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3. Temporal patterns of cancer burden in Asia, 1990–2019: a systematic examination for the Global Burden of Disease 2019 study

Author

Sharma, Rajesh, Abbastabar, Hedayat, Abdulah, Deldar Morad, Abidi, Hassan, Abolhassani, Hassan, Abrehdari-Tafreshi, Zahra, Absalan, Abdorrahim, Ali, Hiwa Abubaker, Abu-Gharbieh, Eman, Acuna, Juan Manuel, Adib, Nasrin, Sakilah Adnani, Qorinah Estiningtyas, Aghaei, Abbas, Ahmad, Aqeel, Ahmad, Sajjad, Ahmadi, Ali, Ahmadi, Sepideh, Ahmed, Luai A., Ajami, Marjan, Al Hamad, Hanadi, Al Hasan, Syed Mahfuz, Alanezi, Fahad Mashhour, Saeed Al-Gheethi, Adel Ali, Al-Hanawi, Mohammed Khaled, Ali, Abid, Ali, Beriwan Abdulqadir, Alimohamadi, Yousef, Aljunid, Syed Mohamed, Ali Al-Maweri, Sadeq Ali, Alqahatni, Saleh A., AlQudah, Mohammad, Al-Raddadi, Rajaa M., Al-Tammemi, Ala'a B., Ansari-Moghaddam, Alireza, Anwar, Sumadi Lukman, Anwer, Razique, Aqeel, Muhammad, Arabloo, Jalal, Arab-Zozani, Morteza, Ariffin, Hany, Artaman, Al, Arulappan, Judie, Ashraf, Tahira, Askari, Elaheh, Athar, Mohammad, Wahbi Atout, Maha Moh'd, Azadnajafabad, Sina, Badar, Muhammad, Badiye, Ashish D., Baghcheghi, Nayereh, Bagherieh, Sara, Bai, Ruhai, Bajbouj, Khuloud, Baliga, Shrikala, Bardhan, Mainak, Bashiri, Azadeh, Baskaran, Pritish, Basu, Saurav, Belgaumi, Uzma Iqbal, Nazer C Bermudez, Amiel, Bhandari, Bharti, Bhardwaj, Nikha, Bhat, Ajay Nagesh, Bitaraf, Saeid, Boloor, Archith, Hashemi, Milad Bonakdar, Butt, Zahid A., Chadwick, Joshua, Kai Chan, Jeffrey Shi, Chattu, Vijay Kumar, Chaturvedi, Pankaj, Cho, William C.S., Darwesh, Aso Mohammad, Dash, Nihar Ranjan, Dehghan, Amin, Dhali, Arkadeep, Dianatinasab, Mostafa, Dibas, Mahmoud, Dixit, Abhinav, Dixit, Shilpi Gupta, Dorostkar, Fariba, Dsouza, Haneil Larson, Elbarazi, Iffat, Elemam, Noha Mousaad, El-Huneidi, Waseem, Elkord, Eyad, Abdou Elmeligy, Omar Abdelsadek, Emamian, Mohammad Hassan, Erkhembayar, Ryenchindorj, Ezzeddini, Rana, Fadoo, Zehra, Faiz, Razana, Fakhradiyev, Ildar Ravisovich, Fallahzadeh, Aida, Faris, MoezAlIslam Ezzat Mahmoud, Farrokhpour, Hossein, Fatehizadeh, Ali, Fattahi, Hamed, Fekadu, Ginenus, Fukumoto, Takeshi, Gaidhane, Abhay Motiramji, Galehdar, Nasrin, Garg, Priyanka, Ghadirian, Fataneh, Ghafourifard, Mansour, Ghasemi, MohammadReza, Nour, Mohammad Ghasemi, Ghassemi, Fariba, Gholamalizadeh, Maryam, Gholamian, Asadollah, Ghotbi, Elena, Golechha, Mahaveer, Goleij, Pouya, Goyal, Sahil, Mohialdeen