Relevant bibliographies by topics / Molecular Targeted Therapy

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Molecular Targeted Therapy'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Molecular Targeted Therapy"

1

Eto, Masatoshi. "PD2-5 The Role of Cytokine Therapy at the Age of Molecular Targeted Therapy." Japanese Journal of Urology 99, no. 2 (2008): 134. http://dx.doi.org/10.5980/jpnjurol.99.134_2.

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Dong, Bing, and Yi-Min Zhu. "Molecular-targeted therapy for cancer." Chinese Journal of Cancer 29, no. 3 (March 5, 2010): 340–45. http://dx.doi.org/10.5732/cjc.009.10313.

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Park, Hee-Sook, and Nam-Su Lee. "Molecular Targeted Therapy in Cancer." Journal of the Korean Medical Association 46, no. 6 (2003): 542. http://dx.doi.org/10.5124/jkma.2003.46.6.542.

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Festuccia, Claudio, Assunta Leda Biordi, Vincenzo Tombolini, Akira Hara, and David Bailey. "Targeted Molecular Therapy in Glioblastoma." Journal of Oncology 2020 (January 14, 2020): 1–3. http://dx.doi.org/10.1155/2020/5104876.

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Gala, Kinisha, and Sarat Chandarlapaty. "Molecular Pathways: HER3 Targeted Therapy." Clinical Cancer Research 20, no. 6 (February 11, 2014): 1410–16. http://dx.doi.org/10.1158/1078-0432.ccr-13-1549.

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Puzanov, Igor, and Keith T. Flaherty. "Targeted Molecular Therapy in Melanoma." Seminars in Cutaneous Medicine and Surgery 29, no. 3 (September 2010): 196–201. http://dx.doi.org/10.1016/j.sder.2010.06.005.

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Le Rhun, Emilie, Matthias Preusser, Patrick Roth, David A. Reardon, Martin van den Bent, Patrick Wen, Guido Reifenberger, and Michael Weller. "Molecular targeted therapy of glioblastoma." Cancer Treatment Reviews 80 (November 2019): 101896. http://dx.doi.org/10.1016/j.ctrv.2019.101896.

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Mischel, Paul S., and Timothy F. Cloughesy. "Targeted Molecular Therapy of GBM." Brain Pathology 13, no. 1 (April 5, 2006): 52–61. http://dx.doi.org/10.1111/j.1750-3639.2003.tb00006.x.

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Stadler, Walter. "IL-6 (S) Progress in Molecular Targeted Therapy for Renal Cell Cancer." Japanese Journal of Urology 98, no. 2 (2007): 59. http://dx.doi.org/10.5980/jpnjurol.98.59.

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Karczmarek-Borowska, Bożenna, and Agata Sałek-Zań. "Review Hepatotoxicity of molecular targeted therapy." Współczesna Onkologia 2 (2015): 87–92. http://dx.doi.org/10.5114/wo.2014.43495.

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Dissertations / Theses on the topic "Molecular Targeted Therapy"

1

Mckiver, Bryan D. "SND1-Targeted Gene Therapy for Hepatocellular Carcinoma." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5676.

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Staphylococcal nuclease and tudor-domain containing 1 (SND1) is an oncogene for a wide variety of cancers, including hepatocellular carcinoma (HCC). SND1 is a multifunctional protein regulating gene expression of proto-oncogenes and tumor suppressor genes, making SND1 a prime target for developing cancer therapeutics. This notion is especially attributed to HCC as most patients are diagnosed in advanced stages and the therapeutic options available for these patients are severely limited. In this study, we evaluated the therapeutic potential of a replication-defective adenovirus vector delivering SND1 shRNA (Ad.SND1sh) to human HCC cell lines, HepG3, HuH-7, and Hep3B. Adenovirus infection in HCC cells was confirmed by Western blotting and immunofluorescence. The efficacy of Ad.SND1sh to knockdown SND1 expression was confirmed via Western blot, qRT-PCR, and immunofluorescence. Ad.SND1sh did not significantly affect proliferation of the three human HCC cells but significantly inhibited their invasive and migratory capacities, as determined by wound healing and Matrigel invasion assays, respectively. As a corollary, Ad.SND1sh treatment resulted in a decrease in mesenchymal markers, such as N-cadherin, Twist, Snail, and Slug, without affecting levels of epithelial marker E-Cadherin, indicating that SND1 knockdown induces mesenchymal conversion in HCC cells. Additionally, reductions in liver cancer stem cell marker CD133 and HCC marker α-fetoprotein (AFP) were observed with SND1 knockdown. HCC cells with aberrant expression of these markers are associated with tumor initiation, recurrence, and multi-drug resistance. Our findings indicate that Ad.SND1sh may potentially be an effective therapy for advanced HCC and needs to be studied further for its clinical application.
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Honarvar, Hadis. "Development of Affibody molecules for radionuclide molecular imaging and therapy of cancer." Doctoral thesis, Uppsala universitet, Medicinsk strålningsvetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-298740.

