Journal articles on the topic 'Precision cancer therapy'

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1

Nalley, Catlin. "Precision Therapy in Lung Cancer." Oncology Times 42, no. 18 (September 20, 2020): 21. http://dx.doi.org/10.1097/01.cot.0000717748.60516.e7.

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2

Al-Janabi, Ismail. "Pharmacogenomics Driving Precision Cancer Medicine." Al-Rafidain Journal of Medical Sciences ( ISSN: 2789-3219 ) 3 (October 24, 2022): 48–63. http://dx.doi.org/10.54133/ajms.v3i.85.

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Genetically-driven variations in the proteins associated with drug action and adverse effects can lead to a significant influence on cancer therapy. Cancer cells can accumulate a plethora of somatic mutations, beyond any existing germline variants, during their progression from normalcy to malignancy. The narrow therapeutic index that characterises cancer drugs and the life-threatening failure of therapy all point to the importance of considering the inclusion of pharmacogenomics when treating cancers. This narrative review discusses the application, merits and challenges of pharmacogenomics knowledge using a few representative examples. The adoption of a properly considered pharmacogenomic program during cancer treatments can be life-saving and rewarding.
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3

Wong, Ada Hang-Heng, and Chu-Xia Deng. "Precision Medicine for Personalized Cancer Therapy." International Journal of Biological Sciences 11, no. 12 (2015): 1410–12. http://dx.doi.org/10.7150/ijbs.14154.

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4

Kato, Shumei, and Razelle Kurzrock. "An avatar for precision cancer therapy." Nature Biotechnology 36, no. 11 (November 2018): 1053–55. http://dx.doi.org/10.1038/nbt.4293.

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Dummer, Reinhard. "Precision medicine and skin cancer therapy." Current Opinion in Oncology 26, no. 2 (March 2014): 182–83. http://dx.doi.org/10.1097/cco.0000000000000059.

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6

Thomas, Anish. "More precision in lung cancer therapy." Science Translational Medicine 7, no. 287 (May 13, 2015): 287ec79. http://dx.doi.org/10.1126/scitranslmed.aab3977.

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7

Schiff, Joshua P., Pedro C. Barata, Evan Y. Yu, and Petros Grivas. "Precision therapy in advanced urothelial cancer." Expert Review of Precision Medicine and Drug Development 4, no. 2 (March 4, 2019): 81–93. http://dx.doi.org/10.1080/23808993.2019.1582298.

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Sapiezynski, Justin, Oleh Taratula, Lorna Rodriguez-Rodriguez, and Tamara Minko. "Precision targeted therapy of ovarian cancer." Journal of Controlled Release 243 (December 2016): 250–68. http://dx.doi.org/10.1016/j.jconrel.2016.10.014.

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9

Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "CAR T Cells: Precision Cancer Immunotherapy." Indonesian Biomedical Journal 10, no. 3 (December 28, 2018): 203–16. http://dx.doi.org/10.18585/inabj.v10i3.635.

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BACKGROUND: Current cancer drugs and treatments are aiming at eradicating tumor cells, but often are more toxic then effective, killing also the normal cells and not selectively the tumor cells. There is good personalized cancer therapy that involves administration to the cancer-bearing host of immune cells with direct anticancer activity, which called adoptive cell therapy (ACT). A review of the unique biology of T cell therapy and of recent clinical experience compels a reassessment of target antigens that traditionally have been viewed from the perspective of weaker immunotherapeutic modalities.CONTENT: Chimeric antigen receptors (CAR) are recombinant receptors which provide both antigen-binding and T cell-activating functions. Many kind of CARs has been reported for the past few years, targeting an array of cell surface tumor antigens. Their biologic functions have extremely changed following the introduction of tripartite receptors comprising a costimulatory domain, termed second-generation CARs. The combination of CARs with costimulatory ligands, chimeric costimulatory receptors, or cytokines can be done to further enhance T cell potency, specificity and safety. CARs reflects a new class of drugs with exciting potential for cancer immunotherapy.SUMMARY: CAR-T cells have been arising as a new modality for cancer immunotherapy because of their potent efficacy against terminal cancers. They are known to exert higher efficacy than monoclonal antibodies and antibodydrug conjugates, and act via mechanisms distinct from T cell receptor-engineered T cells. These cells are constructed by transducing genes encoding fusion proteins of cancer antigen-recognizing single-chain Fv linked to intracellular signaling domains of T cell receptors.KEYWORDS: chimeric antigen receptor, CAR T cells, adoptive cell therapy, ACT, T cell receptor, TCR, cancer, immunotherapy
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10

Henscheid, Nick, Eric Clarkson, Kyle J. Myers, and Harrison H. Barrett. "Physiological random processes in precision cancer therapy." PLOS ONE 13, no. 6 (June 29, 2018): e0199823. http://dx.doi.org/10.1371/journal.pone.0199823.

