdebriders and photoangiolytic lasers; the latter can now be used in the office setting. Numerous adjuvant pharmacologic therapies have been utilized with some success. Also, exciting preliminary data show that HPV vaccines may prolong the time to recurrence in the RRP population. There is also optimism that wide‐spread HPV vaccination could reduce RRP incidence indirectly by preventing vertical HPV transmission to newborns. Conclusion To date, the biology of RRP is not well understood, although it has been noted to become more aggressive in the setting of immune suppression. Additional research is needed to better understand immune system dysfunction in RRP such that immunomodulatory approaches may be developed for RRP management. Level of Evidence 4

Published
2018

46. Prognostic factors in oral cavity and oropharyngeal squamous cell carcinoma

Author

Marcus, Benjamin, Arenberg, Douglas, Lee, Julia, Kleer, Celina, Chepeha, Douglas B., Schmalbach, Cecelia E., Islam, Mozaffarul, Paul, Supriti, Pan, Quintin, Hanash, Samir, Kuick, Rork, Merajver, Sofia D., and Teknos, Theodoros N.

Subjects
Mouth cancer -- Diagnosis, Throat cancer -- Diagnosis, Health
Published
2004

49. Tetrathiomolybdate inhibits head and neck cancer metastasis by decreasing tumor cell motility, invasiveness and by promoting tumor cell anoikis

Author

Merajver Sofia D, Pan Quintin, Islam Mozaffarul, Patel Samip N, Yadav Arti, Kumar Pawan, and Teknos Theodoros N

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background The metastatic spread of solid tumors is directly or indirectly responsible for most cancer-related deaths. Tumor metastasis is very complex and this process requires a tumor cell to acquire enhanced motility, invasiveness and anoikis resistance to successfully establish a tumor at a distal site. Metastatic potential of tumor cells is directly correlated with the expression levels of several angiogenic cytokines. Copper is a mandatory cofactor for the function of many of these angiogenic mediators as well as other proteins that play an important role in tumor cell motility and invasiveness. We have previously shown that tetrathiomolybdate (TM) is a potent chelator of copper and it mediates its anti-tumor effects by suppressing tumor angiogenesis. However, very little is known about the effect of TM on tumor cell function and tumor metastasis. In this study, we explored the mechanisms underlying TM-mediated inhibition of tumor metastasis. Results We used two in vivo models to examine the effects of TM on tumor metastasis. Animals treated with TM showed a significant decrease in lung metastasis in both in vivo models as compared to the control group. In addition, tumor cells from the lungs of TM treated animals developed significantly smaller colonies and these colonies had significantly fewer tumor cells. TM treatment significantly decreased tumor cell motility and invasiveness by inhibiting lysyl oxidase (LOX) activity, FAK activation and MMP2 levels. Furthermore, TM treatment significantly enhanced tumor cell anoikis by activating p38 MAPK cell death pathway and by downregulating XIAP survival protein expression. Conclusions Taken together, these results suggest that TM is a potent suppressor of head and neck tumor metastasis by modulating key regulators of tumor cell motility, invasiveness and anoikis resistance.

Published
2010
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50. Protein kinase Cε: an oncogene and emerging tumor biomarker

Author

Pan Quintin and Gorin Michael A

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Members of the protein kinase C (PKC) family have long been studied for their contributions to oncogenesis. Among the ten different isoforms of this family of serine/threonine kinases, protein kinase Cε (PKCε) is one of the best understood for its role as a transforming oncogene. In vitro, overexpression of PKCε has been demonstrated to increase proliferation, motility, and invasion of fibroblasts or immortalized epithelial cells. In addition, xenograft and transgenic animal models have clearly shown that overexpression of PKCε is tumorigenic resulting in metastatic disease. Perhaps most important in implicating the epsilon isoform in oncogenesis, PKCε has been found to be overexpressed in tumor-derived cell lines and histopathological tumor specimens from various organ sites. Combined, this body of work provides substantial evidence implicating PKCε as a transforming oncogene that plays a crucial role in establishing an aggressive metastatichenotype. Reviewed here is the literature that has led to the current understanding of PKCε as an oncogene. Moreover, this review focuses on the PKCε-mediated signaling network for cell motility and explores the interaction of PKCε with three major PKCε signaling nodes: RhoA/C, STAT3 and Akt. Lastly, the emerging role of PKCε as a tumor biomarker is discussed.

Published
2009
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