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252 results on '"Rodriguez, Paulo"'

1. Transgelin 2 guards T cell lipid metabolism and antitumour function

Author

Hwang, Sung-Min, Awasthi, Deepika, Jeong, Jieun, Sandoval, Tito A., Chae, Chang-Suk, Ramos, Yusibeska, Tan, Chen, Marin Falco, Matías, Salvagno, Camilla, Emmanuelli, Alexander, McBain, Ian T., Mishra, Bikash, Ivashkiv, Lionel B., Zamarin, Dmitriy, Cantillo, Evelyn, Chapman-Davis, Eloise, Holcomb, Kevin, Morales, Diana K., Yu, Xiaoqing, Rodriguez, Paulo C., Conejo-Garcia, Jose R., Kaczocha, Martin, Vähärautio, Anna, Song, Minkyung, and Cubillos-Ruiz, Juan R.

Published
2024
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4. Jagged2 targeting in lung cancer activates anti-tumor immunity via Notch-induced functional reprogramming of tumor-associated macrophages

Author

Mandula, Jay K., Sierra-Mondragon, Rosa A., Jimenez, Rachel V., Chang, Darwin, Mohamed, Eslam, Chang, Shiun, Vazquez-Martinez, Julio A., Cao, Yu, Anadon, Carmen M., Lee, Sae Bom, Das, Satyajit, Rocha-Munguba, Léo, Pham, Vincent M., Li, Roger, Tarhini, Ahmad A., Furqan, Muhammad, Dalton, William, Churchman, Michelle, Moran-Segura, Carlos M., Nguyen, Jonathan, Perez, Bradford, Kojetin, Douglas J., Obermayer, Alyssa, Yu, Xiaoqing, Chen, Ann, Shaw, Timothy I., Conejo-Garcia, Jose R., and Rodriguez, Paulo C.

Published
2024
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6. Enniatin A inhibits the chaperone Hsp90 and unleashes the immune system against triple-negative breast cancer

Author

Eisa, Nada H., Crowley, Vincent M., Elahi, Asif, Kommalapati, Vamsi Krishna, Serwetnyk, Michael A., Llbiyi, Taoufik, Lu, Sumin, Kainth, Kashish, Jilani, Yasmeen, Marasco, Daniela, El Andaloussi, Abdeljabar, Lee, Sukyeong, Tsai, Francis T.F., Rodriguez, Paulo C., Munn, David, Celis, Esteban, Korkaya, Hasan, Debbab, Abdessamad, Blagg, Brian, and Chadli, Ahmed

Published
2023
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7. Targeting intracellular oncoproteins with dimeric IgA promotes expulsion from the cytoplasm and immune-mediated control of epithelial cancers

Author

Biswas, Subir, Mandal, Gunjan, Anadon, Carmen M., Chaurio, Ricardo A., Lopez-Bailon, Luis U., Nagy, Mate Z., Mine, Jessica A., Hänggi, Kay, Sprenger, Kimberly B., Innamarato, Patrick, Harro, Carly M., Powers, John J., Johnson, Joseph, Fang, Bin, Eysha, Mostafa, Nan, Xiaolin, Li, Roger, Perez, Bradford A., Curiel, Tyler J., Yu, Xiaoqing, Rodriguez, Paulo C., and Conejo-Garcia, Jose R.

Published
2023
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11. Increased inflammatory low-density neutrophils in severe obesity and effect of bariatric surgery: Results from case-control and prospective cohort studies

Author

Sanchez-Pino, Maria Dulfary, Richardson, William S., Zabaleta, Jovanny, Puttalingaiah, Ramesh Thylur, Chapple, Andrew G., Liu, Jiao, Kim, Yonghyan, Ponder, Michelle, DeArmitt, Randi, Baiamonte, Lyndsey Buckner, Wyczechowska, Dorota, Zheng, Liqin, Al-Khami, Amir A., Garai, Jone, Martini, Rachel, Davis, Melissa, Gorham, Jessica Koller, Wooldridge, James B., Rodriguez, Paulo C., Miele, Lucio, and Ochoa, Augusto C.

