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Статті в журналах з теми "Target therapies"

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Автор: Grafiati

Опубліковано: 28 січня 2023

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1

Lazzari, Ludovico, Marcella De Paolis, Daniella Bovelli, and Enrico Boschetti. "Target therapies-induced Cardiotoxicity." European Oncology & Haematology 09, no. 01 (2013): 56. http://dx.doi.org/10.17925/eoh.2013.09.1.56.

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2

&NA;. "Rheumatoid arthritis therapies target TNF." Inpharma Weekly &NA;, no. 1173 (February 1999): 2. http://dx.doi.org/10.2165/00128413-199911730-00002.

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3

Bearz, A., M. Berretta, A. Lleshi, and U. Tirelli. "Target Therapies in Lung Cancer." Journal of Biomedicine and Biotechnology 2011 (2011): 1–5. http://dx.doi.org/10.1155/2011/921231.

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Targeting intracellular signaling molecules is an attractive approach for treatment of malignancies. In particular lung cancer has reached a plateau regarding overall survival, and target therapies could offer the possibility to improve patients' outcome beyond cytotoxic activity. The goal for target therapies is to identify agents that target tumor-specific molecules, thus sparing normal tissues; those molecules are called biomarkers, and their identification is recommended because it has a predictive value, for example, provides information on outcome with regard to a specific treatment. The increased specificity should lead to decreased toxicity and better activity. Herein we provide an update of the main target therapies in development or already available for the treatment of nonsmall cell lung cancer.

4

Silvestris, Nicola, Antonio Gnoni, Anna Brunetti, Leonardo Vincenti, Daniele Santini, Giuseppe Tonini, Francesca Merchionne, et al. "Target Therapies in Pancreatic Carcinoma." Current Medicinal Chemistry 21, no. 8 (February 2014): 948–65. http://dx.doi.org/10.2174/09298673113209990238.

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5

Hampton, Tracy. "Novel Therapies Target Myasthenia Gravis." JAMA 298, no. 2 (July 11, 2007): 163. http://dx.doi.org/10.1001/jama.298.2.163.

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6

Meijer, G. A., and J. J. Oudejans. "Targeted Therapies; Who Detects the Target?" Analytical Cellular Pathology 27, no. 3 (January 1, 2005): 165–67. http://dx.doi.org/10.1155/2005/235650.

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7

Wakabayashi, Hiroshi. "Molecular target therapies in rheumatic diseases." Okayama Igakkai Zasshi (Journal of Okayama Medical Association) 126, no. 3 (2014): 227–30. http://dx.doi.org/10.4044/joma.126.227.

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8

Robson, Andrew. "Three different therapies to target PCSK9." Nature Reviews Cardiology 18, no. 8 (June 4, 2021): 541. http://dx.doi.org/10.1038/s41569-021-00581-w.

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9

Hirsch, Etienne. "Parkinson's disease: A target for therapies?" Journal of the Neurological Sciences 429 (October 2021): 118011. http://dx.doi.org/10.1016/j.jns.2021.118011.

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10

Gillis, David. "Two Novel Therapies Target Cellular Microenvironment." Oncology Times 24, no. 2 (February 2002): 38. http://dx.doi.org/10.1097/01.cot.0000294265.17109.36.

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11

Sciarra, Alessandro, Michele Innocenzi, Michele Ravaziol, Francesco Minisola, Andrea Alfarone, Susanna Cattarino, Giuseppe Monti, Vincenzo Gentile, and Franco Di Silverio. "Neuroendocrine target therapies for prostate cancer." Rivista Urologia 78, no. 2 (2011): 137–41. http://dx.doi.org/10.5301/ru.2011.8335.

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12

Nickeleit, Irina, Steffen Zender, Uta Kossatz, and Nisar P. Malek. "p27kip1: a target for tumor therapies?" Cell Division 2, no. 1 (2007): 13. http://dx.doi.org/10.1186/1747-1028-2-13.

