Relevant bibliographies by topics / Therapeutic modality for cancer

Academic literature on the topic 'Therapeutic modality for cancer'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Therapeutic modality for cancer"

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Agarwal, Shashi K. "Exercise: Preventive and Therapeutic Benefits in Cancer." Journal of Cancer Research Updates 10 (October 25, 2021): 10–17. http://dx.doi.org/10.30683/1929-2279.2021.10.02.

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Cancer is soon expected to overtake cardiovascular diseases as the leading cause of death in the world. As newer and often more expensive cancer treatments become available, several complementary modalities are gaining clinical importance. Exercise is one such modality. Increasing scientific data suggests that exercise, besides helping prevent several cancers, can also help improve outcomes across a range of cancer diagnoses. The mechanisms behind this protection and therapeutic effects are numerous and include changes in body composition, insulin sensitivity, oxidative stress, sex hormone levels, systemic inflammation, immune cell function, and DNA integrity. Exercise is easy to do, is inexpensive, and can be modified to the condition of the patient. This review summarizes the various benefits of structured activity in most major cancers affecting humans.
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KOMIYA, Yoshiaki, Tadayoshi MATSUDA, Ikuhiro UTIDA, Syohei IWAMOTO, and Toshiaki KURASHIMA. "Investigation of therapeutic modality for cancer of the tongue." Japanese Journal of Oral & Maxillofacial Surgery 35, no. 6 (1989): 1617–27. http://dx.doi.org/10.5794/jjoms.35.1617.

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Dagnelie, P. C., J. W. O. van den Berg, J. D. Bell, C. S. Foster, T. Rietveld, and G. R. Swart. "Fish oil: a new therapeutic modality in cancer cachexia?" Clinical Nutrition 12 (January 1993): 50. http://dx.doi.org/10.1016/0261-5614(93)90296-g.

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Itoh, Kyogo, and Akira Yamada. "Personalized peptide vaccines: A new therapeutic modality for cancer." Cancer Science 97, no. 10 (October 2006): 970–76. http://dx.doi.org/10.1111/j.1349-7006.2006.00272.x.

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Tordiglione, Michele, Maurizio Kalli, Vittorio Vavassori, and Roberto Luraghi. "Combined Modality Treatment for Esophageal Cancer." Tumori Journal 84, no. 2 (March 1998): 252–58. http://dx.doi.org/10.1177/030089169808400226.

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We have performed a review of recent literature about combined modality therapy in esophageal cancer. Radiobiological principles and radio-chemotherapy interactions modalities in clinical experiences have been considered. Therapeutic schedules, modalities of implementation, and the most relevant clinical results obtained by the major clinical research groups have been emphasized. We also comment on the current role of surgery and on the clinical questions arising in combined radio-chemotherapy treatment.
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Vandghanooni, Somayeh, Morteza Eskandani, Jaleh Barar, and Yadollah Omidi. "Aptamedicine: a new treatment modality in personalized cancer therapy." BioImpacts 9, no. 2 (November 30, 2018): 66–69. http://dx.doi.org/10.15171/bi.2019.09.

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Aptamers (Aps) are short single-strand nucleic acids exhibiting unique 3D structure which facilitate their targeting potential against various cancer molecular markers (CMMs). Such features of Aps not only make them as suitable homing agents in targeted drug delivery systems (DDSs) but also candidate them as macromolecules that inhibit the interaction of the target ligand with other proteins. On the other hand, the conjugation of Aps with another therapeutic molecule such as antisense oligonucleotides (ASOs), siRNAs/miRNAs, Aps, toxins, chemotherapeutic agents, DNAzymes/Ribozymes provides hopeful strategy to eradicate the malignancies and overcome the off-target unwanted side effects. Such prominent features of Aps make them a promising treatment modality to overcome the tumor complexity and heterogeneity, which can be consequently applied for personalized therapy of cancer by using bispecific Ap-based therapeutics.
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Lee, Y., J. Jung, G. Hwang, H. Park, and Y. Im. "Multimodal therapeutic approach in anaplastic thyroid cancer." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 15533. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.15533.