Published
2022
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12. IgA transcytosis and antigen recognition govern ovarian cancer immunity

Author

Biswas, Subir, Mandal, Gunjan, Payne, Kyle K., Anadon, Carmen M., Gatenbee, Chandler D., Chaurio, Ricardo A., Costich, Tara Lee, Moran, Carlos, Harro, Carly M., Rigolizzo, Kristen E., Mine, Jessica A., Trillo-Tinoco, Jimena, Sasamoto, Naoko, Terry, Kathryn L., Marchion, Douglas, Buras, Andrea, Wenham, Robert M., Yu, Xiaoqing, Townsend, Mary K., Tworoger, Shelley S., Rodriguez, Paulo C., Anderson, Alexander R., and Conejo-Garcia, Jose R.

Published
2021
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13. MEK inhibition reprograms CD8+ T lymphocytes into memory stem cells with potent antitumor effects

Author

Verma, Vivek, Jafarzadeh, Nazli, Boi, Shannon, Kundu, Subhadip, Jiang, Zhinuo, Fan, Yiping, Lopez, Jose, Nandre, Rahul, Zeng, Peng, Alolaqi, Fatmah, Ahmad, Shamim, Gaur, Pankaj, Barry, Simon T., Valge-Archer, Viia E., Smith, Paul D., Banchereau, Jacques, Mkrtichyan, Mikayel, Youngblood, Benjamin, Rodriguez, Paulo C., Gupta, Seema, and Khleif, Samir N.

Published
2021
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15. c-Maf: a bad influence in the education of macrophages

Author

Conejo-Garcia, Jose R. and Rodriguez, Paulo C.

Subjects
Macrophages, Tumors -- Development and progression, Beta glucan, Non-small cell lung cancer -- Development and progression, T cells, Transforming growth factors, Small cell lung cancer, Education, Cancer, Immunotherapy, Lung cancer, Health care industry
Abstract

Tumor-associated macrophages (TAMs) represent the most abundant hematopoietic cell type in the solid tumor microenvironment. TAMs drive T cell inhibition, promote angiogenesis, and produce tumor growth factors. Although they can paradoxically exert antitumor activity and prime protective immunity, the pathways driving this phenotype remain unclear. In this issue of theJCI, Liu and colleagues identified the c-Maf transcription factor as a master regulator of protumoral TAM polarization. The authors found that c-Maf promoted TAMs' immunosuppressive activity, governed their metabolic programming, and drove expression of the macrophage differentiation protein, CSF1R. Further, inhibiting c-Maf in myeloid progenitors, and consequent myeloid-lineage cells, including TAMs, delayed tumor growth. Importantly, [beta]-glucan treatment reduced c-MAF expression in macrophages and monocytes from patients with non-small cell lung cancer (NSCLC) where c-MAF is overexpressed. These results reveal mechanisms whereby myeloid cells drive human cancer progression by thwarting protective immunity and could lead to immunotherapy for most solid malignancies., c-Maf upregulation drives M2 attributes and enhances immunosuppressive activity Virtually all solid tumors produce inflammatory factors that pathologically mobilize myeloid cells. At advanced stages of malignant progression, immature cells of [...]

Published
2020
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17. IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity

Author

Song, Minkyung, Sandoval, Tito A., Chae, Chang-Suk, Chopra, Sahil, Tan, Chen, Rutkowski, Melanie R., Raundhal, Mahesh, Chaurio, Ricardo A., Payne, Kyle K., Konrad, Csaba, Bettigole, Sarah E., Shin, Hee Rae, Crowley, Michael J. P., Cerliani, Juan P., Kossenkov, Andrew V., Motorykin, Ievgen, Zhang, Sheng, Manfredi, Giovanni, Zamarin, Dmitriy, Holcomb, Kevin, Rodriguez, Paulo C., Rabinovich, Gabriel A., Conejo-Garcia, Jose R., Glimcher, Laurie H., and Cubillos-Ruiz, Juan R.