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13

Laino, Charlene. "Novel Therapies Target Advanced Kidney Cancer." Oncology Times 31, no. 11 (June 2009): 37–38. http://dx.doi.org/10.1097/01.cot.0000356663.15562.99.

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14

Laino, Charlene. "Novel therapies target advanced kidney cancer." Oncology Times UK 6, no. 5 (May 2009): 10–11. http://dx.doi.org/10.1097/01434893-200905000-00009.

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15

JANCIN, BRUCE. "New Cellulite Therapies Target Fibrous Septae." Skin & Allergy News 43, no. 6 (June 2012): 13. http://dx.doi.org/10.1016/s0037-6337(12)70229-2.

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16

Laino, Charlene. "Novel Therapies Target Advanced Kidney Cancer." Nephrology Times 2, no. 5 (May 2009): 17–18. http://dx.doi.org/10.1097/01.nep.0000352300.55779.b0.

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17

Nair, Pranav, and Kedar S. Prabhavalkar. "Neutrophilic Asthma and Potentially Related Target Therapies." Current Drug Targets 21, no. 4 (March 2, 2020): 374–88. http://dx.doi.org/10.2174/1389450120666191011162526.

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Background: Neutrophilic asthma is generally associated with the absence of eosinophils and activation of non- predominant type 2 immunological pathways. It involves bronchial inflammation followed by different degrees of airway remodeling. Neutrophilic inflammation activates specific cellular and molecular pathways due to inhalation of environmental trigger factors such as exhaust fumes, cigarette smoke, occupation-related agents, and infections. Objective: This review discusses the involvement of neutrophils in asthma and potentially related target therapies. Results: Corticosteroid resistance is the hallmark of neutrophilic asthma which increases disease severity and leads to difficult-to-control asthma. Patients with neutrophil-dominant asthma are characterized by low levels of (or absence of) Th2 cytokines. Due to the shortage of effective treatments for neutrophilic asthma newer biologics are being developed that target type 2 asthma symptoms and phenotypes. Understanding different biomarkers, inflammatory pathways and treatment strategies involved in neutrophilic asthma will help to decrease adverse effects related to corticosteroid insensitivity. Better insight of targets involved in neutrophilic inflammation can lead to improved therapies. Conclusion: Further evaluation and clinical trials of emerging biologics involved in neutrophilic asthma needs to be performed before bringing them into clinical practice.

18

Sciumè, Mariarita, Claudio De Magistris, Nicole Galli, Eleonora Ferretti, Giulia Milesi, Pasquale De Roberto, Sonia Fabris, and Federica Irene Grifoni. "Target Therapies for Systemic Mastocytosis: An Update." Pharmaceuticals 15, no. 6 (June 11, 2022): 738. http://dx.doi.org/10.3390/ph15060738.

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Systemic mastocytosis (SM) results from a clonal proliferation of abnormal mast cells (MCs) in extra-cutaneous organs. It could be divided into indolent SM, smoldering SM, SM with an associated hematologic (non-MC lineage) neoplasm, aggressive SM, and mast cell leukemia. SM is generally associated with the presence of a gain-of-function somatic mutation in KIT at codon 816. Clinical features could be related to MC mediator release or to uncontrolled infiltration of MCs in different organs. Whereas indolent forms have a near-normal life expectancy, advanced diseases have a poor prognosis with short survival times. Indolent forms should be considered for symptom-directed therapy, while cytoreductive therapy represents the first-line treatment for advanced diseases. Since the emergence of tyrosine kinase inhibitors (TKIs), KIT inhibition has been an attractive approach. Initial reports showed that only the rare KITD816V negative cases were responsive to first-line TKI imatinib. The development of new TKIs with activity against the KITD816V mutation, such as midostaurin or avapritinib, has changed the management of this disease. This review aims to focus on the available clinical data of therapies for SM and provide insights into possible future therapeutic targets.

19

&NA;. "'Plausible target' for new obesity therapies identified." Inpharma Weekly &NA;, no. 1287 (May 2001): 8. http://dx.doi.org/10.2165/00128413-200112870-00018.