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15533 Background: Anaplastic thyroid cancer (ATC) is a rare but highly aggressive neoplasm with a dismal prognosis. However, a few patients survive for a long time after treatment. We tried to identify prognostic factors of this disease and analyzed treatment outcomes in patients with ATC. Methods: We reviewed the medical records of 15 patients diagnosed with ATC in our institution between 1988 and 2003. The survival was compared by the Kaplan-Meier log-rank test. Results: The female-to-male ratio was 1.5:1 (9 women and 6 men), and the mean age at diagnosis was 63.9 years (range, 44–91). The mean tumor size was 6.3cm (range, 4–10 cm). Extrathyroidal invasion was present in 12 cases and distant metastasis at diagnosis was present in 6 cases. Surgery was performed in 8 cases. Radiotherapy was used for 10 cases and chemotherapy for 5 cases. The mean overall survival time of the 15 patients was 237 days (range, 28–717 days). The 6-, 12-, 18- and 24-month survival rates were 33%, 26%, 13% and 0%. No association was found between survival and presenting symptoms, age, gender, tumor size, previous goiter history, extrathyroidal invasion, distant metastasis, surgery, radiotherapy or chemotherapy. A significantly better outcome was observed in patients received triple modality treatment (surgery, radiotherapy and chemotherapy) than in those received single or dual modality treatment (P = 0.05). Conclusions: Although most patients with ATC had a poor prognosis, a multimodal approach including surgery, radiotherapy and chemotherapy, might improve survival. No significant financial relationships to disclose.
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Storozynsky, Quinn, and Mary M. Hitt. "The Impact of Radiation-Induced DNA Damage on cGAS-STING-Mediated Immune Responses to Cancer." International Journal of Molecular Sciences 21, no. 22 (November 23, 2020): 8877. http://dx.doi.org/10.3390/ijms21228877.

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Radiotherapy is a major modality used to combat a wide range of cancers. Classical radiobiology principles categorize ionizing radiation (IR) as a direct cytocidal therapeutic agent against cancer; however, there is an emerging appreciation for additional antitumor immune responses generated by this modality. A more nuanced understanding of the immunological pathways induced by radiation could inform optimal therapeutic combinations to harness radiation-induced antitumor immunity and improve treatment outcomes of cancers refractory to current radiotherapy regimens. Here, we summarize how radiation-induced DNA damage leads to the activation of a cytosolic DNA sensing pathway mediated by cyclic GMP-AMP (cGAMP) synthase (cGAS) and stimulator of interferon genes (STING). The activation of cGAS–STING initiates innate immune signaling that facilitates adaptive immune responses to destroy cancer. In this way, cGAS–STING signaling bridges the DNA damaging capacity of IR with the activation of CD8+ cytotoxic T cell-mediated destruction of cancer—highlighting a molecular pathway radiotherapy can exploit to induce antitumor immune responses. In the context of radiotherapy, we further report on factors that enhance or inhibit cGAS–STING signaling, deleterious effects associated with cGAS–STING activation, and promising therapeutic candidates being investigated in combination with IR to bolster immune activation through engaging STING-signaling. A clearer understanding of how IR activates cGAS–STING signaling will inform immune-based treatment strategies to maximize the antitumor efficacy of radiotherapy, improving therapeutic outcomes.
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Chen, Lili, Xiaohong Wang, Fangling Ji, Yongming Bao, Jingyun Wang, Xianwu Wang, Lianying Guo, and Yachen Li. "New bifunctional-pullulan-based micelles with good biocompatibility for efficient co-delivery of cancer-suppressing p53 gene and doxorubicin to cancer cells." RSC Advances 5, no. 115 (2015): 94719–31. http://dx.doi.org/10.1039/c5ra17139c.

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Li, Mingjing, Fan Yu, Chao Yao, Peng George Wang, Yonghui Liu, and Wei Zhao. "Synthetic and immunological studies on trimeric MUC1 immunodominant motif antigen-based anti-cancer vaccine candidates." Organic & Biomolecular Chemistry 16, no. 6 (2018): 993–99. http://dx.doi.org/10.1039/c7ob02976d.

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Dissertations / Theses on the topic "Therapeutic modality for cancer"

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Pozniak, John. "Systemic Delivery of microRNA as a Therapeutic Modality to Treat Cancer." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367939186.