Gubari, Mohammed Ibrahim, Gunasekera, D Sanjeeva, Gunawardane, Damitha Asanga, Gupta, Sapna, Habibzadeh, Parham, Haeri Boroojeni, Helia Sadat, Halboub, Esam S., Hamadeh, Randah R., Hamoudi, Rifat, Harorani, Mehdi, Hasanian, Mohammad, Hassan, Treska S., Hay, Simon I., Heidari, Mohammad, Heidari-Foroozan, Mahsa, Hessami, Kamran, Hezam, Kamal, Hiraike, Yuta, Holla, Ramesh, Hoseini, Mohammad, Hossain, Md Mahbub, Hossain, Sahadat, Hsieh, Vivian Chia-rong, Huang, Junjie, Hussein, Nawfal R., Hwang, Bing-Fang, Iravanpour, Farideh, Ismail, Nahlah Elkudssiah, Iwagami, Masao, Merin J, Linda, Jadidi-Niaragh, Farhad, Jafarinia, Morteza, Jahani, Mohammad Ali, Jahrami, Haitham, Jaiswal, Abhishek, Jakovljevic, Mihajlo, Jalili, Mahsa, Jamshidi, Elham, Jayarajah, Umesh, Jayaram, Shubha, Jha, Sweety Suman, Jokar, Mohammad, Joseph, Nitin, Kabir, Ali, Kabir, Md. Awal, Kadir, Dler Hussein, Kakodkar, Pradnya Vishal, Kalankesh, Laleh R., Kalankesh, Leila R., Kalhor, Rohollah, Kaliyadan, Feroze, Kamal, Vineet Kumar, Kamal, Zul, Kamath, Ashwin, Kar, Sitanshu Sekhar, Karimi, Hanie, Kaur, Navjot, Keikavoosi-Arani, Leila, Keykhaei, Mohammad, Khader, Yousef Saleh, Khajuria, Himanshu, Khan, Ejaz Ahmad, Khan, M Nuruzzaman, Khan, Maseer, Khan, Moien A.B., Khan, Yusra H., Khanmohammadi, Shaghayegh, Khatatbeh, Moawiah Mohammad, Khateri, Sorour, Khayamzadeh, Maryam, Khayat Kashani, Hamid Reza, Kim, Min Seo, Kompani, Farzad, Koohestani, Hamid Reza, Koulmane Laxminarayana, Sindhura Lakshmi, Krishan, Kewal, Kumar, Narinder, Kumar, Naveen, Kutluk, Tezer, Kuttikkattu, Ambily, Ching Lai, Daphne Teck, Lal, Dharmesh Kumar, Lami, Faris Hasan, Lasrado, Savita, Lee, Sang-Woong, Lee, Seung Won, Lee, Yeong Yeh, Lee, Yo Han, Leong, Elvynna, Li, Ming-Chieh, Liu, Jue, Madadizadeh, Farzan, Mafi, Ahmad R., Mahjoub, Soleiman, Malekzadeh, Reza, Malik, Ahmad Azam, Malik, Iram, Mallhi, Tauqeer Hussain, Mansournia, Mohammad Ali, Martini, Santi, Mathews, Elezebeth, Mathur, Manu Raj, Meena, Jitendra Kumar, Menezes, Ritesh G., Mirfakhraie, Reza, Mirinezhad, Seyed Kazem, Mirza-Aghazadeh-Attari, Mohammad, Mithra, Prasanna, Mohamadkhani, Ashraf, Mohammadi, Soheil, Mohammadzadeh, Maryam, Mohan, Syam, Mokdad, Ali H., Al Montasir, Ahmed, Montazeri, Fateme, Moradi, Maryam, Sarabi, Mostafa Moradi, Moradpour, Farhad, Moradzadeh, Maliheh, Moraga, Paula, Mosapour, Abbas, Motaghinejad, Majid, Mubarik, Sumaira, Muhammad, Jibran