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11

Dienstmann, Rodrigo, Kate Connor, Annette T. Byrne, W. H. Fridman, D. Lambrechts, A. Sadanandam, L. Trusolino, J. H. M. Prehn, J. Tabernero, and W. Kolch. "Precision Therapy in RAS Mutant Colorectal Cancer." Gastroenterology 158, no. 4 (March 2020): 806–11. http://dx.doi.org/10.1053/j.gastro.2019.12.051.

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12

Koch, Linda. "A network to guide precision cancer therapy." Nature Reviews Genetics 17, no. 9 (August 8, 2016): 505. http://dx.doi.org/10.1038/nrg.2016.105.

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13

Reimers, M. S., E. C. M. Zeestraten, P. J. K. Kuppen, G. J. Liefers, and C. J. H. van de Velde. "Biomarkers in precision therapy in colorectal cancer." Gastroenterology Report 1, no. 3 (August 23, 2013): 166–83. http://dx.doi.org/10.1093/gastro/got022.

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14

Zhang, Xiaoli, Jinming Yu, and Min Li. "Precision regimen for personalized pancreatic cancer therapy." Precision Radiation Oncology 1, no. 2 (June 2017): 44–45. http://dx.doi.org/10.1002/pro6.19.

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15

Knisely, Jonathan P. S. "Precision Medicine—Targeted Therapy." International Journal of Radiation Oncology*Biology*Physics 102, no. 4 (November 2018): 734. http://dx.doi.org/10.1016/j.ijrobp.2018.07.190.

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16

Chen, Guoli, Zhaohai Yang, James R. Eshleman, George J. Netto, and Ming-Tseh Lin. "Molecular Diagnostics for Precision Medicine in Colorectal Cancer: Current Status and Future Perspective." BioMed Research International 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/9850690.

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Precision medicine, a concept that has recently emerged and has been widely discussed, emphasizes tailoring medical care to individuals largely based on information acquired from molecular diagnostic testing. As a vital aspect of precision cancer medicine, targeted therapy has been proven to be efficacious and less toxic for cancer treatment. Colorectal cancer (CRC) is one of the most common cancers and among the leading causes for cancer related deaths in the United States and worldwide. By far, CRC has been one of the most successful examples in the field of precision cancer medicine, applying molecular tests to guide targeted therapy. In this review, we summarize the current guidelines for anti-EGFR therapy, revisit the roles of pathologists in an era of precision cancer medicine, demonstrate the transition from traditional “one test-one drug” assays to multiplex assays, especially by using next-generation sequencing platforms in the clinical diagnostic laboratories, and discuss the future perspectives of tumor heterogeneity associated with anti-EGFR resistance and immune checkpoint blockage therapy in CRC.
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17

Shneider, Olga V., Tatyana A. Kamilova, Alexander S. Golota, Andrey M. Sarana, and Sergey G. Sсherbak. "Biomarkers and Target Therapy for Lung Cancer." Physical and rehabilitation medicine, medical rehabilitation 3, no. 1 (April 28, 2021): 74–94. http://dx.doi.org/10.36425/rehab63268.

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Precision (target) medicine is proposed as a new strategy to identify and develop new highly selective drugs against specific targets for the disease and more precise tailoring of medicines to the target populations of patients. Precision medicine can be an important approach to create more novel and safer therapeutics (tyrosine kinase inhibitors, tumour specific monoclonal antibodies) for patients with gene mutation, aberrations, or protein over-expression. Precision medicine requires an understanding mutational processes, and heterogeneity between cancer cells during tumor evolution. The present review briefly define various heterogeneities and potential associations with drug efficacy and resistance, emphasize the importance to develop functional biomarkers to monitor drug efficacy and resistance, and define opportunities and challenges of precision medicine for clinical practice.
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18

Strand, Matthew S., Hua Pan, Julie G. Grossman, Peter S. Goedegebuure, Timothy Fleming, Samuel A. Wickline, and Ryan C. Fields. "Precision cancer therapy through nanoparticle delivery of siRNA against KRAS." Journal of Clinical Oncology 34, no. 4_suppl (February 1, 2016): 260. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.260.