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McCarthy, Alexandra Leigh. "A rebellious distemper : a Foucaultian history of breast cancer to 1900." Thesis, Queensland University of Technology, 2005. https://eprints.qut.edu.au/16030/1/Alexandra_McCarthy_Thesis.pdf.

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This dissertation explores some of the conditions of possibility underpinning contemporary breast cancer discourse, which is imbued with harsh moral, social and spiritual nuance. I have therefore explored a set of questions concerned with the past state of things in breast cancer care that laid the foundation for present approaches. I wanted to know how it became possible to speak what we now regard as the only truth about breast cancer. I wanted to understand how this truth was determined; who determined it, and who or what gave them the right to assert that their truth was the only truth. I wanted to acquire insight into the ways that thinking about and managing breast cancer based on this truth came to dominate the post-modern consciousness (rather than other, perhaps equally valid ways). And if it was possible, I wanted to open up a space for thinking differently about breast cancer. Finally, I wanted to test the fit of the ideas of the philosopher-historian, Michel Foucault, to these questions. Foucault's notions of discontinuity, discipline, the gaze, normalising judgements and to a lesser extent, some aspects of power/knowledge and the ethics of the self are here tested on the surgical archive of breast cancer, which housed the discourse that best represented Western societal beliefs about the disease, and which had been invested by society with the greatest authority in its conception and management. The analytic framework - modes of consciousness - suggested by Foucault provided a coherent structure with which to explore the archive. I found that there are numerous elements in the archive instrumental in cementing the conditions of possibility for breast cancer discourse in our own time. This dissertation demonstrates that, as is the case in the present day, these were based on unstable truths about breast cancer that were a result of a complex of sociocultural and political norms rather than an objective truth.
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McCarthy, Alexandra Leigh. "A Rebellious Distemper: A Foucaultian History of Breast Cancer to 1900." Queensland University of Technology, 2005. http://eprints.qut.edu.au/16030/.

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This dissertation explores some of the conditions of possibility underpinning contemporary breast cancer discourse, which is imbued with harsh moral, social and spiritual nuance. I have therefore explored a set of questions concerned with the past state of things in breast cancer care that laid the foundation for present approaches. I wanted to know how it became possible to speak what we now regard as the only truth about breast cancer. I wanted to understand how this truth was determined; who determined it, and who or what gave them the right to assert that their truth was the only truth. I wanted to acquire insight into the ways that thinking about and managing breast cancer based on this truth came to dominate the post-modern consciousness (rather than other, perhaps equally valid ways). And if it was possible, I wanted to open up a space for thinking differently about breast cancer. Finally, I wanted to test the fit of the ideas of the philosopher-historian, Michel Foucault, to these questions. Foucault's notions of discontinuity, discipline, the gaze, normalising judgements and to a lesser extent, some aspects of power/knowledge and the ethics of the self are here tested on the surgical archive of breast cancer, which housed the discourse that best represented Western societal beliefs about the disease, and which had been invested by society with the greatest authority in its conception and management. The analytic framework - modes of consciousness - suggested by Foucault provided a coherent structure with which to explore the archive. I found that there are numerous elements in the archive instrumental in cementing the conditions of possibility for breast cancer discourse in our own time. This dissertation demonstrates that, as is the case in the present day, these were based on unstable truths about breast cancer that were a result of a complex of sociocultural and political norms rather than an objective truth.
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Walker, Teneille. "Therapeutic Drugs in Cancer." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1722.