Sualeh, Murray, Christopher J.L., Nagarajan, Ahamarshan Jayaraman, Naghavi, Mohsen, Nargus, Shumaila, Natto, Zuhair S., Nayak, Biswa Prakash, Nejadghaderi, Seyed Aria, Nguyen, Phuong The, Niazi, Robina Khan, Noroozi, Nafise, Okati-Aliabad, Hassan, Okekunle, Akinkunmi Paul, Ong, Sokking, Oommen, Anu Mary, Padubidri, Jagadish Rao, Pandey, Ashok, Park, Eun-Kee, Park, Seoyeon, Pati, Siddhartha, Patil, Shankargouda, Paudel, Rajan, Paudel, Uttam, Pirestani, Majid, Podder, Indrashis, Pourali, Ghazaleh, Pourjafar, Mona, Pourshams, Akram, Syed, Zahiruddin Quazi, Radhakrishnan, Raghu Anekal, Radhakrishnan, Venkatraman, Rahman, Mosiur, Rahmani, Shayan, Rahmanian, Vahid, Ramesh, Pushkal Sinduvadi, Rana, Juwel, Rao, Indu Ramachandra, Rao, Sowmya J., Rashedi, Sina, Rashidi, Mohammad-Mahdi, Rezaei, Nazila, Rezaei, Negar, Rezaei, Nima, Rezaei, Saeid, Rezaeian, Mohsen, Roshandel, Gholamreza, Chandan, S.N., Saber-Ayad, Maha Mohamed, Sabour, Siamak, Sabzmakan, Leila, Saddik, Basema, Saeed, Umar, Safi, Sher Zaman, Sharif-Askari, Fatemeh Saheb, Sahebkar, Amirhossein, Sahoo, Harihar, Sajedi, Seyed Aidin, Sajid, Mirza Rizwan, Salehi, Mohammad Amin, Farrokhi, Amir Salek, Sarasmita, Made Ary, Sargazi, Saman, Sarode, Gargi Sachin, Sarode, Sachin C., Sathian, Brijesh, Satpathy, Maheswar, Semwal, Prabhakar, Senthilkumaran, Subramanian, Sepanlou, Sadaf G., Shafeghat, Melika, Shahabi, Saeed, Shahbandi, Ataollah, Shahraki-Sanavi, Fariba, Shaikh, Masood Ali, Shannawaz, Mohammed, Sheikhi, Rahim Ali, Shobeiri, Parnian, Shorofi, Seyed Afshin, Shrestha, Sunil, Siabani, Soraya, Singh, Garima, Singh, Paramdeep, Singh, Surjit, Sinha, Dhirendra Narain, Siwal, Samarjeet Singh, Sreeram, Saraswathy, Suleman, Muhammad, Abdulkader, Rizwan Suliankatchi, Sultan, Iyad, Sultana, Abida, Tabish, Mohammad, Tabuchi, Takahiro, Taheri, Majid, Talaat, Iman M., Tehrani-Banihashemi, Arash, Temsah, Mohamad-Hani, Thangaraju, Pugazhenthan, Thomas, Nihal, Thomas, Nikhil Kenny, Tiyuri, Amir, Tobe-Gai, Ruoyan, Toghroli, Razie, Tovani-Palone, Marcos Roberto, Ullah, Sana, Unnikrishnan, Bhaskaran, Upadhyay, Era, Tahbaz, Sahel Valadan, Valizadeh, Rohollah, Varthya, Shoban Babu, Waheed, Yasir, Wang, Song, Wickramasinghe, Dakshitha Praneeth, Wickramasinghe, Nuwan Darshana, Xiao, Hong, Yonemoto, Naohiro, Younis, Mustafa Z., Yu, Chuanhua, Zahir, Mazyar, Zaki, Nazar, Zamanian, Maryam, Zhang, Zhi-Jiang, Zhao, Hanqing, Zitoun, Osama A., and Zoladl, Mohammad