Published
2018
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19. Methyltransferase inhibitors restore SATB1 protective activity against cutaneous T cell lymphoma in mice

Author

Harro, Carly M., Perez-Sanz, Jairo, Costich, Tara Lee, Payne, Kyle K., Anadon, Carmen M., Chaurio, Ricardo A., Biswas, Subir, Mandal, Gunjan, Rigolizzo, Kristen E., Sprenger, Kimberly B., Mine, Jessica A., Showe, Louise C., Yu, Xiaoqing, Liu, Kebin, Rodriguez, Paulo C., Pinilla-Ibarz, Javier, Sokol, Lubomir, and Conejo-Garcia, Jose R.

Subjects
Enzyme inhibitors -- Genetic aspects -- Health aspects, Methyltransferases -- Physiological aspects -- Health aspects, T cell lymphoma -- Models -- Genetic aspects -- Development and progression, Transcription factors -- Physiological aspects -- Health aspects, Health care industry
Abstract

Cutaneous T cell lymphoma (CTCL) has a poorly understood etiology and no known cure. Using conditional knockout mice, we found that ablation of the genomic organizer special AT-rich sequence-binding protein 1 (Satb1) caused malignant transformation of mature, skin-homing, Notch-activated CD[4.sup.+] and CD[8.sup.+] T cells into progressively fatal lymphoma. Mechanistically, Satb1 restrained Stat5 phosphorylation and the expression of skin-homing chemokine receptors in mature T cells. Notably, methyltransferase-dependent epigenetic repression of SATB1 was universally found in human Sezary syndrome, but not in other peripheral T cell malignancies. H3K27 and H3K9 trimethylation occluded the SATB1 promoter in Sezary cells, while inhibition of SUV39H1/2 methyltransferases (unlike EZH2 inhibition) restored protective SATB1 expression and selectively abrogated the growth of primary Sezary cells more effectively than romidepsin. Therefore, inhibition of methyltransferases that silence SATB1 could address an unmet need for patients with mycosis fungoides/Sezary syndrome, a set of incurable diseases., Introduction Peripheral T cell lymphomas (PTCLs) represent a collection of aggressive disorders with unfavorable outcome that account for approximately 12% of lymphoid tumors worldwide (1). Cutaneous T cell lymphoma (CTCL) [...]

Published
2021
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21. Publisher Correction: ER stress-induced mediator C/EBP homologous protein thwarts effector T cell activity in tumors through T-bet repression

Author

Cao, Yu, Trillo-Tinoco, Jimena, Sierra, Rosa A., Anadon, Carmen, Dai, Wenjie, Mohamed, Eslam, Cen, Ling, Costich, Tara L., Magliocco, Anthony, Marchion, Douglas, Klar, Richard, Michel, Sven, Jaschinski, Frank, Reich, Richard R., Mehrotra, Shikhar, Cubillos-Ruiz, Juan R., Munn, David H., Conejo-Garcia, Jose R., and Rodriguez, Paulo C.

Published
2019
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22. ER stress-induced mediator C/EBP homologous protein thwarts effector T cell activity in tumors through T-bet repression

Author

Cao, Yu, Trillo-Tinoco, Jimena, Sierra, Rosa A., Anadon, Carmen, Dai, Wenjie, Mohamed, Eslam, Cen, Ling, Costich, Tara L., Magliocco, Anthony, Marchion, Douglas, Klar, Richard, Michel, Sven, Jaschinski, Frank, Reich, Richard R., Mehrotra, Shikhar, Cubillos-Ruiz, Juan R., Munn, David H., Conejo-Garcia, Jose R., and Rodriguez, Paulo C.

Published
2019
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23. Relationships among Inflammatory Biomarkers and Objectively Assessed Physical Activity and Sleep during and after Chemotherapy for Gynecologic Malignancies.