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20

Cascinu, S., L. Verdecchia, N. Valeri, R. Berardi, and M. Scartozzi. "New target therapies in advanced pancreatic cancer." Annals of Oncology 17 (May 2006): v148—v152. http://dx.doi.org/10.1093/annonc/mdj971.

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21

Kuznar, W., and M. Gheorghiade. "Emerging Therapies for HF Target Different Pathophysiology." MD Conference Express 14, no. 12 (July 1, 2014): 29–30. http://dx.doi.org/10.1177/155989771412019.

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22

Stevenson, Lynne Warner, Gregory Couper, Barbara Natterson, Gregg Fonarow, Michele A. Hamilton, Mary Woo, and Julie W. Creaser. "Target Heart Failure Populations for Newer Therapies." Circulation 92, no. 9 (November 1995): 174–81. http://dx.doi.org/10.1161/01.cir.92.9.174.

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23

Turhan, Ali G. "STAT5 as a CML target: STATinib therapies?" Blood 117, no. 12 (March 24, 2011): 3252–53. http://dx.doi.org/10.1182/blood-2011-01-332569.

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24

&NA;. "Scientists identify protein target for vaccine therapies." Oncology Times UK 5, no. 7 (July 2008): 6. http://dx.doi.org/10.1097/01434893-200807000-00008.

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25

Vitali, Francesca, Francesca Mulas, Pietro Marini, and Riccardo Bellazzi. "Network-based target ranking for polypharmacological therapies." Journal of Biomedical Informatics 46, no. 5 (October 2013): 876–81. http://dx.doi.org/10.1016/j.jbi.2013.06.015.

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26

Tesser-Gamba, Francine, Antonio Sergio Petrilli, Mario Del Giudice Paniago, Maria Teresa Seixas Alves, Reynaldo Jesus Garcia-Filho, and Silvia R. C. Toledo. "MAPK7 gene: A target for multimodal therapies." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 10533. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.10533.

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10533 Background: Osteosarcoma (OS) is a class of cancer originating from the bone, affecting mainly children and young adults. In a previous work we observed that the overexpression of MAPK7 gene was significantly associated to tumor progression, a poor response to treatment, and worse overall survival, suggesting that MAPK7 could play an important role in osteosarcoma tumorigenesis. This present study investigated if any genomic structural alteration could be related to MAPK7 overexpression in OS samples. Methods: The MAPK7 gene was fully sequenced in 33 OS samples (15 prechemotherapy,15 post-chemotherapy and 3 OS cell lines) using the 3500 Genetic Analyser (Applied Biosystem) and 15 custom primers pairs that amplified overlapping genomic fragments. Results: From the 30 patient samples analyzed, 16 could not be completely sequenced. Samples containing these deleted regions were significantly correlated to clinical and pathologic features of patients with OS. No deletions were observed in patients with the favorable outcome (non-metastatic at diagnosis, >90% degree of necrosis in the surgical specimen and with complete remission at end of treatment). There was no correlation found between deletions and overexpression in pre-chemotherapy, even in patients that after chemotherapy still overexpressed MAPK7. Conclusions: Progress related to improved survival of patients with OS is at a plateau, and the intensification of therapy or incorporation of new therapeutic agents has not been successful, especially in patients metastatic at diagnosis. To our knowledge, no molecular marker for OS that could be related to its development, evolution or progression has been described yet. Based on our findings, we observed that patients who have no genomic deletion of MAPK7 gene respond better to treatment and have a favorable outcome. Studies available to date suggest that a single targeted therapy may not provide clinically significant anti-tumor effects, therefore we believe that specific inhibitors of the MAPK/ERK pathway are emerging as a relevant addition to multimodal therapies.

27

Gass, Jennifer, Mercedes Prudencio, Caroline Stetler, and Leonard Petrucelli. "Progranulin: An emerging target for FTLD therapies." Brain Research 1462 (June 2012): 118–28. http://dx.doi.org/10.1016/j.brainres.2012.01.047.