Published
2024
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7. The molecular mechanisms of apoptosis accompanied with the epigenetic regulation of the NY-ESO-1 antigen in non-small lung cancer cells treated with decitabine (5-aza-CdR)

Author

Inchakalody, Varghese P., Hydrose, Shereena P., Krishnankutty, Roopesh, Merhi, Maysaloun, Therachiyil, Lubna, Sasidharan Nair, Varun, Elashi, Asma A., Khan, Abdul Q., Taleb, Sara, Raza, Afsheen, Yoosuf, Zeenath Safira K.M., Fernandes, Queenie, Al-Zaidan, Lobna, Mestiri, Sarra, Taib, Nassiba, Bedhiafi, Takwa, Moustafa, Dina, Assami, Laila, Maalej, Karama Makni, Elkord, Eyad, Uddin, Shahab, Al Homsi, Ussama, and Dermime, Said

Published
2023
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12. Contributors

Author

Ahmad, Gulzar, primary, Ahmed, Nadia Tasnim, additional, Amedei, Amedeo, additional, Amiji, Mansoor M., additional, Asrani, Kirtika H., additional, Boem, Federico, additional, Cassady, Kevin A., additional, Chen, Yu, additional, Culp, Patty A., additional, Degenhardt, Jeremiah D., additional, Dettling, Danielle E., additional, Djamgoz, Mustafa B.A., additional, Doshi, Aatman S., additional, Elkord, Eyad, additional, Firmenich, Laetitia, additional, Gauthier, Lauren M., additional, Ghoneim, Hazem E., additional, Goto, Taichiro, additional, Hernandez-Aguirre, Ilse, additional, Jang, Hae Lin, additional, Li, Yongsheng, additional, Liu, Xiang, additional, Mackenzie, Gerardo G., additional, May, Chad, additional, Milane, Lara Scheherazade, additional, Russo, Edda, additional, Saadey, Abbey A., additional, Saleh, Reem, additional, Sasidharan Nair, Varun, additional, Sengupta, Shiladitya, additional, Su, Ting, additional, Toor, Salman M., additional, Yousif, Amir, additional, Zhou, Shurong, additional, and Zhu, Guizhi, additional

Published
2022
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19. Designing a broad-spectrum integrative approach for cancer prevention and treatment

Author

Block, Keith I, Gyllenhaal, Charlotte, Lowe, Leroy, Amedei, Amedeo, Amin, ARM Ruhul, Amin, Amr, Aquilano, Katia, Arbiser, Jack, Arreola, Alexandra, Arzumanyan, Alla, Ashraf, S Salman, Azmi, Asfar S, Benencia, Fabian, Bhakta, Dipita, Bilsland, Alan, Bishayee, Anupam, Blain, Stacy W, Block, Penny B, Boosani, Chandra S, Carey, Thomas E, Carnero, Amancio, Carotenuto, Marianeve, Casey, Stephanie C, Chakrabarti, Mrinmay, Chaturvedi, Rupesh, Chen, Georgia Zhuo, Chen, Helen, Chen, Sophie, Chen, Yi Charlie, Choi, Beom K, Ciriolo, Maria Rosa, Coley, Helen M, Collins, Andrew R, Connell, Marisa, Crawford, Sarah, Curran, Colleen S, Dabrosin, Charlotta, Damia, Giovanna, Dasgupta, Santanu, DeBerardinis, Ralph J, Decker, William K, Dhawan, Punita, Diehl, Anna Mae E, Dong, Jin-Tang, Dou, Q Ping, Drew, Janice E, Elkord, Eyad, El-Rayes, Bassel, Feitelson, Mark A, Felsher, Dean W, Ferguson, Lynnette R, Fimognari, Carmela, Firestone, Gary L, Frezza, Christian, Fujii, Hiromasa, Fuster, Mark M, Generali, Daniele, Georgakilas, Alexandros G, Gieseler, Frank, Gilbertson, Michael, Green, Michelle F, Grue, Brendan, Guha, Gunjan, Halicka, Dorota, Helferich, William G, Heneberg, Petr, Hentosh, Patricia, Hirschey, Matthew D, Hofseth, Lorne J, Holcombe, Randall F, Honoki, Kanya, Hsu, Hsue-Yin, Huang, Gloria S, Jensen, Lasse D, Jiang, Wen G, Jones, Lee W, Karpowicz, Phillip A, Keith, W Nicol, Kerkar, Sid P, Khan, Gazala N, Khatami, Mahin, Ko, Young H, Kucuk, Omer, Kulathinal, Rob J, Kumar, Nagi B, Kwon, Byoung S, Le, Anne, Lea, Michael A, Lee, Ho-Young, Lichtor, Terry, Lin, Liang-Tzung, Locasale, Jason W, Lokeshwar, Bal L, Longo, Valter D, Lyssiotis, Costas A, MacKenzie, Karen L, Malhotra, Meenakshi, Marino, Maria, Martinez-Chantar, Maria L, and Matheu, Ander

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Rare Diseases, Precision Medicine, Aetiology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, Good Health and Well Being, Antineoplastic Agents, Phytogenic, Drug Resistance, Neoplasm, Genetic Heterogeneity, Humans, Molecular Targeted Therapy, Neoplasms, Signal Transduction, Tumor Microenvironment, Multi-targeted, Cancer hallmarks, Phytochemicals, Targeted therapy, Integrative medicine, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Targeted therapies and the consequent adoption of "personalized" oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are not reliant upon the same mechanisms as those which have been targeted). To address these limitations, an international task force of 180 scientists was assembled to explore the concept of a low-toxicity "broad-spectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspects of relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a wide range of high-priority targets (74 in total) that could be modified to improve patient outcomes. For these targets, corresponding low-toxicity therapeutic approaches were then suggested, many of which were phytochemicals. Proposed actions on each target and all of the approaches were further reviewed for known effects on other hallmark areas and the tumor microenvironment. Potential contrary or procarcinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixed evidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of the relationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. This novel approach has potential to be relatively inexpensive, it should help us address stages and types of cancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for future research is offered.