Author

Tometich, Danielle B., Hoogland, Aasha I., Small, Brent J., Janelsins, Michelle C., Bryant, Crystal, Rodriguez, Yvelise, Gonzalez, Brian D., Li, Xiaoyin, Bulls, Hailey W., James, Brian W., Arboleda, Bianca, Colon-Echevarria, Claudia, Townsend, Mary K., Tworoger, Shelley S., Rodriguez, Paulo, Oswald, Laura B., Bower, Julienne E., Apte, Sachin M., Wenham, Robert M., and Chon, Hye Sook

Subjects
SEDENTARY lifestyles, SLEEP latency, CANCER chemotherapy, INFLAMMATION, RESEARCH methodology, REGRESSION analysis, PHYSICAL activity, SLEEP duration, CANCER patients, SLEEP disorders, HEALTH behavior, TUMOR markers, FEMALE reproductive organ tumors, LONGITUDINAL method
Abstract

Simple Summary: Physical inactivity and sleep problems are commonly reported by women going through chemotherapy for gynecologic cancer. Inflammation from cancer and its treatment might contribute to these issues, but existing findings are limited. We examined relationships between biomarkers of inflammation and data from wearable devices to objectively measure physical activity and sleep. We collected data from women with gynecologic cancer during chemotherapy and followed up with them for a year after completing chemotherapy. We also compared their results to women without cancer who were assessed at similar time intervals. We found that women with cancer were less active and had more sleep problems than controls even a year after completing chemotherapy. Greater inflammation was also related to less physical activity and more sleep problems. Future research should test whether interventions aimed at reducing inflammation can help women with cancer to be more active and have fewer sleep problems. Little is known regarding associations between inflammatory biomarkers and objectively measured physical activity and sleep during and after chemotherapy for gynecologic cancer; thus, we conducted a longitudinal study to address this gap. Women with gynecologic cancer (patients) and non-cancer controls (controls) completed assessments before chemotherapy cycles 1, 3, and 6 (controls assessed contemporaneously), as well as at 6- and 12-month follow-ups. Physical activity and sleep were measured using wrist-worn actigraphs and sleep diaries, and blood was drawn to quantify circulating levels of inflammatory markers. Linear and quadratic random-effects mixed models and random-effects fluctuation mixed models were used to examine physical activity and sleep over time, as well as the associations with inflammatory biomarkers. On average, patients (n = 97) and controls (n = 104) were 62 and 58 years old, respectively. Compared to controls, patients were less active, more sedentary, had more time awake after sleep onset, and had lower sleep efficiency (p-values < 0.05). Across groups, higher levels of TNF-α were associated with more sedentary time and less efficient sleep (p-values ≤ 0.05). Higher levels of IL-1β, TNF-α, and IL-6 were associated with lower levels of light physical activity (p-values < 0.05). Associations between inflammatory biomarkers, physical activity, and sleep did not differ between patients and controls. Given these results, we speculate that inflammation may contribute to less physical activity and more sleep problems that persist even 12 months after completing chemotherapy. [ABSTRACT FROM AUTHOR]

Published
2023
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30. Relationships among Inflammatory Biomarkers and Self-Reported Treatment-Related Symptoms in Patients Treated with Chemotherapy for Gynecologic Cancer: A Controlled Comparison.

Author

Hoogland, Aasha I., Small, Brent J., Oswald, Laura B., Bryant, Crystal, Rodriguez, Yvelise, Gonzalez, Brian D., Li, Xiaoyin, Janelsins, Michelle C., Bulls, Hailey W., James, Brian W., Arboleda, Bianca, Colon-Echevarria, Claudia, Townsend, Mary K., Tworoger, Shelley S., Rodriguez, Paulo C., Bower, Julienne E., Apte, Sachin M., Wenham, Robert M., and Jim, Heather S. L.