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The first study examined the interaction between low doses of the multi-kinase inhibitor sorafenib and the histone deacetylase inhibitor vorinostat in colon cancer cells. Sorafenib and vorinostat synergized to kill HCT116 and SW480 cells. In SW480 cells, sorafenib+vorinostat toxicity correlated with CD95 activation and CD95-stimulated autophagy. Drug lethality in SW480 cells was blocked by knock down of CD95. In SW620 cells that are patient matched to SW480 cells, sorafenib+vorinostat toxicity was significantly reduced that correlated with a lack of CD95 activation and lower expression of ceramide synthase 6 (LASS6). Overexpression of LASS6 in SW620 cells enhanced drug-induced CD95 activation and tumor cell killing, whereas knock down of LASS6 in SW480 cells suppressed CD95 activation. In HCT116 cells, sorafenib+vorinostat did not increase CD95 plasma membrane levels, weakly induced caspase 8 association with CD95, and knock down of CD95 enhanced drug lethality. In HCT116 cells sorafenib+vorinostat treatment caused CD95-dependent autophagy that was a protective signal. Thus, treatment of tumor cells with sorafenib+vorinostat activates CD95 that promotes viability via autophagy or degrades survival via extrinsic or intrinsic pathways. Drug-induced activation of the de novo ceramide synthesis pathway plays a key role in CD95 activation. The second project explores the mechanism by which the combination of 17AAG, an hsp90 inhibitor, and PD184352, a MEK1/2 inhibitor alters survival in colon cancer cells. 17AAG and PD184352 synergized to kill HCT116 and SW480 cells. In HCT116 cells drug-exposure increased CD95 plasma membrane levels In SW620 cells, 17AAG and PD184352 toxicity was significantly reduced that correlated with a lack of CD95 activation and lower expression LASS6. Overexpression of LASS6 in SW620 cells enhanced drug-induced CD95 activation and tumor cell killing. In Mia Paca2 cells, a pancreatic cell line, inhibition of caspase 8 or overexpression of c-FLIP-s suppressed cell killing by PD184352 and 17AAG exposure. Drug lethality in Mia Paca2 cells was blocked by knock down of CD95. Additionally, overexpression of Bcl-xL or knockdown of caspase 9 decreased cell killing in 17AAG and PD184352 combination treatment. Thus, 17AAG+PD184352 exposure activates the extrinsic and intrinsic apoptotic pathways to kill Mia Paca2 cells. This document was created in Microsoft Word 2000.
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Wang, Chao. "Integrative Analysis of Multi-modality Data in Cancer." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1429791373.

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Wall, Richard Andrew. "Multi-Modality Endoscopic Imaging for the Detection of Colorectal Cancer." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/301761.

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Optical coherence tomography (OCT) is an imaging method that is considered the optical analog to ultrasound, using the technique of optical interferometry to construct two-dimensional depth-resolved images of tissue microstructure. With a resolution on the order of 10 μm and a penetration depth of 1-2 mm in highly scattering tissue, fiber optics-coupled OCT is an ideal modality for the inspection of the mouse colon with its miniaturization capabilities. In the present study, the complementary modalities laser-induced fluorescence (LIF), which offers information on the biochemical makeup of the tissue, and surface magnifying chromoendoscopy, which offers high contrast surface visualization, are combined with OCT in endoscopic imaging systems for the greater specificity and sensitivity in the differentiation between normal and neoplastic tissue, and for the visualization of biomarkers which are indicative of early events in colorectal carcinogenesis. Oblique incidence reflectometry (OIR) also offers advantages, allowing the calculation of bulk tissue optical properties for use as a diagnostic tool. The study was broken up into three specific sections. First, a dual-modality OCTLIF imaging system was designed, capable of focusing light over 325-1300 nm using a reflective distal optics design. A dual-modality fluorescence-based SMC-OCT system was then designed and constructed, capable of resolving the stained mucosal crypt structure of the in vivo mouse colon. The SMC-OCT instrument's OIR capabilities were then modeled, as a modified version of the probe was used measure tissue scattering and absorption coefficients.
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Martin, Aditi Pandya. "Therapeutic drugs in cancer and resistance." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1717.