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Affibody molecules are a promising class of scaffold-based targeting proteins for radionuclide-based imaging and therapy of cancer. This thesis work is based on 5 original research articles (papers I-V), which focus on optimization of molecular design of HER2-binding Affibody variants for high contrast imaging of this predictive biomarker as well as development of Affibody molecules suitable for radionuclide-based targeted therapies.  Papers I and II were dedicated to evaluation of the influence of the macrocyclic chelator DOTA positioning at N-terminus, in the middle of helix-3 and at C terminus of a synthetic Affibody molecule, ZHER2:S1. These synthetic variants were labelled with different radionuclides i.e. 111In and 68Ga to study also the effect of different labels on their biodistribution properties. In paper III a 2-helix variant, Z342min, was developed using native ligation cyclization to cross-link helices one and two resulting in a stable 2-helix scaffold and characterized in vivo. This study was performed with the aim to obtain structure-properties relationship for development of smaller Affibody molecules.   Papers IV and V were devoted to development of therapeutic strategies. In paper IV, a series of peptide based chelators was investigated for labelling of Affibody molecules with 188Re to provide low renal retention. In paper V, a pretargeting approach using peptide nucleic acid was investigated. These studies were performed with the aim to overcome the high renal retention of Affibody molecules when labelled with residualizing therapeutic radionuclides. Otherwise, the particle emitting radiometals could damage the kidneys more than the tumours. The results obtained for anti-HER2 Affibody molecules summarized in this thesis might be of importance for the development of other scaffold protein based targeting agents.
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Jokinen, E. (Elina). "Targeted therapy sensitivity and resistance in solid malignancies." Doctoral thesis, Oulun yliopisto, 2014. http://urn.fi/urn:isbn:9789526205755.

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Abstract Cancer is a major global killer and a challenge for the healthcare worldwide. Earlier cancer has been treated with surgery, radiation, chemotherapy and hormonal therapy. Unfortunately the efficiency of these therapies has shown to be limited and this has raised an enthusiasm for development of new, targeted cancer therapies that are based on activated oncogenes. The challenge of the targeted therapies is therapy resistance, de novo, adaptive and acquired. This work investigated targeted therapy sensitivity and resistance in lung cancer, breast cancer, colorectal cancer, and melanoma cell lines. The results of this study indicate that in some non-small cell lung cancer cell lines, dual PI3K and MEK inhibition is a more efficacious treatment than inhibition of either solely. It was also showed that the maximal effect of the dual inhibition can be achieved with alternative dosing schedules that are potentially more tolerable in clinical use. Furthermore, by combining ABT-263, entinostat or dasatinib to the dual PI3K and MEK inhibition, the efficiency of the therapy can be increased. Bcl-xl downregulation is a major determinant of the apoptotic response to the triple inhibitor treatment. The current work showed that cancer stem cells can mediate resistance to targeted therapies. Since these cells follow the stochastic model, concurrent therapy with a targeted agent and a stem cell targeting drug might be needed for maximal therapeutic efficiency. This study also showed that Gö6976 acts as a potent inhibitor of mutant EGFR despite the presence of T790M, the most important mechanism of acquired resistance for EGFR tyrosine kinase inhibitors in lung cancer, both in vitro and in vivo
Tiivistelmä Syöpä on yksi johtavia kuolemanaiheuttajia ja tauti on maailmanlaajuinen haaste terveydenhuollolle. Perinteiset syöpähoidot käsittävät kirurgian, sädehoidon, kemoterapian ja hormonaalisen hoidon, mutta näiden rinnalle on noussut uusia, aktivoituneiden onkogeenien signaalien estoon perustuvia hoitoja. Tämä työ tutki kohdennettuja syöpähoitoja ja näihin hoitoihin liittyvää resistenssiä keuhko-, rinta- ja paksusuolen syövän sekä melanooman solulinjoissa. Tulokset osoittavat, että joissakin ei-pienisoluisen keuhkosyövän solulinjoissa yhdistetty PI3K- ja MEK-esto aiheuttaa tehokkaamman vasteen kuin kummankaan signaalireitin esto yksistään. Tässä työssä näytettiin myös, että maksimaalinen vaste yhdistetylle PI3K- ja MEK-estolle voidaan saavuttaa vaihtoehtoisilla annostelutavoilla, jotka ovat voisivat olla paremmin siedettyjä kliinisessä käytössä kuin kahden lääkkeen jatkuva annostelu. Tämä tutkimus osoitti lisäksi, että kaksoiseston tehokkuutta voidaan lisätä yhdistämällä hoitoon kolmas lääkeaine, ABT-263, entinostaatti tai dasatinibi. Bcl-xl proteiinilla on keskeinen rooli apoptoottisen vasteen määrittäjänä näille kolmen lääkkeen käsittelyille. Tämä työ osoitti, että syövän kantasolut voivat välittää resistenssiä kohdennetuille syöpähoidoille. Nämä solut noudattavat niin kutsuttua stokastista mallia, joten parhaan vasteen saaminen saattaa edellyttää että hoito kohdentuu sekä erilaistuneisiin että kantasolutyyppisiin syöpäsoluihin. Tässä tutkimuksessa osoitettin lisäksi, että Gö6976 toimii mutatoituneen EGFR:n estäjänä, huolimatta kehittyvää keuhkosyövissä resistenssiä välittävästä T90M mutaatiosta, sekä in vitro -että in vivo -malleissa
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MAUCERI, MATTEO. "New Targeted Molecules for the Therapy of Ovarian Cancer." Doctoral thesis, Università degli Studi di Trieste, 2022. http://hdl.handle.net/11368/3031106.