Subjects
BIOMARKERS, INFLAMMATION, SELF-evaluation, CANCER chemotherapy, CANCER patients, COMPARATIVE studies, SLEEP, DESCRIPTIVE statistics, TUMOR necrosis factors, MENTAL depression, RESEARCH funding, FATIGUE (Physiology), FEMALE reproductive organ tumors, DISEASE complications, SYMPTOMS
Abstract

Simple Summary: Treatment-related symptoms such as fatigue, depression, and disruptions in sleep and physical activity are common and distressing in gynecologic cancer patients. The aim of our study was to examine whether higher levels of inflammation are associated with worse symptomatology, and if these associations are stronger for patients with gynecologic cancer (n = 121) than age-matched women without a cancer history (i.e., controls; n = 105). Elevated levels of C-reactive protein were associated with depression and disrupted physical activity, but there were no other significant associations between inflammation and treatment-related symptoms. Findings suggest that inflammation may not play a significant role in the development of fatigue or sleep disturbance among gynecologic cancer patients but may contribute to depression and physical inactivity. Previous research suggests that inflammation triggers cancer-treatment-related symptoms (i.e., fatigue, depression, and disruptions in sleep and physical activity), but evidence is mixed. This study examined relationships between inflammatory biomarkers and symptoms in patients with gynecologic cancer compared to age-matched women with no cancer history (i.e., controls). Patients (n = 121) completed assessments before chemotherapy cycles 1, 3, and 6, and 6 and 12 months later. Controls (n = 105) completed assessments at similar timepoints. Changes in inflammation and symptomatology were evaluated using random-effects mixed models, and cross-sectional differences between patients and controls in inflammatory biomarkers and symptoms were evaluated using least squares means. Associations among inflammatory biomarkers and symptoms were evaluated using random-effects fluctuation mixed models. The results indicated that compared to controls, patients typically have higher inflammatory biomarkers (i.e., TNF-alpha, TNFR1, TNFR2, CRP, IL-1ra) and worse fatigue, depression, and sleep (ps < 0.05). Patients reported lower levels of baseline physical activity (p = 0.02) that became more similar to controls over time. Significant associations were observed between CRP, depression, and physical activity (ps < 0.05), but not between inflammation and other symptoms. The results suggest that inflammation may not play a significant role in fatigue or sleep disturbance among gynecologic cancer patients but may contribute to depression and physical inactivity. [ABSTRACT FROM AUTHOR]

Published
2023
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34. Activation of p53 in Immature Myeloid Precursor Cells Controls Differentiation into Ly6c+CD103+ Monocytic Antigen-Presenting Cells in Tumors

Author

Sharma, Madhav D., Rodriguez, Paulo C., Koehn, Brent H., Baban, Babak, Cui, Yan, Guo, Gang, Shimoda, Michiko, Pacholczyk, Rafal, Shi, Huidong, Lee, Eun-Joon, Xu, Hongyan, Johnson, Theodore S., He, Yukai, Mergoub, Taha, Venable, Christopher, Bronte, Vincenzo, Wolchok, Jedd D., Blazar, Bruce R., and Munn, David H.

Published
2018
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37. Inhibition of a BTK-IDO-mTOR axis promotes differentiation of monocyte-lineage inflammatory dendritic cells and enhances anti-tumor T cell immunity

Author

Sharma, Madhav D., Pacholczyk, Rafal, Shi, Huidong, Berrong, Zuzana J., Zakharia, Yousef, Greco, Austin, Chang, Chang-Sheng S., Eathiraj, Sudharshan, Kennedy, Eugene, Cash, Thomas, Bollag, Roni J., Kolhe, Ravindra, Sadek, Ramses, McGaha, Tracy L., Rodriguez, Paulo, Mandula, Jessica, Blazar, Bruce R., Johnson, Theodore S., and Munn, David H.