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We investigated the mechanism of toxicity and resistance development of small molecule tyrosine kinase inhibitor lapatinib in HCT 116 colon cancer cells. Lapatinib mediated cell death in HCT 116 cells was caspase independent and involved cytosolic release of apoptosis inducing factor. Treatment of HCT 116 cells with 10µM Lapatinib lead to the outgrowth of lapatinib resistant HCT 116 cells. Our studies show that alterations in the expression and activation of Bcl-2 family proteins allow lapatinib resistant HCT 116 cells to resist cytotoxic effects of lapatinib as well as of other commonly used chemotherapeutic agents. In hepatoma and pancreatic cancer cells, the effects of combining multi-kinase inhibitor sorafenib with histone deacetylase inhibitors (HDACIs) namely, vorinostat and sodium valproate were investigated. It was found that sorafenib synergizes with HDACIs resulting in enhanced cell death compared to death induced by the drugs individually. The mechanism of action of sorafenib and vorinostat combination treatment as well as sorafenib and sodium valproate combined treatment was shown to involve activation of the CD95 death receptor pathway. Alterations in the CD95 pathway can render cancer cells resistant to chemotherapeutic agents. Hence, we combined sorafenib+sodium valproate with a BH-3 domain mimetic named obatoclax (GX-15-070) which resulted in enhanced toxicity to cancer cells. More importantly, knock-down of CD95 (to mimic non-functional CD95 pathway) reduced cell death induced by sorafenib+sodium valproate combined but failed to protect cells from cell death induced by sorafenib+sodium valproate+obatoclax combined. This suggests that combining sorafenib+HDACI with obatoclax may not only enhance toxicity to cancer cells but may also reduce chances of resistance development via alterations in the CD95 pathway. These studies enhance our knowledge of existing treatment strategies for cancer as well as throw light on how current approaches can be improved in order to better diagnose and treat cancer. Understanding mechanisms of drug action as well as resistance development will allow us to combine existing therapies effectively in order best target cancer cells as well as provide us with information that can help us design new cancer treatment strategies.
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Quinn, Bridget A. "Novel Therapeutic Strategies for Pancreatic Cancer." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/4671.

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Pancreatic cancer is a devastating disease that leaves patients with a very poor prognosis and few therapeutic options. Many of the treatment options available are the same that have been used for almost 2 decades. There is a dire need for both novel treatments for this disease as well as novel strategies of treatment. This body of work will introduce and provide evidence in support of a novel combination therapy for pancreatic cancer treatment, a novel strategy of modifying currently used chemotherapeutics for pancreatic cancer therapy, and a novel transgenic preclinical mouse model of pancreatic cancer. Sabutoclax, an antagonist of the anti-apoptotic Bcl-2 proteins, and Minocycline, a commonly used antibiotic, show potent synergy when used in combination in both pancreatic cancer cells and in multiple immune-deficient and immune-competent mouse models of pancreatic cancer. Sabutoclax alone is capable of inducing cell cycle arrest and apoptosis in cells and its cytotoxicity is enhanced significantly when combined with Minocycline. This combination results in the loss of Stat3 activation both in vitro and in vivo, which is essential for its toxicity. It also inhibits tumor growth and prolongs survival in the KPC transgenic mouse model of pancreatic cancer. Also presented here are studies that demonstrate efficacy in vivo of modified versions of Gemcitabine and Paclitaxel. These drugs are linked to a peptide that shows specificity for the EphA2 receptor, which is overexpressed on the surface of pancreatic cancer cells and only minimally on normal cells. This peptide results in increased cellular uptake of drug, as it is bypassing its normal mechanism of entry. These normal mechanisms are often dysregulated in cancer, leading to decreased uptake and drug resistance. The use of these modified drugs show significantly increased tumor growth inhibition as compared to the parent drug alone. Finally, we provide data on the characterization of a novel transgenic mouse model of pancreatic cancer. This model, the Pan Met View (PMV) mouse, combines the commonly used KPC transgenic mouse model of pancreatic cancer and a mouse that expresses a Luciferase reporter gene under the control of the cancer-specific promoter, CCN1. Our data shows that double transgenic PMV mice can now be used to follow primary tumor and metastasis development in real time by Bioluminescent imaging (BLI) through disease progression and potentially therapy. This strategy will enhance the use of genetically engineered mouse models (GEMMS) to study cancer initiation and progression with potential to non-invasively monitor therapy. These chapters present novel and exciting data that have the potential to open multiple avenues of translational study and result in significant advances in pancreatic cancer therapy.
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Kurtyka, Courtney A. "Novel Therapeutic Strategies in Lung Cancer." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5363.