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260 Background: Small interfering RNA (siRNA) has potential for highly specific gene manipulation, making it attractive for delivering precision therapy to cancer patients. However, efforts to employ siRNA therapeutically have been limited by its short half-life in circulation, low target tissue specificity, and cellular entrapment within endosomes. We utilized serum-stable, cell-penetrating, and endosomolytic peptide-based nanoparticles (NPs) to overcome these obstacles and deliver siRNA against KRAS to KRAS-mutant human and mouse pancreas and colorectal cancers. Methods: Human and mouse pancreas and colorectal cancer cell lines were tested for NP uptake in vitro utilizing fluorescent siRNAs. Uptake was assessed via fluorescent microscopy and flow cytometry (FC). Mice bearing tumors from these cells were injected IV with the same NP, and uptake was assessed with an in vivo imaging system (IVIS), and FC. Cell lines were treated with KRAS-siRNA NP and KRAS knockdown was assessed by real-time PCR. Results: Mouse and human pancreas and colorectal cancer cell lines took up NP in vitro, with signal detected within > 93% of cells at 24 hours. Tumors from these cells grown in mice were strongly fluorescent after IV injection of fluorescent NP within 2 hours, and until at least 30 hours. FC of a tumor treated with fluorescent NP showed that 86% of tumor cells expressed fluorescent signal 24 hours post-injection. IVIS revealed signal in mouse liver and kidneys, but when assessed by FC, only 17.8% and 13.5% of cells from these tissues were fluorescent, respectively. The brain, heart, lungs, spleen, and pancreas of mice receiving injections were negative. Cancer cell lines exposed to KRAS-siRNA NP for 48 hours express KRAS at levels that are 4.5 to 15.1% of untreated cells. Conclusions: Human and mouse pancreas and colorectal cancers efficiently and specifically take up NP in vitro and in vivo. Selected limitations of siRNA are overcome with this NP delivery system, and NP-packaged siRNA effectively inhibits KRAS. This platform represents a highly specific approach to targeting tumor genes of interest, which may ultimately enable selective knockdown of putative drivers of tumor progression.
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19

Fazio, Maurizio, Julien Ablain, Yan Chuan, David M. Langenau, and Leonard I. Zon. "Zebrafish patient avatars in cancer biology and precision cancer therapy." Nature Reviews Cancer 20, no. 5 (April 6, 2020): 263–73. http://dx.doi.org/10.1038/s41568-020-0252-3.

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20

De Ruysscher, Dirk, Jianyue Jin, Tim Lautenschlaeger, Jin-Xiong She, Zhongxing Liao, and Feng-Ming Spring Kong. "Blood-based biomarkers for precision medicine in lung cancer: precision radiation therapy." Translational Lung Cancer Research 6, no. 6 (December 2017): 661–69. http://dx.doi.org/10.21037/tlcr.2017.09.12.

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21

Hudis, Clifford A., and Maura Dickler. "Increasing Precision in Adjuvant Therapy for Breast Cancer." New England Journal of Medicine 375, no. 8 (August 25, 2016): 790–91. http://dx.doi.org/10.1056/nejme1607947.

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22

Tydings, Caitlin, and AeRang Kim. "Technology and precision therapy delivery in childhood cancer." Current Opinion in Pediatrics 32, no. 1 (February 2020): 1–6. http://dx.doi.org/10.1097/mop.0000000000000865.

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23

Labrie, Marilyne, Nicholas D. Kendsersky, Hongli Ma, Lydia Campbell, Jennifer Eng, Koei Chin, and Gordon B. Mills. "Proteomics advances for precision therapy in ovarian cancer." Expert Review of Proteomics 16, no. 10 (September 13, 2019): 841–50. http://dx.doi.org/10.1080/14789450.2019.1666004.