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28

Chung, Clement. "Current targeted therapies in lymphomas." American Journal of Health-System Pharmacy 76, no. 22 (October 3, 2019): 1825–34. http://dx.doi.org/10.1093/ajhp/zxz202.

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Abstract Purpose This article summarizes current targeted therapies that have received regulatory approval for the treatment of B- and T-cell lymphomas. Summary Over the last 20 years, new drug therapies for lymphomas of B cells and T cells have expanded considerably. Targeted therapies for B-cell lymphomas include: (1) monoclonal antibodies directed at the CD20 lymphocyte antigen, examples of which are rituximab, ofatumumab, and obinutuzumab; (2) gene transfer therapy, an example of which is chimeric antigen receptor–modified T-cell (CAR-T) therapy directed at the CD19 antigen expressed on the cell surface of both immature and mature B cells; and (3) small-molecule inhibitors (ibrutinib, acalabrutinib, copanlisib, duvelisib, and idelalisib) that target the B-cell receptor signaling pathway. Of note, brentuximab vedotin is an antibody–drug conjugate that targets CD30, another lymphocyte antigen expressed on the cell surface of both Hodgkin lymphoma (a variant of B-cell lymphoma) and some T-cell lymphomas. Although aberrant epigenetic signaling pathways are present in both B- and T-cell lymphomas, epigenetic inhibitors (examples include belinostat, vorinostat, and romidepsin) are currently approved by the Food and Drug Administration for T-cell lymphomas only. In addition, therapies that target the tumor microenvironment have been developed. Examples include mogamulizumab, bortezomib, lenalidomide, nivolumab, and pembrolizumab. In summary, the efficacy of these agents has led to the development of supportive care to mitigate adverse effects, due to the presence of on- or off-target toxicities. Conclusion The therapeutic landscape of lymphomas has continued to evolve. In turn, the efficacy of these agents has led to the development of supportive care to mitigate adverse effects, due to the presence of on- or off-target toxicities. Further opportunities are warranted to identify patients who are most likely to achieve durable response and reduce the risk of disease progression. Ongoing trials with current and investigational agents may further elucidate their place in therapy and therapeutic benefits.

29

Perna, Fabiana, Samuel Berman, Rajesh K. Soni, Jorge Mansilla-Soto, Justin Eyquem, Mohamad Hamieh, Ronald C. Hendrickson, Cameron Brennan, and Michel Sadelain. "Systematic Combinatorial Chimeric Antigen Receptor Therapies to AML." Blood 130, Suppl_1 (December 7, 2017): 856. http://dx.doi.org/10.1182/blood.v130.suppl_1.856.856.