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Lung cancer is the leading cause of cancer-related death and the second most diagnosed cancer in the United States. Unfortunately, many patients either do not have any common mutations for which there are already targetable agents, or they eventually become resistant to these compounds. As such, there is a high demand for new, effective methods of treating this disease as well as predicting patient prognosis and potential benefit from chemotherapy. In this work, numerous strategies for treating lung cancer are explored. The first method described here is through the use of a pan-early 2 factor (E2F) inhibitor, HLM006474, which is shown to synergize with paclitaxel in non-small cell lung cancer (NSCLC). Next, we explored the creation and utilization of an E2F signature that is prognostic and predictive of early-stage NSCLC patient benefit from adjuvant chemotherapy (ACT). The third project examined possible targets to enhance sensitivity to cisplatin in NSCLC lacking Kirsten rat sarcoma viral oncogene homolog (KRAS) and epidermal growth factor receptor (EGFR) mutations and anaplastic lymphoma receptor tyrosine kinase (ALK) fusions (triple-negative), for which cisplatin is one of the few treatment options. These studies led to the identification of a kinase that is overexpressed in NSCLC and whose knockdown sensitizes cells to platinum agents.
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Young, Jennifer Denise. "Imaging and therapeutic radiotracers for prostate cancer." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/imaging-and-therapeutic-radiotracers-for-prostate-cancer(4822a0bb-f8a4-4738-bd61-23bb1b500e8d).html.

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Radiotracers that target glutamate carboxypeptidase II, also known as the prostate specific membrane antigen (GCP(II)/PSMA), have shown exceptional promise for prostate cancer imaging and molecular radiotherapy. A number of bioconjugates have been developed to target GCP(II)/PSMA which utilise the simple and robust targeting motif (Lys-C(O)-Glu) (referred to as PSMA ligand), functionalised with a chelator for radiometal incorporation. This work utilised and evaluated the tris(hydroxypyridinone) (THP) chelator due to the simplicity, speed and selectivity of its radiolabelling with gallium radioisotopes, and its potential to be developed into one-step radiopharmaceutical kits. [68Ga]Ga-THP-PSMA was assessed as a PET imaging agent and [67Ga]Ga-THP-PSMA for molecular radiotherapy due to its Auger electron emissions. The first objective was to synthesise THP-PSMA and assess its radiolabelling with gallium-68. [68Ga]Ga-THP-PSMA with over 95% radiochemical purity was produced at room temperature, and pH 7 in just 5 minutes. A one-step kit was developed, suitable for use with gallium-68 directly from a generator. [68Ga]Ga-THP-PSMA exhibited specific uptake in GCP(II)/PSMA-expressing prostate cancer cells and 50% inhibition of binding at a concentration of 361 ± 60 nM. In vivo PET imaging showed specific uptake in GCP(II)/PSMA-expressing tumours, reaching 5.6 ± 1.2 percentage injected dose per cubic centimetre. Overall, [68Ga]Ga-THP-PSMA had equivalent imaging properties but greatly simplified radiolabelling compared to other [68Ga]Ga-PSMA tracers. Clinical studies were then conducted by collaborators which found that [68Ga]Ga-THP-PSMA could delineate prostate cancer in both initial staging and biochemical recurrence. The second objective was to assess [67Ga]Ga-THP-PSMA for molecular radiotherapy. Extremely high molar activity was achieved: 326 MBq/nmol (22% chelator occupancy). Despite this, the activity delivered to GCP(II)/PSMA expressing cells was low (max 0.1 Bq/cell) and the tracer showed rapid efflux. These findings were confirmed with in vivo studies showing poor retention of [67Ga]Ga-THP-PSMA in GCP(II)/PSMA-expressing prostate cancer tumours. These results suggest that the affinity and retention, but not the molar activity, limit the use of [67Ga]Ga-THP-PSMA for molecular radiotherapy. The third objective was to determine whether replacing the urea with a thiourea in the GCP(II)/PSMA targeting motif resulted in higher affinity. This was studied using the inhibitors Glu-C(O)-Glu and Glu-C(S)-Glu, the syntheses of which are described. The in vitro inhibition assays showed that the affinity was made much weaker by the presence of the thiourea (135 μM compared to 1.34 μM) and therefore this is not an effective strategy for improving affinity. Overall the THP-PSMA bioconjugate shows excellent radiolabelling properties, with both gallium-68 and gallium-67. [68Ga]Ga-THP-PSMA is a good PET imaging agent for prostate cancer however, improved affinity for GCP(II)/PSMA and retention of the tracer may potentially enhance the utility of [67Ga]Ga-THP-PSMA for molecular radiotherapy.
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Books on the topic "Therapeutic modality for cancer"

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George, Coukos, and Rubin Stephen C, eds. Cancer of the uterus. New York: Marcel Dekker, 2005.