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24

Pillarsetty, Nagavarakishore, Komal Jhaveri, Tony Taldone, Eloisi Caldas-Lopes, Blesida Punzalan, Suhasini Joshi, Alexander Bolaender, et al. "Paradigms for Precision Medicine in Epichaperome Cancer Therapy." Cancer Cell 36, no. 5 (November 2019): 559–73. http://dx.doi.org/10.1016/j.ccell.2019.09.007.

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25

Meng, Ling-hua, and XF Steven Zheng. "Toward rapamycin analog (rapalog)-based precision cancer therapy." Acta Pharmacologica Sinica 36, no. 10 (August 24, 2015): 1163–69. http://dx.doi.org/10.1038/aps.2015.68.

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26

Sayed, Ahmed, Malak Munir, Noor Eweis, Doaa Wael, Omar Shazly, Ahmed K. Awad, Marihan A. Elbadawy, and Sanaa Eissa. "An overview on precision therapy in bladder cancer." Expert Review of Precision Medicine and Drug Development 5, no. 5 (August 16, 2020): 347–61. http://dx.doi.org/10.1080/23808993.2020.1801346.

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27

Sun, Huanli, Yangyang Dong, Jan Feijen, and Zhiyuan Zhong. "Peptide-decorated polymeric nanomedicines for precision cancer therapy." Journal of Controlled Release 290 (November 2018): 11–27. http://dx.doi.org/10.1016/j.jconrel.2018.09.029.

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28

Lin, Jessica J., and Alice T. Shaw. "Refining precision cancer therapy in ALK-positive NSCLC." EBioMedicine 41 (March 2019): 9–10. http://dx.doi.org/10.1016/j.ebiom.2019.01.059.

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29

Janakiraman, Harinarayanan, Yun Zhu, Scott A. Becker, Cindy Wang, Ashley Cross, Emily Curl, David Lewin, et al. "Modeling rectal cancer to advance neoadjuvant precision therapy." International Journal of Cancer 147, no. 5 (February 3, 2020): 1405–18. http://dx.doi.org/10.1002/ijc.32876.

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30

Turano, Mimmo, Paolo Delrio, Daniela Rega, Francesca Cammarota, Alessia Polverino, Francesca Duraturo, Paola Izzo, and Marina De Rosa. "Promising Colorectal Cancer Biomarkers for Precision Prevention and Therapy." Cancers 11, no. 12 (December 4, 2019): 1932. http://dx.doi.org/10.3390/cancers11121932.

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Colorectal cancer (CRC) has been ranked as the third most prevalent cancer worldwide. Indeed, it represents 10.2% of all cancer cases. It is also the second most common cause of cancer mortality, and accounted for about 9.2% of all cancer deaths in 2018. Early detection together with a correct diagnosis and staging remains the most effective clinical strategy in terms of disease recovery. Thanks to advances in diagnostic techniques, and improvements of surgical adjuvant and palliative therapies, the mortality rate of CRC has decreased by more than 20% in the last decade. Cancer biomarkers for the early detection of CRC, its management, treatment and follow-up have contributed to the decrease in CRC mortality. Herein, we provide an overview of molecular biomarkers from tumor tissues and liquid biopsies that are approved for use in the CRC clinical setting for early detection, follow-up, and precision therapy, and of biomarkers that have not yet been officially validated and are, nowadays, under investigation.
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31

McCrea, Edel M., Daniel K. Lee, Tristan M. Sissung, and William D. Figg. "Precision medicine applications in prostate cancer." Therapeutic Advances in Medical Oncology 10 (January 1, 2018): 175883591877692. http://dx.doi.org/10.1177/1758835918776920.

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Aided by developments in diagnostics and therapeutics, healthcare is increasingly moving toward precision medicine, in which treatment is customized to each individual. We discuss the relevance of precision medicine in prostate cancer, including gene targets, therapeutics and resistance mechanisms. We foresee precision medicine becoming an integral component of prostate cancer management to increase response to therapy and prolong survival.
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32

Roychowdhury, Sameek, and Arul M. Chinnaiyan. "Advancing Precision Medicine for Prostate Cancer Through Genomics." Journal of Clinical Oncology 31, no. 15 (May 20, 2013): 1866–73. http://dx.doi.org/10.1200/jco.2012.45.3662.