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Patients with high-grade serous ovarian cancer (HGSOC), the most aggressive epithelial ovarian cancer (EOC) subtype, have a 5-year survival rate of about 93% when diagnosed at an early stage, but it drops to 30-40% when diagnosed in the advanced stage. HGSOC aggressiveness is mainly caused by the late diagnosis (51% stage III, 29% stage IV) when the tumor has already spread in the peritoneal cavity. PIN1 is a unique peptidyl-prolyl isomerase that targets the phosphorylated Ser/Thr(Pro) motifs to regulate several key proteins in different signaling pathways. Pin1 is overexpressed in several cancer types and it regulates more than 40 oncogenes and 20 tumor suppressors. Many functions are modulated through PIN1-mediated isomerization such as cell cycle progression, cellular proliferation, invasion, migration, and apoptosis. Downregulation of Pin1 decreases tumor progression. Recently, Pin1 was shown to be overexpressed in ovarian cancer (OC) which, together with the high number of interactions with other proteins, makes Pin1 a promising target for HGSOC. The aim of this work is to investigate the effects of the PIN1 inhibitor VS10 on cancer cell lines and to find the molecular signaling pathways in which Pin1 is involved. Migration, mesothelial clearance assay, and the effects on spheroid formation and preformed spheroids were studied to better understand the effects on the metastatic process. Furthermore, in order to clarify the molecular mechanism that triggers the cytotoxicity induced by Pin1 inhibition in several OC cell lines, silencing Pin1 has been demonstrated to be associated with Ser473pAkt dephosphorylation by Western Blot (WB) analysis. Additionally, cell viability and colony-forming assays showed that Akt overexpression rescued the lethal phenotype due to Pin1 knockdown in OVCAR3 and KURAMOCHI OC cell lines. Among PIN1 inhibitors, All-trans retinoic acid (ATRA), a drug in clinic for the treatment of acute promyelocytic leukemia, has been demonstrated to be active on PIN1. Our group developed many PIN1 inhibitors including VS10, a non-covalent and selective molecule, which is active in killing cancer cells. ATRA and VS10 have been combined with first- and second-line chemotherapy drugs to treat SKOV3 cell line whether these drug combinations could work synergistically to improve current therapy. This drug combination screening showed that Doxorubicin and Caelyx act in synergy with both VS10 and ATRA. This drug combination was studied in 5 sensible and 2 OC cell lines resistant to cisplatin treatment. These results candidate Pin1 as a promising new molecular target for HGSOC patients' therapy.
Patients with high-grade serous ovarian cancer (HGSOC), the most aggressive epithelial ovarian cancer (EOC) subtype, have a 5-year survival rate of about 93% when diagnosed at an early stage, but it drops to 30-40% when diagnosed in the advanced stage. HGSOC aggressiveness is mainly caused by the late diagnosis (51% stage III, 29% stage IV) when the tumor has already spread in the peritoneal cavity. PIN1 is a unique peptidyl-prolyl isomerase that targets the phosphorylated Ser/Thr(Pro) motifs to regulate several key proteins in different signaling pathways. Pin1 is overexpressed in several cancer types and it regulates more than 40 oncogenes and 20 tumor suppressors. Many functions are modulated through PIN1-mediated isomerization such as cell cycle progression, cellular proliferation, invasion, migration, and apoptosis. Downregulation of Pin1 decreases tumor progression. Recently, Pin1 was shown to be overexpressed in ovarian cancer (OC) which, together with the high number of interactions with other proteins, makes Pin1 a promising target for HGSOC. The aim of this work is to investigate the effects of the PIN1 inhibitor VS10 on cancer cell lines and to find the molecular signaling pathways in which Pin1 is involved. Migration, mesothelial clearance assay, and the effects on spheroid formation and preformed spheroids were studied to better understand the effects on the metastatic process. Furthermore, in order to clarify the molecular mechanism that triggers the cytotoxicity induced by Pin1 inhibition in several OC cell lines, silencing Pin1 has been demonstrated to be associated with Ser473pAkt dephosphorylation by Western Blot (WB) analysis. Additionally, cell viability and colony-forming assays showed that Akt overexpression rescued the lethal phenotype due to Pin1 knockdown in OVCAR3 and KURAMOCHI OC cell lines. Among PIN1 inhibitors, All-trans retinoic acid (ATRA), a drug in clinic for the treatment of acute promyelocytic leukemia, has been demonstrated to be active on PIN1. Our group developed many PIN1 inhibitors including VS10, a non-covalent and selective molecule, which is active in killing cancer cells. ATRA and VS10 have been combined with first- and second-line chemotherapy drugs to treat SKOV3 cell line whether these drug combinations could work synergistically to improve current therapy. This drug combination screening showed that Doxorubicin and Caelyx act in synergy with both VS10 and ATRA. This drug combination was studied in 5 sensible and 2 OC cell lines resistant to cisplatin treatment. These results candidate Pin1 as a promising new molecular target for HGSOC patients' therapy.
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Almqvist, Ylva. "Targeted Therapy of Colorectal Cancer : Preclinical Evaluation of a Radiolabelled Antibody." Doctoral thesis, Uppsala University, Radiology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8657.