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William, Small, ed. Combining targeted biological agents with radiotherapy: Current status and future directions. New York, NY: Demos Medical Pub., 2008.

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Marshall, John L., ed. Cancer Therapeutic Targets. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-6613-0.

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MA, Howard Pam, ed. The therapeutic encounter: A cross-modality approach. London: SAGE, 2012.

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Schlag, Peter, Peter Hohenberger, and Urs Metzger, eds. Combined Modality Therapy of Gastrointestinal Tract Cancer. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83293-2.

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Omlor, Georg H. Isolated hyperthermic limb perfusion. New York: Springer-Verlag, 1995.

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Baronzio, Gianfranco, Gianfranco Fiorentini, and Christopher R. Cogle, eds. Cancer Microenvironment and Therapeutic Implications. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9576-4.

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Hugh, Allen H., and Nisker Jeffrey A, eds. Cancer in pregnancy: Therapeutic guidelines. Mount Kisco, N.Y: Futura Pub. Co., 1986.

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Gianfranco, Fiorentini, Cogle Christopher R, and SpringerLink (Online service), eds. Cancer Microenvironment and Therapeutic Implications: Tumor Pathophysiology Mechanisms and Therapeutic Strategies. Dordrecht: Springer Netherlands, 2009.

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service), ScienceDirect (Online, ed. Bone cancer: Progression and therapeutic approaches. Amsterdam: Academic, 2010.

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Book chapters on the topic "Therapeutic modality for cancer"

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Bengmark, S. "Biliary Duct Cancer: Therapeutic Nihilism or Prospect." In Combined Modality Therapy of Gastrointestinal Tract Cancer, 74–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83293-2_10.

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Wils, J. A. "Treatment of Pancreatic Carcinoma: Therapeutic Nihilism?" In Combined Modality Therapy of Gastrointestinal Tract Cancer, 87–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83293-2_12.

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Kaur, Satinder, and H. S. Darling. "Immunotherapy in Endometrial Cancer: An Evolving Therapeutic Modality." In Recent Advances in Endometrial Cancer, 245–56. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5317-2_13.

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Papillon, J. "Current Therapeutic Concepts in Management of Carcinoma of the Anal Canal." In Combined Modality Therapy of Gastrointestinal Tract Cancer, 146–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83293-2_22.

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Chambon, Adrienne, and Daniel Simeoni. "Modality in the therapeutic dialogue." In Linguistic Choice across Genres, 239. Amsterdam: John Benjamins Publishing Company, 1998. http://dx.doi.org/10.1075/cilt.158.17cha.

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Jones, Adele D., Ena Trotman Jemmott, Hazel Da Breao, and Priya E. Maharaj. "Art as a Therapeutic Modality." In Treating Child Sexual Abuse in Family, Group and Clinical Settings, 281–323. London: Palgrave Macmillan UK, 2016. http://dx.doi.org/10.1057/978-1-137-37769-2_6.

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Ventafridda, V. "Therapeutic Strategy." In Cancer Pain, 57–67. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9139-8_6.

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Suppes, Bethany C. "Differentiating Therapeutic Theory and Clinical Modality." In Family Systems Theory Simplified, 23–33. New York: Routledge, 2022. http://dx.doi.org/10.4324/9781003088196-4.

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Baumel, H., and B. Deixonne. "Therapeutic Management." In Exocrine Pancreatic Cancer, 124–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71178-7_7.

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Ling, Morris, and T. C. Wu. "Therapeutic Human Papillomavirus Vaccines." In Cancer Prevention — Cancer Causes, 345–75. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/1-4020-2016-3_13.

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Conference papers on the topic "Therapeutic modality for cancer"

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Hobson, Dexter, Laura Curiel, Jean-Yves Chapelon, and Samuel Pichardo. "Dual-modality image guided high intensity focused ultrasound device design for prostate cancer: A numerical study." In 11TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND. AIP, 2012. http://dx.doi.org/10.1063/1.4757323.