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Prostate cancer is the most common type of cancer in men and the second leading cause of cancer death in men in the United States. The recent surge of high-throughput sequencing of cancer genomes has supported an expanding molecular classification of prostate cancer. Translation of these basic science studies into clinically valuable biomarkers for diagnosis and prognosis and biomarkers that are predictive for therapy is critical to the development of precision medicine in prostate cancer. We review potential applications aimed at improving screening specificity in prostate cancer and differentiating aggressive versus indolent prostate cancers. Furthermore, we review predictive biomarker candidates involving ETS gene rearrangements, PTEN inactivation, and androgen receptor signaling. These and other putative biomarkers may signify aberrant oncogene pathway activation and provide a rationale for matching patients with molecularly targeted therapies in clinical trials. Lastly, we advocate innovations for clinical trial design to incorporate tumor biopsy and molecular characterization to develop biomarkers and understand mechanisms of resistance.
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Song, Cheeun, Seung Ju Jang, Woo Hyeok Jeon, Sejung Maeng, Jong Hyun Tae, and In Ho Chang. "Nanomedicines for Therapy of Bladder Cancer." Korean Journal of Urological Oncology 20, no. 4 (November 30, 2022): 235–47. http://dx.doi.org/10.22465/kjuo.2022.20.4.235.

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Bladder cancer is one of most common malignant urinary tract tumor types, and transurethral resection of nonmuscle invasive bladder cancer followed by intravesical instillation of immunochemotherapy is the standard treatment approach to minimize recurrence and delay progression of bladder cancer. In general, conventional intravesical immunochemotherapy lacks selectivity for tumor tissues and the effect of drug is reduced with the excretion of urine leading to frequent administration and bladder irritation symptoms. Recently, nanomedicines which adhere to the bladder tumors for a long time, and continuously and efficiently release drug to bladder cancers may overcome all the above problems. Moreover, the advances in nanomedicine based targeted therapy have led to significant improvements in drug efficacy and precision of targeted drug delivery. This review shows the available nano-systems of targeted drug delivery to bladder cancer tissues.
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34

Liow, Elizabeth, and Ben Tran. "Precision oncology in urothelial cancer." ESMO Open 5, Suppl 1 (March 2020): e000616. http://dx.doi.org/10.1136/esmoopen-2019-000616.

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Genomics-driven, precision medicine has been adopted in virtually every tumour type and underlies the significant advances in cancer management to date. The paradigm shift from the indiscriminate use of chemotherapeutics, to strategies that harness our mechanistic knowledge of cancer biology has led to profound clinical benefit for patients, and will continue to mould present and future treatment approaches. In the realm of urothelial cancer, the present status of precision medicine includes a rich landscape that encompasses molecularly-matched therapy, predictive biomarkers that could help inform response to chemotherapy and immunotherapy, as well as novel strategies such as antibody drug conjugates that exploit the use of target proteins for enhanced tumour killing. Here, we present an overview on these clinically-impactful discoveries in urothelial cancer, discuss the limitations and challenges in the implementation of precision oncology, and offer our vision for its future.
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35

Jadvar, Hossein. "Targeted Radionuclide Therapy: An Evolution Toward Precision Cancer Treatment." American Journal of Roentgenology 209, no. 2 (August 2017): 277–88. http://dx.doi.org/10.2214/ajr.17.18264.

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36

Yan, Xiang, and Bingliang Fang. "Harnessing plasma genotyping for precision therapy against lung cancer." Journal of Thoracic Disease 8, no. 10 (October 2016): E1387—E1390. http://dx.doi.org/10.21037/jtd.2016.10.95.

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37

Ferreira, Meghaan. "OncoDNA's Research Projects Seek to Enable Precision Cancer Therapy." Clinical OMICs 4, no. 2 (March 2017): 33. http://dx.doi.org/10.1089/clinomi.04.02.30.

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38

Kurnit, Katherine C., Ann M. Bailey, Jia Zeng, Amber M. Johnson, Md Abu Shufean, Lauren Brusco, Beate C. Litzenburger, et al. "“Personalized Cancer Therapy”: A Publicly Available Precision Oncology Resource." Cancer Research 77, no. 21 (October 31, 2017): e123-e126. http://dx.doi.org/10.1158/0008-5472.can-17-0341.