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Targeted radiotherapy (TRT) of cancer is a promising approach that enables selective treatment of tumour cells, while sparing normal tissue. The humanized monoclonal antibody A33 (huA33) is a potential targeting agent for TRT of colorectal cancer, since its antigen is expressed in more than 95 % of all colorectal carcinomas. The aim of this thesis was to evaluate the therapeutic potential of the two huA33-based TRT-conjugates, 177Lu-huA33, and 211At-huA33.

The conjugates 177Lu-huA33, and 211At-huA33, bound specifically to colorectal cancer cells, both in vitro and in vivo. A dose dependent cytotoxic effect of 211At-huA33 was also demonstrated in vitro. From a therapeutic perspective, both conjugates had a favourable biodistribution in tumour-bearing nude mice, with high tumour uptake and a low uptake in normal organs (with the exception of an expected thyroid uptake of 211At). After injection of 211At-huA33, the blood absorbed a slightly higher dose than the tumour, but for 177Lu-huA33, the tumour received a 12 times higher dose than blood. Two days after intravenous injection of 177Lu-huA33 in tumour-bearing mice, the tumours could be clearly visualised by gamma camera imaging, with very low interference from normal tissue radioactivity. In an experimental therapy study, also performed in tumour-bearing mice, there was an excellent therapeutic effect of 177Lu-huA33. About 50 % of the treated animals were tumour free 140 days after injection of 177Lu-huA33, while none of the non-radioactive controls survived beyond 20 days after injection of treatment substances.

In conclusion, this thesis demonstrates that the therapeutic conjugates 177Lu-huA33, and 211At-huA33, are promising targeting agents that might help improve therapy of colorectal cancer.

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Pak, Ekaterina. "Resistance to Targeted Therapy in Sonic Hedgehog Subgroup Medulloblastoma: Mechanisms and Treatment Strategies." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493334.