Published
2015

23. Editorial: Novel biomarkers in tumor immunity and immunotherapy.

Author

Takaji Matsutani, Akbay, Esra, and Elkord, Eyad

Subjects
TUMOR markers, IMMUNOTHERAPY, PLATELET lymphocyte ratio, THYROID cancer, IMMUNITY, PROGNOSIS
Abstract

This document provides an overview of various studies conducted to identify novel biomarkers and predictive methods for cancer immunotherapy across different types of cancer. The research utilizes advanced technologies and techniques to uncover promising biomarkers that can help predict treatment response and prognosis in cancer patients. The role of the gut microbiota in modulating the tumor microenvironment and response to immunotherapy is also explored. The document highlights the value of serological methods and technological advancements in immunohistochemical methods for identifying biomarkers. Overall, this body of work contributes to the advancement of cancer diagnosis, prognosis, and treatment. [Extracted from the article]

Published
2024
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41. T‐cell responses and therapies against SARS‐CoV‐2 infection

Author

Toor, Salman M., Saleh, Reem, Sasidharan Nair, Varun, Taha, Rowaida Z., and Elkord, Eyad

Subjects
Immunity, Cellular, COVID-19 Vaccines, SARS-CoV-2, T-Lymphocytes, Immunology, coronavirus, T cells, COVID-19, Review Article, Adoptive Transfer, Antiviral Agents, immune responses, SARS‐CoV‐2, COVID-19 Drug Treatment, COVID‐19, Host-Pathogen Interactions, Immunology and Allergy, Animals, Humans, Immunologic Factors, Immunotherapy, Review Articles, Lung
Abstract

Coronavirus disease 2019 (COVID‐19) is caused by SARS‐CoV‐2, a novel coronavirus strain. Some studies suggest that COVID‐19 could be an immune‐related disease, and failure of effective immune responses in initial stages of viral infection could contribute to systemic inflammation and tissue damage, leading to worse disease outcomes. T cells can act as a double‐edge sword with both pro‐ and anti‐roles in the progression of COVID‐19. Thus, better understanding of their roles in immune responses to SARS‐CoV‐2 infection is crucial. T cells primarily react to the spike protein on the coronavirus to initiate antiviral immunity; however, T‐cell responses can be suboptimal, impaired or excessive in severe COVID‐19 patients. This review focuses on the multifaceted roles of T cells in COVID‐19 pathogenesis and rationalizes their significance in eliciting appropriate antiviral immune responses in COVID‐19 patients and unexposed individuals. In addition, we summarize the potential therapeutic approaches related to T cells to treat COVID‐19 patients. These include adoptive T‐cell therapies, vaccines activating T‐cell responses, recombinant cytokines, Th1 activators and Th17 blockers, and potential utilization of immune checkpoint inhibitors alone or in combination with anti‐inflammatory drugs to improve antiviral T‐cell responses against SARS‐CoV‐2., This review focuses on the multi‐faceted roles of T cells in COVID‐19 pathogenesis and rationalizes their significance in eliciting appropriate antiviral immune responses in COVID‐19 patients and unexposed individuals. In addition, wesummarize the potential therapeutic approaches related to T cells to treat COVID‐19 patients.

Published
2020

42. Expression of immune checkpoints and T cell exhaustion markers in early and advanced stages of colorectal cancer

Author

Saleh, Reem, Taha, Rowaida Z., Toor, Salman M., Sasidharan Nair, Varun, Murshed, Khaled, Khawar, Mahwish, Al-Dhaheri, Mahmood, Petkar, Mahir Abdulla, Abu Nada, Mohamed, and Elkord, Eyad

Subjects
Adult, Male, Prognostic biomarker, Therapeutic target, T-Lymphocytes, Programmed Cell Death 1 Receptor, Young Adult, Lymphocytes, Tumor-Infiltrating, Biomarkers, Tumor, Humans, CTLA-4 Antigen, Receptors, Immunologic, Aged, Neoplasm Staging, T cell exhaustion, Aged, 80 and over, Oncology and carcinogenesis, Middle Aged, Colorectal cancer, Gene Expression Regulation, Neoplastic, Case-Control Studies, Immune checkpoints, Original Article, Female, Colorectal Neoplasms, Follow-Up Studies
Abstract