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39

Li, Yujing, Jianxun Ding, Xiaoding Xu, Run Shi, Phei Er Saw, Junqing Wang, Shirley Chung, et al. "Dual Hypoxia-Targeting RNAi Nanomedicine for Precision Cancer Therapy." Nano Letters 20, no. 7 (June 1, 2020): 4857–63. http://dx.doi.org/10.1021/acs.nanolett.0c00757.

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40

Efstathiou, Eleni. "Attaining precision therapy in prostate cancer: A tall order." European Journal of Cancer 81 (August 2017): 226–27. http://dx.doi.org/10.1016/j.ejca.2017.05.011.

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41

Ciecielski, Katrin Jana, Alexandra Berninger, and Hana Algül. "Precision Therapy of Pancreatic Cancer: From Bench to Bedside." Visceral Medicine 36, no. 5 (2020): 373–80. http://dx.doi.org/10.1159/000509232.

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<b><i>Background:</i></b> Pancreatic ductal adenocarcinoma (PDAC), with a mortality rate of 94% and a 5-year-survival rate of only 8%, is one of the deadliest cancer entities worldwide, and early diagnostic methods as well as effective therapies are urgently needed. <b><i>Summary:</i></b> This review summarizes current clinical procedure and recent developments of oncological therapy in the palliative setting of metastatic PDAC. It further gives examples of successful, as well as failed, targeted therapy approaches and finally discusses promising ongoing research into the decade-old question of the “undruggability” of KRAS. <b><i>Key Messages:</i></b> Bench-driven concepts change the clinical landscape from “one size fits all” towards precision medicine. With growing insight into the molecular mechanisms of pancreatic cancer the era of targeted therapy in PDAC is gaining a new momentum.
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42

Thiagalingam, S. "The road to precision cancer therapy – history and strategies." Journal of the National Science Foundation of Sri Lanka 50 (November 10, 2022): 321. http://dx.doi.org/10.4038/jnsfsr.v50i0.11247.

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43

Bae, JuneSung, Yun Sik Choi, Gunsik Cho, and Se Jin Jang. "The Patient-Derived Cancer Organoids: Promises and Challenges as Platforms for Cancer Discovery." Cancers 14, no. 9 (April 25, 2022): 2144. http://dx.doi.org/10.3390/cancers14092144.

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The cancer burden is rapidly increasing in most countries, and thus, new anticancer drugs for effective cancer therapy must be developed. Cancer model systems that recapitulate the biological processes of human cancers are one of the cores of the drug development process. PDCO has emerged as a unique model that preserves the genetic, physiological, and histologic characteristics of original cancer, including inter- and intratumoral heterogeneities. Due to these advantages, the PCDO model is increasingly investigated for anticancer drug screening and efficacy testing, preclinical patient stratification, and precision medicine for selecting the most effective anticancer therapy for patients. Here, we review the prospects and limitations of PDCO compared to the conventional cancer models. With advances in culture success rates, co-culture systems with the tumor microenvironment, organoid-on-a-chip technology, and automation technology, PDCO will become the most promising model to develop anticancer drugs and precision medicine.
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44

Bae, JuneSung, Yun Sik Choi, Gunsik Cho, and Se Jin Jang. "The Patient-Derived Cancer Organoids: Promises and Challenges as Platforms for Cancer Discovery." Cancers 14, no. 9 (April 25, 2022): 2144. http://dx.doi.org/10.3390/cancers14092144.

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The cancer burden is rapidly increasing in most countries, and thus, new anticancer drugs for effective cancer therapy must be developed. Cancer model systems that recapitulate the biological processes of human cancers are one of the cores of the drug development process. PDCO has emerged as a unique model that preserves the genetic, physiological, and histologic characteristics of original cancer, including inter- and intratumoral heterogeneities. Due to these advantages, the PCDO model is increasingly investigated for anticancer drug screening and efficacy testing, preclinical patient stratification, and precision medicine for selecting the most effective anticancer therapy for patients. Here, we review the prospects and limitations of PDCO compared to the conventional cancer models. With advances in culture success rates, co-culture systems with the tumor microenvironment, organoid-on-a-chip technology, and automation technology, PDCO will become the most promising model to develop anticancer drugs and precision medicine.
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45

Zeng, Zihua, Ching-Hsuan Tung, and Youli Zu. "Aptamer-Equipped Protamine Nanomedicine for Precision Lymphoma Therapy." Cancers 12, no. 4 (March 25, 2020): 780. http://dx.doi.org/10.3390/cancers12040780.