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Aberrant activation of the Sonic Hedgehog (Shh) signaling network is implicated in many human cancers, including the most common cancer, basal cell carcinoma (BCC) and the brain tumor medulloblastoma. Suppressing Shh signaling is thus a promising strategy in oncology. The largest and most clinically advanced group of Shh signaling inhibitors comprises selective antagonists of the pathway component Smoothened (Smo). In 2012, the Food and Drug Administration approved the first Smo antagonist, and others are now approved or in clinical trials. However, there is already evidence that some patients can have primary or develop secondary resistance to therapy. Accordingly, a more comprehensive understanding of resistance mechanisms and alternative treatment approaches are needed. Here, we describe a genome-wide transposon mutagenesis screen to identify candidate resistance genes for Smo antagonists using an in vitro model of Shh-dependent medulloblastoma. Top hits from the screen include Suppressor of fused (Sufu), a known resistance gene and negative regulator in Shh signaling, and Oral-facial-digital syndrome 1 (Ofd1), a gene associated with an X-linked developmental syndrome. Independent gain- and loss-of-function experiments confirm Ofd1 as a bona fide resistance gene. Ofd1 mutant cells have reduced numbers of primary cilia, which are necessary for transducing canonical Shh signaling. Reduction of Kif3a and Ift88, two other cilia genes, also causes resistance. Strikingly, resistant cilia mutants are still dependent on active Shh signaling downstream of Smo. These mutants lack the truncated repressor form of the Shh transcription factor Gli2, but maintain full-length Gli2 levels and therefore shift the overall balance of transcriptional activators and repressors toward pathway reactivation. Importantly, we present evidence that resistance by loss of primary cilia may have clinical relevance. Subcutaneous medulloblastoma tumors in mice that acquire de novo resistance to Smo inhibition exhibit decreased numbers of primary cilia compared to tumors that remain sensitive. Additionally, resistant BCCs from patients treated with Smo antagonists have significantly more cilia gene mutations compared to untreated BCCs. Recognizing the need for more options to treat resistant tumors, we carried out a high-throughput small molecule screen in Shh-dependent medulloblastoma cells. From a set of over 900 small molecules, we identify histone deacetylase (HDAC) inhibitors as a class of promising therapeutics. While not all HDAC inhibitors are effective, we present some with similar chemical structures that work consistently within the nanomolar range across cell lines that are both sensitive and resistant to Smo inhibitors. Preliminary results indicate that inhibition of HDACs works within the Shh signaling axis and that specific HDACs may play a role in resistant human tumors. Together, these studies reveal new resistance mechanisms and explore the development of next-generation treatments in Shh-dependent tumors.
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Fröhner, Michael, Oliver W. Hakenberg, and Manfred P. Wirth. "Molecular Therapy in Urologic Oncology." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-133789.

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During recent years, significant advances have been made in the field of molecular therapy in urologic oncology, mainly for advanced renal cell carcinoma. In this hitherto largely treatment-refractory disease, several agents have been developed targeting the von Hippel-Lindau metabolic pathway which is involved in carcinogenesis and progression of the majority of renal cell carcinomas. Although cure may not be expected, new drugs, such as the multikinase inhibitors sorafenib and sunitinib and the mammalian target of rapamycine inhibitor temsirolimus, frequently stabilize the disease course and may improve survival. Fewer data are available supporting molecular therapies in prostate, bladder, and testicular cancers. Preliminary data suggest a potential role of high-dose calcitriol and thalidomide in hormone-refractory prostate cancer, whereas targeted therapies in bladder and testicular cancers are still more or less limited to single-case experiences. The great theoretical potential and the multitude of possible targets and drug combinations, however, support further research into this exciting field of medical treatment of urologic malignancies
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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Fröhner, Michael, Oliver W. Hakenberg, and Manfred P. Wirth. "Molecular Therapy in Urologic Oncology." Karger, 2007. https://tud.qucosa.de/id/qucosa%3A27535.

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During recent years, significant advances have been made in the field of molecular therapy in urologic oncology, mainly for advanced renal cell carcinoma. In this hitherto largely treatment-refractory disease, several agents have been developed targeting the von Hippel-Lindau metabolic pathway which is involved in carcinogenesis and progression of the majority of renal cell carcinomas. Although cure may not be expected, new drugs, such as the multikinase inhibitors sorafenib and sunitinib and the mammalian target of rapamycine inhibitor temsirolimus, frequently stabilize the disease course and may improve survival. Fewer data are available supporting molecular therapies in prostate, bladder, and testicular cancers. Preliminary data suggest a potential role of high-dose calcitriol and thalidomide in hormone-refractory prostate cancer, whereas targeted therapies in bladder and testicular cancers are still more or less limited to single-case experiences. The great theoretical potential and the multitude of possible targets and drug combinations, however, support further research into this exciting field of medical treatment of urologic malignancies.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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Trisolini, Elena. "Targeted molecular characterization of adult midline and circumscribed gliomas for the identification of new potential targets for personalized therapy." Doctoral thesis, Università del Piemonte Orientale, 2020. http://hdl.handle.net/11579/114872.