Despite recent advances in colorectal cancer (CRC) treatment, a large proportion of patients show limited responses to therapies, especially in advanced stages. There is an urgent need to identify prognostic biomarkers and/or therapeutic targets in advanced stages, aiming to improve the efficacy of current treatments. We aimed to determine prognostic biomarkers in tumor tissue and circulation of CRC patients, with a special focus on T cell exhaustion markers. We found that mRNA levels of PD-1, TIM-3, CTLA-4, TIGIT, CD160, CD244, KLRG1, TOX2, TOX3, Ki-67, and PRDM1 were elevated in CRC tumor tissues. We also investigated differences in gene expression between early and advanced disease stages. We found that TOX and potentially TIM-3, CTLA-4, VISTA, TIGIT, KLRG1, TOX2, SIRT1, Ki-67, and Helios mRNA levels in tumor tissue were elevated in advanced disease stages, suggesting their potential roles in CRC progression. In contrast, PD-1 and CD160 levels in tumor tissue were downregulated in advanced stages. In the circulation of CRC patients, mRNA levels of PD-1, VISTA and LAG-3 were higher than those of healthy individuals. Moreover, in circulation, PD-1, CTLA-4 and TIGIT mRNA levels were reduced in advanced stages. Interestingly, levels of PD-1 in both tumor tissue and circulation were reduced in advanced stages, suggesting that targeting PD-1 in patients with advanced stages could be less effective. Altogether, these findings suggest some potential T cell exhaustion markers that could be utilized as prognostic biomarkers and/or therapeutic targets for CRC. However, further investigations and validations in larger cohorts are required to confirm these findings.Other Information Published in: Cancer Immunology, Immunotherapy License: https://creativecommons.org/licenses/by/4.0See article on publisher's website: http://dx.doi.org/10.1007/s00262-020-02593-w

Published
2022
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43. Identification of two HLA-A*0201 immunogenic epitopes of lactate dehydrogenase C (LDHC): potential novel targets for cancer immunotherapy

Author

Thomas, Remy, Shaath, Hibah, Naik, Adviti, Toor, Salman M., Elkord, Eyad, and Decock, Julie

Subjects
Oncology and carcinogenesis
Abstract

Lactate dehydrogenase C (LDHC) is an archetypical cancer testis antigen with limited expression in adult tissues and re-expression in tumors. This restricted expression pattern together with the important role of LDHC in cancer metabolism renders LDHC a potential target for immunotherapy. This study is the first to investigate the immunogenicity of LDHC using T cells from healthy individuals. LDHC-specific T cell responses were induced by in vitro stimulation with synthetic peptides, or by priming with autologous peptide-pulsed dendritic cells. We evaluated T cell activation by IFN-γ ELISpot and determined cytolytic activity of HLA-A*0201-restricted T cells in breast cancer cell co-cultures. In vitro T cell stimulation induced IFN-γ secretion in response to numerous LDHC-derived peptides. Analysis of HLA-A*0201 responses revealed a significant T cell activation after stimulation with peptide pools 2 (PP2) and 8 (PP8). The PP2- and PP8-specific T cells displayed cytolytic activity against breast cancer cells with endogenous LDHC expression within a HLA-A*0201 context. We identified peptides LDHC41−55 and LDHC288−303 from PP2 and PP8 to elicit a functional cellular immune response. More specifically, we found an increase in IFN-γ secretion by CD8 + T cells and cancer-cell-killing of HLA-A*0201/LDHC positive breast cancer cells by LDHC41−55- and LDHC288−303-induced T cells, albeit with a possible antigen recognition threshold. The majority of induced T cells displayed an effector memory phenotype. To conclude, our findings support the rationale to assess LDHC as a targetable cancer testis antigen for immunotherapy, and in particular the HLA-A*0201 restricted LDHC41–55 and LDHC288–303 peptides within LDHC.Other Information Published in: Cancer Immunology, Immunotherapy License: https://creativecommons.org/licenses/by/4.0See article on publisher's website: http://dx.doi.org/10.1007/s00262-020-02480-4