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Anaplastic large cell lymphoma (ALCL) is the most common T-cell lymphoma in children. ALCL cells characteristically express surface CD30 molecules and carry the pathogenic ALK oncogene, both of which are diagnostic biomarkers and are also potential therapeutic targets. For precision therapy, we report herein a protamine nanomedicine incorporated with oligonucleotide aptamers to selectively target lymphoma cells, a dsDNA/drug payload to efficiently kill targeted cells, and an siRNA to specifically silence ALK oncogenes. The aptamer-equipped protamine nanomedicine was simply fabricated through a non-covalent charge-force reaction. The products had uniform structure morphology under an electron microscope and a peak diameter of 103 nm by dynamic light scattering measurement. Additionally, flow cytometry analysis demonstrated that under CD30 aptamer guidance, the protamine nanomedicine specifically bound to lymphoma cells, but did not react to off-target cells in control experiments. Moreover, specific cell targeting and intracellular delivery of the nanomedicine were also validated by electron and confocal microscopy. Finally, functional studies demonstrated that, through combined cell-selective chemotherapy using a drug payload and oncogene-specific gene therapy using an siRNA, the protamine nanomedicine effectively killed lymphoma cells with little toxicity to off-target cells, indicating its potential for precision therapy.
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46

Sgouros, George, and David M. Goldenberg. "Radiopharmaceutical therapy in the era of precision medicine." European Journal of Cancer 50, no. 13 (September 2014): 2360–63. http://dx.doi.org/10.1016/j.ejca.2014.04.025.

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47

Radich, Jerald P., Edward Briercheck, Daniel T. Chiu, Manoj P. Menon, Olga Sala Torra, Cecilia C. S. Yeung, and Edus H. Warren. "Precision Medicine in Low- and Middle-Income Countries." Annual Review of Pathology: Mechanisms of Disease 17, no. 1 (January 24, 2022): 387–402. http://dx.doi.org/10.1146/annurev-pathol-042320-034052.

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Most cancer cases occur in low- and middle-income countries (LMICs). The sophisticated technical and human infrastructure needed for optimal diagnosis, treatment, and monitoring of cancers is difficult enough in affluent countries; it is especially challenging in LMICs. In Western, educated, industrial, rich, democratic countries, there is a growing emphasis on and success with precision medicine, whereby targeted therapy is directed at cancers based on the specific genetic lesions in the cancer. Can such precision approaches be delivered in LMICs? We offer some examples of novel partnerships and creative solutions that suggest that precision medicine may be possible in LMICs given heavy doses of will, creativity, and persistence and a little luck.
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48

Cagle, Philip T., and Timothy Craig Allen. "Lung Cancer Genotype-Based Therapy and Predictive Biomarkers: Present and Future." Archives of Pathology & Laboratory Medicine 136, no. 12 (December 1, 2012): 1482–91. http://dx.doi.org/10.5858/arpa.2012-0508-ra.

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Context.—The advent of genotype-based therapy and predictive biomarkers for lung cancer has thrust the pathologist into the front lines of precision medicine for this deadly disease. Objective.—To provide the clinical background, current status, and future perspectives of molecular targeted therapy for lung cancer patients, including the pivotal participation of the pathologist. Data Sources.—Data were obtained from review of the pertinent peer-reviewed literature. Conclusions.—First-generation tyrosine kinase inhibitors have produced clinical response in a limited number of non–small cell lung cancers demonstrated to have activating mutations of epidermal growth factor receptor or anaplastic lymphoma kinase rearrangements with fusion partners. Patients treated with first-generation tyrosine kinase inhibitors develop acquired resistance to their therapy. Ongoing investigations of second-generation tyrosine kinase inhibitors and new druggable targets as well as the development of next-generation genotyping and new antibodies for immunohistochemistry promise to significantly expand the pathologist's already crucial role in precision medicine of lung cancer.
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49

Frankel, Arthur E., Kenya Honda, Bruce Roberts, Rose Szabady, Amit Reddy, Johnny Lightcap, Steve McClellan, Sachin Kumar Deshmukh, and Andrew Y. Koh. "Precision probiotic therapy enhances immune checkpoint therapy efficacy in melanoma bearing mice." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e14195-e14195. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14195.