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Diffuse midline gliomas (MLG) are primary brain tumours arising from thalamus, hypothalamus, brainstem, cerebellum or spinal cord, mainly occurring in children. In adults, less than 10% of diffuse gliomas arises in midline structures and recent works suggested that this subset of tumours may present with phenotypic and molecular characteristics differing from both pediatric MLG and adult supratentorial gliomas. Circumscribed gliomas (CG) are low-grade tumours but may progress to anaplasia. They have lower genetic complexity than diffuse gliomas and could be better candidate for targeted therapies, when complete surgical resection is not feasible. Unravelling the genomic landscape of MLG and CG will better define the prognostic value of molecular biomarkers and identify new therapeutic strategies that could improve patient care. Adult patients with diagnosis of MLG and CG were retrospectively identified from «Maggiore della Carità» Hospital and GH Pitié-Salpêtrière (Paris). Mutation analysis was performed by Sanger sequencing of the major hot-spots: IDH1, IDH2, H3F3A, HIST1H3B, FGFR1, TERT promoter. FISH analyses of NTRK1-2-3 rearrangements were performed by break-apart probes on tissue microarray of MLG cases. We identified 116 (French) and 47 (Italian) patients. The two cohorts showed a lower percentage of H3F3A mutations (20% vs 33%), the mutation was not associated to a worse prognosis. FGFR1 mutations were identified in 18% of cases and are restricted to MLG. NTRKs analysis in the Italian cohort showed NTRK1 translocations in 15% of cases. We reported a high rate of FGFR1 mutations in optic nerve pilocytic astrocitomas and the presence of alternative BRAF activating mutations (Thr599_Val600insThr and Val600_Lys601>Glu). Our finding of frequent and potentially targetable FGFR1 and BRAF mutations and NTRK1 translocations have important therapeutical implications in the current context of clinical trials, and further reinforces the need for molecular analyses.
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Zhang, Zhenfeng. "Study of Molecular Mechanisms of Sensitivity and Resistance to EGFR-Targeted Therapy in Lung Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1278615774.

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Books on the topic "Molecular Targeted Therapy"

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Vallabhajosula, Shankar. Molecular Imaging and Targeted Therapy. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23205-3.

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Takiguchi, Yuichi, ed. Molecular Targeted Therapy of Lung Cancer. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2002-5.

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N, Syrigos Konstantinos, and Harrington Kevin J. 1958-, eds. Targeted therapy for cancer. Oxford: Oxford University Press, 2003.

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Anderson, Kenneth C., Razelle Kurzrock, and Apostolia-Maria Tsimberidou. Targeted therapy in translational cancer research. Hoboken, New Jersey: John Wiley & Sons, Inc., 2016.

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Houghton, Peter J., and Robert Arceci. Molecularly targeted therapy for childhood cancer. New York: Springer, 2010.

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International Washington Spring Symposium (10th 1990 George Washington University). Advances in molecular biology and targeted treatment for AIDS. New York: Plenum Press, 1991.

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Bo, Xuenong, and Joost Verhaagen. Gene delivery and therapy for neurological disorders. New York: Humana Press, 2015.

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1950-, Cambrosio Alberto, ed. Cancer on trial: Oncology as a new style of practice. Chicago: The University of Chicago Press, 2012.

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Slabý, Ondřej. MicroRNAs in solid cancer: From biomarkers to therapeutic targets. Hauppauge, N.Y: Nova Science, 2011.

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Prazeres, Duarte Miguel F., and Sofia Aires M. Martins. G protein-coupled receptor screening assays: Methods and protocols. New York: Humana Press, 2015.

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Book chapters on the topic "Molecular Targeted Therapy"

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Hunt, Arabella, and Kate L. Newbold. "Targeted Molecular Therapy." In The Thyroid and Its Diseases, 647–54. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-72102-6_42.

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Dougherty, Graeme J., and Shona T. Dougherty. "Vascular-Targeted Molecular Therapy." In Tumor Microenvironment, 401–19. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470669891.ch18.

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Liu, Jinhong. "Cancer Targeted Molecular Therapy." In Anesthesia for Oncological Surgery, 27–34. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-50977-3_4.

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Cieszykowska, Izabela, Wioletta Wojdowska, Dariusz Pawlak, and Renata Mikołajczak. "Radiometals in Molecular Imaging and Therapy." In Targeted Metallo-Drugs, 319–46. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003272250-12.