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Avadisian, Miriam, Steven Fletcher, Baoxu Liu, Wei Zhao, Peibin Yue, James Turkson, Claudiu Gradinaru, and Patrick Gunning. "Abstract B220: Artificially inducing protein-membrane anchorage: Introducing a new therapeutic modality." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b220.

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Braun, Alexandra, Aniko Palfi, Christoph Mueller, Torsten Hechler, Andreas Pahl, and Michael Kulke. "Abstract 910: Amanitin-based ADCs targeting PSMA as novel therapeutic modality for prostate cancer therapy." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-910.

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Cao, Lizhi, Adam Petrone, Wayne Gatlin, Jenny Che, Abhishek Das, Robert LeBlanc, Zakir Siddiquee, et al. "Abstract LB-109: A novel therapeutic modality of inhibiting the glyco-immune checkpoint axis to treat cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-lb-109.

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Cao, Lizhi, Adam Petrone, Wayne Gatlin, Jenny Che, Abhishek Das, Robert LeBlanc, Zakir Siddiquee, et al. "Abstract LB-109: A novel therapeutic modality of inhibiting the glyco-immune checkpoint axis to treat cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-lb-109.

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OBrien, Zhihong (Julie), Li Wang, Cima Cina, Bharat Majeti, James Chu, Xiaoen Wang, Robiel Baclig, et al. "Abstract 4060: Discovery and preclinical development of KRAS-targeting siRNA therapeutic modality for the treatment of pancreatic cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4060.

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Zaman, Mohd, Cai Huang, Sachith Gallolu Kankanamalage, Amit K. Chaudhary, Jianbo Dong, and Yue Liu. "Abstract LB069: Development of cMET/cMET/EGFR Trispecific antibody as therapeutic modality for Non-small Cell Lung Cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-lb069.

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Gupta, Sounak, Mir Maria, John Bomalaski, Paul J. Elson, Kamini Singh, Jyoti Harwalkar, Paula Carver, Alex Almasan, and Donna E. Hansel. "Abstract 11: Arginine deprivation therapy using ADI-PEG20 as a novel therapeutic modality in the treatment of bladder cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-11.

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Prodromidou, Anastasia, Sofia Lekka, Alexandros Fotiou, Victoria Psomiadou, Dimitrios Giannoulopoulos, and Christos R. Iavazzo. "500 Metformin as a preventive and therapeutic modality in endometrial cancer: a systematic review and meta-analysis of randomized control trials." In ESGO SoA 2020 Conference Abstracts. BMJ Publishing Group Ltd, 2020. http://dx.doi.org/10.1136/ijgc-2020-esgo.78.

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Yemelyanov, Alexander, Pankaj Bhalla, Andrey Ugolkov, Ximing Yang, and Irina Budunova. "Abstract 3929: Differential targeting of androgen and glucocorticoid receptors induces ER stress and apoptosis in prostate cancer cells: A novel therapeutic modality." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3929.

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Reports on the topic "Therapeutic modality for cancer"

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Williams, Mark B. Dual Modality Imaging System for Breast Cancer Research. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada405549.

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Williams, Mark B. Dual Modality Imaging System for Breast Cancer Research. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada429091.

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Williams, Mark. Dual Modality Imaging System for Breast Cancer Research. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada390538.

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LaVeist, Thomas A. Disparities in Prostate Cancer Treatment Modality and Quality of Life. Fort Belvoir, VA: Defense Technical Information Center, November 2010. http://dx.doi.org/10.21236/ada567845.

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Sarkar, Devanand. Novel Therapeutic Approach for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada428427.

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Gomez, Christian R. Enhancing Therapeutic Cellular Prostate Cancer Vaccines. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada606946.

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Gomez, Christian R. Enhancing Therapeutic Cellular Prostate Cancer Vaccines. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada592082.

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Sarkar, Devanand. Novel Therapeutic Approach for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada459211.

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Faller, Douglas V. Virus-Targeted Therapeutic for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada378792.

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Gomez, Christian. Enhancing Therapeutic Cellular Prostate Cancer Vaccines. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada547341.

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