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e14195 Background: Immune checkpoint inhibitor therapy, ICT, achieves remissions in melanoma patients but factors modulating response are not well defined. Our group (Frankel et al. Neoplasia 2017) and others have identified specific gut microbiota associated with improved ICT response. Recently, we identified specific gut microbiota that induce adaptive immune responses and potentiate ICT (Tanoue et al. Nature 2019). In this study, we determined whether this predefined consortia of gut microbiota augment ICT efficacy in melanoma bearing mice. Methods: Mice (C57BL/6, 6-8wk old, female, Jackson, n = 4-12 mice) received ± antibiotic water (penicillin G 1500U/mL + streptomycin 2mg/mL) for 6 d to deplete gut microbiota. Mice were then inoculated with 105 B16F10 melanoma cells SQ. At d 4, 8, 12 post-tumor inoculation, 0.2 mg anti-mCTLA4 + anti-mPD1 antibodies (Bio X Cell) were administered IP. Precision probiotic therapies included Vedanta Bioscience VE800 (Tanoue et al., Nature 2019), VE804 (same as VE800 without R. lactatiformans and F. ulcerans), VE411 (four Clostridial firmicutes) (Narushima, 2014), and Lactobacillus acidophilus (ATCC 4356) probiotics were given via gavage (1x109 cfu) starting day +1 after tumor inoculation and 3xwkly. Loss of survival was defined as death or tumor diameters ≥ 2 cm. Tumor growth inhibition, TGI = (1- mean treated tumor volume/mean control tumor volume) x 100%. Tumor mononuclear cells were isolated for flow cytometry for murine CD4, CD8, and CD11c. Results: TGI in mice with intact gut microbiota and treated with ICT was 84 ± 4% (SEM). Pre-treatment antibiotics reduced TGI to 38 ± 11%. Groups treated with Vedanta VE800, VE804, and VE411 exhibited TGIs of 77 ± 9, 61 ± 8, and 69%, respectively, whereas treatment with Lactobacillus acidophilus achieved TGIs 57%. VE800 treated mice had significantly increased length of survival compared to mice treated with antibiotics (p = 0.0008, log-rank test). Length of survival was not significantly different between groups with intact gut microbiota and those pretreated with antibiotics and dosed with VE800 (p = 0.52, log-rank test). ICT increased tumor CD4 cells to 11% from 2% and CD8 cells to 9% from 1%., however pre-treatment with antibiotics reduced CD4 cells to 4% and CD8 cells to 1%. Conclusions: Defined consortia of gut microbiota facilitate ICT efficacy. These preclinical studies lay the foundation for optimizing the host response to ICT.
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50

Nishino, Mizuki, Hiroto Hatabu, F. Stephen Hodi, and Nikhil H. Ramaiya. "Drug-Related Pneumonitis in the Era of Precision Cancer Therapy." JCO Precision Oncology, no. 1 (November 2017): 1–12. http://dx.doi.org/10.1200/po.17.00026.

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Drug-related pneumonitis as a result of novel cancer therapy provides new challenges for providers of cancer care in the era of precision medicine. Awareness of this emerging entity and knowledge of its manifestations and management guidelines are essential for state-of-the-art practice of clinical oncology. Here, we provide a detailed review of drug-related pneumonitis that develops during precision cancer therapies using immune-checkpoint inhibitors and molecular targeting agents, and we summarize the emerging data that have been obtained by recent investigations to provide a state-of-the-art overview for clinicians involved in cancer care. We focus on immune-checkpoint inhibitor–related pneumonitis, which is an immune-related adverse event of growing interest and increasing clinical significance in current oncology practice that has rapidly expanding access to these agents. Clinical characteristics, radiographic spectrum, and risk factors and outcome of pneumonitis are described for each class of agents, and current treatment guidelines and monitoring recommendations are discussed. This review also indicates the area of unmet clinical need and provides direction for future investigations, as well as emphasizing the importance of a multidisciplinary approach to further understand the mechanisms, develop methods for accurate diagnosis, and optimize management guidelines of drug-related pneumonitis in the era of precision oncology.
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