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Deonarain, Mahendra, Ioanna Stamati, and Gokhan Yahioglu. "Antibody-Targeted Photodynamic Therapy." In Molecular and Cellular Therapeutics, 103–24. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781119967309.ch4.

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Mossé, Yaël P., and John M. Maris. "Molecular Therapy for Neuroblastoma." In Molecularly Targeted Therapy for Childhood Cancer, 351–71. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-69062-9_17.

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Kurmasheva, Raushan T., Hajime Hosoi, Ken Kikuchi, and Peter J. Houghton. "Molecular Therapy for Rhabdomyosarcoma." In Molecularly Targeted Therapy for Childhood Cancer, 425–58. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-69062-9_20.

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Vallabhajosula, Shankar. "Radiopharmaceuticals for Therapy." In Molecular Imaging and Targeted Therapy, 461–99. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23205-3_17.

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Lundqvist, Hans, Bo Stenerlöw, and Lars Gedda. "The Auger Effect in Molecular Targeting Therapy." In Targeted Radionuclide Tumor Therapy, 195–214. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-8696-0_11.

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Gown, Allen M. "Modern Immunohistochemistry in Targeted Therapy." In Molecular Genetic Pathology, 181–96. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4800-6_7.

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Conference papers on the topic "Molecular Targeted Therapy"

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Wang, Yu “Winston”, Soyoung Kang, and Jonathan T. C. Liu. "Multiplexed Molecular Imaging with Targeted SERS Nanoparticles for Rapid Tumor Detection." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.cth2a.4.

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Boppart, Stephen A. "Magnetomotive molecular probes for targeted contrast enhancement and therapy." In SPIE BiOS, edited by Samuel Achilefu and Ramesh Raghavachari. SPIE, 2011. http://dx.doi.org/10.1117/12.873862.

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Voloshynska, Katerina, Tetjana Ilashchuk, and Sergey Yermolenko. "Spectropolarimetry of blood plasma in optimal molecular targeted therapy." In Advanced Topics in Optoelectronics, Microelectronics, and Nanotechnologies 2014, edited by Ionica Cristea, Marian Vladescu, and Razvan Tamas. SPIE, 2015. http://dx.doi.org/10.1117/12.2068189.

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Shuming Nie. "Biomedical nanotechnology for molecular imaging, diagnostics, and targeted therapy." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5332688.

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Chen, Yongping, Toufic Jabbour, and Xingde Li. "Functional Fluorescent Nanocapsules for Molecular Imaging and Potential Targeted Therapy." In CLEO: Applications and Technology. Washington, D.C.: OSA, 2011. http://dx.doi.org/10.1364/cleo_at.2011.jme1.

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Sorace, Anna G., Reshu Saini, Marshall J. Mahoney, and Kenneth Hoyt. "Targeted molecular ultrasound therapy improves chemotherapeutic drug delivery in cancer cells." In 2012 IEEE International Ultrasonics Symposium. IEEE, 2012. http://dx.doi.org/10.1109/ultsym.2012.0106.

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Hanly, Elyse K., Neha Y. Tuli, Robert Suriano, Robert Bednarczyk, Zbigniew Darzynkiewicz, Augustine L. Moscatello, Edward J. Shin, Jan Geliebter, and Raj K. Tiwari. "Abstract 3709: Resistance mechanisms to targeted molecular therapy in thyroid cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3709.

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McCormick, Frank. "Abstract PL05-03: Future challenges of targeted therapy." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-pl05-03.

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Schmidtlein, Charles Ross, Matthew K. Maroun, Andrzej Krol, Howard Gifford, Lisa Bodei, Joseph O'Donoghue, Ida Häggström, and Yuesheng Xu. "A deblurring/denoising corrected scintigraphic planar image reconstruction model for targeted alpha therapy." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor S. Gimi and Andrzej Krol. SPIE, 2021. http://dx.doi.org/10.1117/12.2584736.

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Wang, Sijia, Gereon Hüttmann, Tayyaba Hasan, and Ramtin Rahmanzadeh. "Molecular targeted PDT with selective delivery of ICG Photo-Immunoconjugates (Conference Presentation)." In Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXV, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2016. http://dx.doi.org/10.1117/12.2217572.

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Reports on the topic "Molecular Targeted Therapy"

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Xu, Liang. (-)-Gossypol, A Potent Small Molecule Inhibitor of BcL-XL as a Novel Molecular Targeted Therapy for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada452527.

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Wang, Xiaoyue, Hui Lu, Zhihao Liang, Liang Wang, and Ji Ma. Ixazomib combined with autologous stem cell transplantation for POEMS syndrome: a case report and meta‑analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0061.