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Abstract Chimeric antigen receptor (CAR) therapy targeting CD19 yields remarkable outcomes in patients with ALL. Three molecules (CD123, CD33 and CLEC12A) are currently targeted in clinical trials by CAR T cells for patients with AML. However, they do not feature expression profiles favorable as that of CD19. An ideal target should be expressed in all tumor cells, at high density and in most patients. To prevent undue toxicity, the ideal target should not be expressed on any normal tissue, or at least not in vital tissues, including normal counterparts. This task requires comprehensive sources of antigen annotation, as well as analytical tools specifically designed to identify potential CAR targets. To identify CAR targets in AML in an unbiased manner, we probed the AML surfaceome for highly abundant molecules with little to no expression in vital tissues. We assembled a comprehensive database of 4,942 AML surface molecules by combining public protein repositories and our own cell-surface proteomics from 6 distinct AML cell lines. We computed molecule-specific AML/normal HSPC expression ratios by comparing the RNA expression levels of 26 genetically defined AML subtypes to normal BM CD34+ CD38- CD90+ CD45RA- HSCs and MPP, GMP, CMP, MEP progenitor cells, identifying 682 molecules. We combined three proteomics databases including both immunohistochemistry (HPA) and mass spectrometry (HPM and PDB) data, prioritizing antigens with membrane-associated sub-localization and expression data supported by multiple sources, thus removing 321 molecules. Finally, we selected top 24 molecules exhibiting low average expression across 43 clusters of normal tissues, and no high expression in any normal tissue, excluding blood, bone marrow and spleen. We further defined the expression of these candidate targets in a panel of 30 primary AML samples and AML LSCs, and focused on nine candidate molecules with >75% expression in most patients. Four of these, ADGRE2, CCR1, CD70 and LILRB2, showed <5% expression in normal BM HSCs and T cells, which is critical to prevent HSC toxicity and T cell self-elimination. While they may have therapeutic potential, they are not ideal or as good as CD19. This prompted us to explore combinatorial targeting strategies, which fall in two major categories (Figure 1). One is based on cumulative CAR targeting through the generation of bi-specific T cells that co-express two CARs and recognize target cells expressing any of two given antigens (CAR/CAR). Some low or moderate expression in normal tissues, albeit not optimal, may be tolerable depending on the tissues in question. The other takes advantage of split signaling to target two antigens, using one antigen to direct costimulation to enhance or rescue the suboptimal function of a CAR or TCR targeting the other antigen. In the latter approach (CAR/CCR), T cells are more restricted to dual-antigen positive tumor cells, thus relaxing the expression criteria for at least one of the paired antigens. However, pan-tumor expression of the CAR target is required. In both instances, target pairings depend on the systemic expression and co-expression of the two prospective matches to minimize cumulative expression in normal tissues. We optimized target selection by pairing targets with non-overlapping expression in normal tissues. Starting from 12 molecules with the best expression profiles (9 candidate targets described above in addition to CD123, CD33, and CLEC12A), the 66 possible pairings, yielded few promising therapeutic combinations. We studied four combinations: CD33+ADGRE2, CLEC12A+CCR1, CD33+CD70, and LILRB2+CLEC12A, which exhibit expression profiles unlikely to exacerbate on-target/off-tumor activity of either target alone and stained <5% of normal HSCs and T cells. Three pairings positively stained >97% of cells in AML samples, significantly above either marker alone. It is however noteworthy that total positivity was significantly higher than dual-positivity, suggesting the presence of cells expressing one antigen only. This finding is consistent with AML clonal heterogeneity and favors using such antigen pairs in the dual-targeting approach (CAR/CAR). This present study represents a new approach to the discovery of CAR targets and will help advance the development of CAR therapy for AML and other cancers. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

30

Consuegra-Fernandez, Marta, Fernando Aranda, Ines Simoes, Marc Orta, Adelaida Sarukhan, and Francisco Lozano. "CD5 as a Target for Immune-Based Therapies." Critical Reviews in Immunology 35, no. 2 (2015): 85–115. http://dx.doi.org/10.1615/critrevimmunol.2015013532.

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31

Aroldi, Francesca, Paola Bertocchi, Edoardo Rosso, Tiziana Prochilo, and Alberto Zaniboni. "Pancreatic Cancer: Promises and Failures of Target Therapies." Reviews on Recent Clinical Trials 11, no. 1 (January 25, 2016): 33–38. http://dx.doi.org/10.2174/1574887110666150930122720.

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32

Williams, Sarah C. P. "Early-stage therapies target surgery-induced erectile dysfunction." Nature Medicine 18, no. 10 (October 2012): 1444. http://dx.doi.org/10.1038/nm1012-1444.

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33

van Herpen, Carla M. L., Winette T. A. van der Graaf, and Wim J. G. Oyen. "Time to target evaluation criteria of targeted therapies." Nuclear Medicine Communications 30, no. 7 (July 2009): 487–89. http://dx.doi.org/10.1097/mnm.0b013e3283294d32.

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34

Pillai, Krishna, Mohammad H. Pourgholami, Terence C. Chua, and David L. Morris. "MUC1 as a Potential Target in Anticancer Therapies." American Journal of Clinical Oncology 38, no. 1 (February 2015): 108–18. http://dx.doi.org/10.1097/coc.0b013e31828f5a07.