Published
2022
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45. DNA methylation in the promoters of PD-L1, MMP9, ARG1, galectin-9, TIM-3, VISTA and TGF-β genes in HLA-DR– myeloid cells, compared with HLA-DR+ antigen-presenting cells

Author

Saleh, Reem, Toor, Salman M., Taha, Rowaida Z., Al-Ali, Dana, Sasidharan Nair, Varun, and Elkord, Eyad

Subjects
DNA methylation, immunosuppression, B7 Antigens, epigenetics, Arginase, MDSC, Sialic Acid Binding Ig-like Lectin 3, Antigen-Presenting Cells, HLA-DR Antigens, B7-H1 Antigen, Epigenesis, Genetic, Matrix Metalloproteinase 9, Genetic Loci, Transforming Growth Factor beta, Humans, Myeloid Cells, Promoter Regions, Genetic, Hepatitis A Virus Cellular Receptor 2, Research Article, Research Paper
Abstract

Myeloid cells, including antigen-presenting cells (APCs) and myeloid-derived suppressor cells (MDSCs) play opposing roles to orchestrate innate and adaptive immune responses during physiological and pathological conditions. We investigated the role of DNA methylation in regulating the transcription of inhibitory/suppressive molecules in myeloid suppressive cells (identified as CD33+HLA-DR–) in comparison to APCs. We selected a number of immune checkpoints (ICs), IC ligands, and immunosuppressive molecules that have been implicated in MDSC function, including PD-L1, TIM-3, VISTA, galectin-9, TGF-β, ARG1 and MMP9. We examined their mRNA expression levels, and investigated whether DNA methylation regulates their transcription in sorted myeloid cell subpopulations. We found that mRNA levels of PD-L1, TIM-3, TGF-β, ARG1 and MMP9 in CD33+HLA-DR– cells were higher than APCs. However, VISTA and galectin-9 mRNA levels were relatively similar in both myeloid subpopulations. CpG islands in the promoter regions of TGF-β1, TIM-3 and ARG1 were highly unmethylated in CD33+HLA-DR–cells, compared with APCs, suggesting that DNA methylation is one of the key mechanisms, which regulate their expression. However, we did not find differences in the methylation status of PD-L1 and MMP9 between CD33+HLA-DR– and APCs, suggesting that their transcription could be regulated via other genetic and epigenetic mechanisms. The promoter methylation status of VISTA was relatively similar in both myeloid subpopulations. This study provides novel insights into the epigenetic mechanisms, which control the expression of inhibitory/suppressive molecules in circulating CD33+HLA-DR– cells in a steady-state condition, possibly to maintain immune tolerance and haemostasis.

Published
2020

46. Complement C5a and Clinical Markers as Predictors of COVID-19 Disease Severity and Mortality in a Multi-Ethnic Population

Author

Cyprian, Farhan S., primary, Suleman, Muhammad, additional, Abdelhafez, Ibrahim, additional, Doudin, Asmma, additional, Masud Danjuma, Ibn Mohammed, additional, Mir, Fayaz Ahmad, additional, Parray, Aijaz, additional, Yousaf, Zohaib, additional, Siddiqui, Mohammed Yaseen Ahmed, additional, Abdelmajid, Alaaedin, additional, Mulhim, Mohammad, additional, Al-Shokri, Shaikha, additional, Abukhattab, Mohammad, additional, Shaheen, Ranad, additional, Elkord, Eyad, additional, Al-khal, Abdul Latif, additional, Elzouki, Abdel-Naser, additional, and Girardi, Guillermina, additional

Published
2021
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47. SnoRNAs and miRNAs Networks Underlying COVID-19 Disease Severity

Author

Parray, Aijaz, primary, Mir, Fayaz Ahmad, additional, Doudin, Asmma, additional, Iskandarani, Ahmad, additional, Danjuma, Ibn Mohammed Masud, additional, Kuni, Rahim Ayadathil Thazhhe, additional, Abdelmajid, Alaaedin, additional, Abdelhafez, Ibrahim, additional, Arif, Rida, additional, Mulhim, Mohammad, additional, Abukhattab, Mohammad, additional, Dar, Shoukat Rashhid, additional, Moustafa, Ala-Eddin Al, additional, Elkord, Eyad, additional, Al Khal, Abdul Latif, additional, Elzouki, Abdel-Naser, additional, and Cyprian, Farhan, additional

Published
2021
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