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Review question / Objective: POEMS syndrome is a rare monoclonal plasma cell proliferation disorder. At present, there is no unified treatment for POEMS syndrome. Here, we describe one case with POEMS syndrome. And we made a meta­analysis to assess the efficacy of treatment strategies in recent ten years. Search strategy: We searched relevant articles in PubMed, Embase and MEDLINE database for the period up to July 2021.The search strategy included the keywords: POEMS, Therapy, Drug Therapy, Biological Therapy, Combined Modality Therapy, Hematopoietic Stem Cell Transplantation, Immunotherapy, Molecular Targeted Therapy, Chemoradiotherapy, Salvage Therapy, Controlled Clinical Trial, Randomized Controlled Trial et al. In addition, we checked all the references of eligible articles that our search retrieved to identify potentially eligible papers.
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Xu, Liang. Tumor-Targeted Silencing of Bcl-2/Bcl-xl by Self-Assembled Sirna-Nanovectors as a Novel Molecular Therapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada475350.

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Wang, Lu-Hai. Exploring the Molecular Targets for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada442297.

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Tzfira, Tzvi, Michael Elbaum, and Sharon Wolf. DNA transfer by Agrobacterium: a cooperative interaction of ssDNA, virulence proteins, and plant host factors. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7695881.bard.

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Agrobacteriumtumefaciensmediates genetic transformation of plants. The possibility of exchanging the natural genes for other DNA has led to Agrobacterium’s emergence as the primary vector for genetic modification of plants. The similarity among eukaryotic mechanisms of nuclear import also suggests use of its active elements as media for non-viral genetic therapy in animals. These considerations motivate the present study of the process that carries DNA of bacterial origin into the host nucleus. The infective pathway of Agrobacterium involves excision of a single-stranded DNA molecule (T-strand) from the bacterial tumor-inducing plasmid. This transferred DNA (T-DNA) travels to the host cell cytoplasm along with two virulence proteins, VirD2 and VirE2, through a specific bacteriumplant channel(s). Little is known about the precise structure and composition of the resulting complex within the host cell and even less is known about the mechanism of its nuclear import and integration into the host cell genome. In the present proposal we combined the expertise of the US and Israeli labs and revealed many of the biophysical and biological properties of the genetic transformation process, thus enhancing our understanding of the processes leading to nuclear import and integration of the Agrobacterium T-DNA. Specifically, we sought to: I. Elucidate the interaction of the T-strand with its chaperones. II. Analyzing the three-dimensional structure of the T-complex and its chaperones in vitro. III. Analyze kinetics of T-complex formation and T-complex nuclear import. During the past three years we accomplished our goals and made the following major discoveries: (1) Resolved the VirE2-ssDNA three-dimensional structure. (2) Characterized VirE2-ssDNA assembly and aggregation, along with regulation by VirE1. (3) Studied VirE2-ssDNA nuclear import by electron tomography. (4) Showed that T-DNA integrates via double-stranded (ds) intermediates. (5) Identified that Arabidopsis Ku80 interacts with dsT-DNA intermediates and is essential for T-DNA integration. (6) Found a role of targeted proteolysis in T-DNA uncoating. Our research provide significant physical, molecular, and structural insights into the Tcomplex structure and composition, the effect of host receptors on its nuclear import, the mechanism of T-DNA nuclear import, proteolysis and integration in host cells. Understanding the mechanical and molecular basis for T-DNA nuclear import and integration is an essential key for the development of new strategies for genetic transformation of recalcitrant plant species. Thus, the knowledge gained in this study can potentially be applied to enhance the transformation process by interfering with key steps of the transformation process (i.e. nuclear import, proteolysis and integration). Finally, in addition to the study of Agrobacterium-host interaction, our research also revealed some fundamental insights into basic cellular mechanisms of nuclear import, targeted proteolysis, protein-DNA interactions and DNA repair.
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Wahl, Geoffrey M. Amplified Genes in Breast Cancer: Molecular Targets for Investigation and Therapy. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada382811.

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Lilly, Michael. PIM1: A Molecular Target to Modulate Cellular Resistance to Therapy in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada494338.

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Lilly, Michael. Pim-1: A Molecular Target to Modulate Cellular Resistance to Therapy in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada453390.

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Lilly, Michael B. Pim-1: A Molecular Target to Modulate Cellular Resistance to Therapy in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada465489.

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Lilly, Michael. Pim-1: A Molecular Target to Modulate Cellular Resistance to Therapy in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada482582.

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