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35

Ingram, G. M., and J. H. Kinnaird. "Ribonucleotide Reductase: A New Target for Antiparasite Therapies." Parasitology Today 15, no. 8 (August 1999): 338–42. http://dx.doi.org/10.1016/s0169-4758(99)01478-7.

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36

Moise, Alexander R., Noa Noy, Krzysztof Palczewski, and William S. Blaner. "Delivery of Retinoid-Based Therapies To Target Tissues†." Biochemistry 46, no. 15 (April 2007): 4449–58. http://dx.doi.org/10.1021/bi7003069.

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37

McClellan, Karen. "Cytokine-target therapies cost effective in Crohn’s disease?" PharmacoEconomics & Outcomes News 196, no. 1 (January 1999): 3. http://dx.doi.org/10.1007/bf03274779.

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38

Henderson, Beric. "Nuclear transport as a target for cancer therapies." Drug Discovery Today 8, no. 6 (March 2003): 249. http://dx.doi.org/10.1016/s1359-6446(03)02628-x.

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39

Firth, Jill, and Sarah Critchley. "Treating to target in rheumatoid arthritis: biologic therapies." British Journal of Nursing 20, no. 20 (November 8, 2011): 1284–91. http://dx.doi.org/10.12968/bjon.2011.20.20.1284.

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40

Thangaraju, Pugazhenthan, ShobanBabu Varthya, and Sajitha Venkatesan. "Target/therapies for chronic recurrent erythema nodosum leprosum." Indian Journal of Pharmacology 52, no. 3 (2020): 222. http://dx.doi.org/10.4103/ijp.ijp_788_19.

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41

VanAuker, Michael D., and Elizabeth Hood. "Delivery strategies to target therapies to inflammatory tissue." Expert Opinion on Drug Delivery 5, no. 7 (July 2008): 767–74. http://dx.doi.org/10.1517/17425247.5.7.767.

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42

Holinstat, M., and PF Bray. "Protease receptor antagonism to target blood platelet therapies." Clinical Pharmacology & Therapeutics 99, no. 1 (November 18, 2015): 72–81. http://dx.doi.org/10.1002/cpt.282.

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43

Saberinia, Amin, Amin Alinezhad, Fatemeh Jafari, Setareh Soltany, and Reza Akhavan Sigari. "Oncogenic miRNAs and target therapies in colorectal cancer." Clinica Chimica Acta 508 (September 2020): 77–91. http://dx.doi.org/10.1016/j.cca.2020.05.012.

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44

Hampton, Tracy. "Researchers Identify New Candidate Target for Asthma Therapies." JAMA 310, no. 9 (September 4, 2013): 894. http://dx.doi.org/10.1001/jama.2013.277035.

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45

Stein, Eytan M. "Molecularly targeted therapies for acute myeloid leukemia." Hematology 2015, no. 1 (December 5, 2015): 579–83. http://dx.doi.org/10.1182/asheducation-2015.1.579.

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Abstract The past 15 years have seen major leaps in our understanding of the molecular genetic mutations that act as drivers of acute myeloid leukemia (AML). Clinical trials of agents against specific mutant proteins, such as FLT3-internal tandem duplications (ITDs) and isocitrate dehydrogenase mutations (IDHs) are ongoing. This review discusses agents in clinical trials that target specific gene mutations and/or epigenetic targets.

46

Gayan, Chathura. "Evaluate the response of Apoptosis, Angiogenesis and Cancer Therapies." Cancer Research and Cellular Therapeutics 2, no. 1 (March 28, 2018): 01–08. http://dx.doi.org/10.31579/2640-1053/022.