Subjects
Male, T-Lymphocytes, TOR Serine-Threonine Kinases, Cell Differentiation, Dendritic Cells, Article, Monocytes, Mice, Neoplasms, Agammaglobulinaemia Tyrosine Kinase, Animals, Humans, Indoleamine-Pyrrole 2,3,-Dioxygenase, Female, Signal Transduction
Abstract

Monocytic-lineage inflammatory Ly6c+CD103+ dendritic cells (DCs) promote anti-tumor immunity, but these DCs are infrequent in tumors, even upon chemotherapy. Here we examined how targeting pathways that inhibit the differentiation of inflammatory myeloid cells impact anti-tumor immunity. Pharmacologic inhibition of Bruton’s Tyrosine Kinase (BTK) and the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO), or deletion of Btk or Ido1, allowed robust differentiation of inflammatory Ly6c+CD103+ DCs during chemotherapy, promoting anti-tumor T cell responses and inhibiting tumor growth. Immature Ly6c+c-kit+ precursor cells had epigenetic profiles similar to conventional DC precursors; deletion of Btk or Ido1 promoted differentiation of these cells. Mechanistically, a BTK-IDO axis inhibited a tryptophan-sensitive differentiation pathway driven by GATOR2 and mTORC1, and disruption of the GATOR2 in monocyte-lineage precursors prevented differentiation into inflammatory DCs in vivo. IDO-expressing DCs and monocytic cells were present across a range of human tumors. Thus, a BTK-IDO axis represses differentiation of inflammatory DCs during chemotherapy, with implications for targeted therapies.

Published
2021

40. CAR-T Phenotype and Efficacy Is Impaired By Lymphoma-Associated CD39 + T Cells

Author

Jain, Michael D., Yu, Xiaoqing, Atkins, Reginald, Turner, Joel G., Noble, Jerald, Menges, Meghan, Reid, Kayla, Corallo, Salvatore, Cen, Ling, Yoder, Sean J., Abraham Miranda, Julieta, Naderinezhad, Samira, Liu, Hien, Shah, Bijal D., Chavez, Julio C, Dean, Erin, Fahrmann, Johannes, Saini, Neeraj Y., Hanash, Samir, Hesterberg, Rebecca S., Rodriguez, Paulo C., Cleveland, John L., Davila, Marco, Wang, Xuefeng, and Locke, Frederick L.

Published
2023
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41. preclinical model of patient-derived cerebrospinal fluid circulating tumor cells for experimental therapeutics in leptomeningeal disease from melanoma.

Author

Law, Vincent, Chen, Zhihua, Vena, Francesca, Smalley, Inna, Macaulay, Robert, Evernden, Brittany R, Tran, Nam, Pina, Yolanda, Puskas, John, Caceres, Gisela, Bayle, Simon, Johnson, Joseph, Liu, James K C, Etame, Arnold, Vogelbaum, Michael, Rodriguez, Paulo, Duckett, Derek, Czerniecki, Brian, Chen, Ann, and Smalley, Keiran S M

Published
2022
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45. Using principles of community participatory research: Groundwork for a collaboration in Brazil

Author

Pinto, Rogerio M., Schmidt, Clency N.T., Rodriguez, Paulo S.O., and Solano, Renata

Subjects
Brazil -- Social policy, Community -- Analysis, Community development -- Analysis, Human growth -- Analysis, Research teams -- Analysis, Sociology and social work
Abstract

Partnership between researchers and community is very important for any international research to be effective. The model has shown that the interaction of both the social and the physical environment might affect many levels of human growth and community development in the host country, from the individual to the family and social group to the country.

Published
2007

49. Tumor-directed dysregulation of erythroid progenitors drives immunosuppressive myeloid cells.

Author

Mandula, Jessica K. and Rodriguez, Paulo C.

Subjects
*MYELOID cells, *MYELOID-derived suppressor cells, *IMMUNE checkpoint inhibitors, *PROGENITOR cells, *CANCER cells
Abstract

In this issue of Cancer Cell , Long et al. demonstrate that tumors can reprogram erythroid progenitors into myeloid-erythroid cells that promote immunosuppression. Erythroid-differentiated myeloid cells (EDMCs) expand in cancer-bearing individuals, resemble the functionality of myeloid-derived suppressor cells (MDSCs), and correlate with poor response to immune-checkpoint inhibitors (ICIs) and tumor-related anemia. [ABSTRACT FROM AUTHOR]

Published
2022
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