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Angiogenesis, the growth of new blood vessels from the existing vasculature, and is maintained in adult tissues by the balanced presence of both angiogenic inducers and inhibitors in the tissue milieu. When inducers predominate, vascular endothelial cells (VECs) become activated and in this activated VECs, distinct cell signaling pathways are initiated providing the specificity of anti-angiogenic therapies to the tumor vasculature. VEC apoptosis has been well documented in regressing vessels, and it has been shown that, in addition to activating the VECs, some inducers such as vascular endothelial growth factor also up-regulate Fas expression, thus sensitizing the cell to apoptotic stimuli. Endogenous angiogenesis inhibitors, such as thrombospondin-1(TSP-1) and pigment epithelium-derived factor (PEDF), stimulate signaling cascades within the VECs and also induce the expression of Fas ligand in activated VECs. Therefore, when inhibitors predominate, the apoptotic cascade is initiated ,thus anti-angiogenic therapies can target the inducer supply or directly target the VECs. Although clinical studies suggest that anti-angiogenic therapies may prove to be most effective when used in combination with traditional therapies

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Gluba-Brzózka, Anna, Beata Franczyk, Magdalena Rysz-Górzyńska, Janusz Ławiński, and Jacek Rysz. "Emerging Anti-Atherosclerotic Therapies." International Journal of Molecular Sciences 22, no. 22 (November 9, 2021): 12109. http://dx.doi.org/10.3390/ijms222212109.

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Cardiovascular disease (CAD) is the main cause of morbidity and deaths in the western world. The development of atherosclerosis underlying CAD development begins early in human life. There are numerous genetic and environmental risk factors accelerating its progression which then leads to the occurrence of acute events. Despite considerable progress in determining risk factors, there is still a lot of work ahead since identified determinants are responsible only for a part of overall CAD risk. Current therapies are insufficient to successfully reduce the risk of atherosclerosis development. Therefore, there is a need for effective preventive measures of clinical manifestations of atherosclerosis since the currently available drugs cannot prevent the occurrence of even 70% of clinical events. The shift of the target from lipid metabolism has opened the door to many new therapeutic targets. Currently, the majority of known targets for anti-atherosclerotic drugs focus also on inflammation (a common mediator of many risk factors), mechanisms of innate and adaptive immunity in atherosclerosis, molecule scavengers, etc. The therapeutic potential of cyclodextrins, protein kinase inhibitors, colchicine, inhibitors of p38 mitogen-activated protein kinase (MAPK), lipid dicarbonyl scavengers, a monoclonal antibody targeting interleukin-1β, and P-selectin inhibitors is still not fully confirmed and requires confirmation in large clinical trials. The preliminary results look promising.

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Godbole, Abhijit M., and Vincent C. O. Njar. "New Insights into the Androgen-Targeted Therapies and Epigenetic Therapies in Prostate Cancer." Prostate Cancer 2011 (2011): 1–13. http://dx.doi.org/10.1155/2011/918707.

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Prostate cancer is the most common cancer in men in the United States, and it is the second leading cause of cancer-related death in American men. The androgen receptor (AR), a receptor of nuclear family and a transcription factor, is the most important target in this disease. While most efforts in the clinic are currently directed at lowering levels of androgens that activate AR, resistance to androgen deprivation eventually develops. Most prostate cancer deaths are attributable to this castration-resistant form of prostate cancer (CRPC). Recent work has shed light on the importance of epigenetic events including facilitation of AR signaling by histone-modifying enzymes, posttranslational modifications of AR such as sumoylation. Herein, we provide an overview of the structure of human AR and its key structural domains that can be used as targets to develop novel antiandrogens. We also summarize recent findings about the antiandrogens and the epigenetic factors that modulate the action of AR.

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Serrano, Manuel. "SHP2: a new target for pro‐senescence cancer therapies." EMBO Journal 34, no. 11 (April 27, 2015): 1439–41. http://dx.doi.org/10.15252/embj.201591616.

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Järvinen, Tero, Ulrike May, and Stuart Prince. "Systemically Administered, Target Organ-Specific Therapies for Regenerative Medicine." International Journal of Molecular Sciences 16, no. 10 (September 30, 2015): 23556–71. http://dx.doi.org/10.3390/ijms161023556.

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