Relevant bibliographies by topics / Cancer molecular targets

Academic literature on the topic 'Cancer molecular targets'

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

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Journal articles on the topic "Cancer molecular targets"

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Weigelt, Britta, and Susana Banerjee. "Molecular targets and targeted therapeutics in endometrial cancer." Current Opinion in Oncology 24, no. 5 (September 2012): 554–63. http://dx.doi.org/10.1097/cco.0b013e328354e585.

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Kummar, Shivaani, and James H. Doroshow. "Molecular targets in cancer therapy." Expert Review of Anticancer Therapy 13, no. 3 (March 2013): 267–69. http://dx.doi.org/10.1586/era.12.170.

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Lorch, Jochen H. "Molecular Targets for Thyroid Cancer." Oncology Times 35 (June 2013): 2–3. http://dx.doi.org/10.1097/01.cot.0000431825.52663.3e.

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Lazo, John S., and Elizabeth R. Sharlow. "Drugging Undruggable Molecular Cancer Targets." Annual Review of Pharmacology and Toxicology 56, no. 1 (January 6, 2016): 23–40. http://dx.doi.org/10.1146/annurev-pharmtox-010715-103440.

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Gale, Danielle M. "Molecular targets in cancer therapy." Seminars in Oncology Nursing 19, no. 3 (August 2003): 193–205. http://dx.doi.org/10.1016/s0749-2081(03)00047-0.

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Westwell, Andrew D. "Molecular targets and cancer therapeutics." Drug Discovery Today 9, no. 24 (December 2004): 1042–44. http://dx.doi.org/10.1016/s1359-6446(04)03287-8.

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William, William N., John V. Heymach, Edward S. Kim, and Scott M. Lippman. "Molecular targets for cancer chemoprevention." Nature Reviews Drug Discovery 8, no. 3 (March 2009): 213–25. http://dx.doi.org/10.1038/nrd2663.

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Zaenker, K. S., G. Mustacchi, and E. Mihich. "Molecular targets of cancer chemotherapy." Cancer Chemotherapy and Pharmacology 58, no. 2 (December 24, 2005): 279–82. http://dx.doi.org/10.1007/s00280-005-0170-9.

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Rossig, Claudia. "Immune modulation by molecular cancer targets and targeted therapies." OncoImmunology 1, no. 3 (May 2012): 358–60. http://dx.doi.org/10.4161/onci.18401.

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Wang, Shihao, Jinqiu Shen, Boyang Zhang, Jiao Tian, Wei Zhao, and Wenzheng Wu. "Molecular mechanism study of cancer treatment based on network pharmacology of lily." Highlights in Science, Engineering and Technology 14 (September 29, 2022): 397–403. http://dx.doi.org/10.54097/hset.v14i.1852.

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OBJECTIVE: To make predictions related to the treatment of cancer by lily. METHODS: A systematic study of the constituents, targets and pathways of lily and cancer treatment was conducted using network pharmacology and molecular docking methods. The active ingredients of lily were screened and selected for investigation using TCMSP, Uniprot and PubChem databases, and the "ingredient-target-pathway" correlation axis was established. PubChem was used to collect the compounds in lily, and the active ingredients and targets with OB≥30% and DL≥0.18 in lily were obtained using the TCMSP Chinese medicine database. The active ingredients that met the criteria were also screened, and the binding patterns of the core targets and active ingredients were verified using molecular docking techniques before the active ingredients in lily were genetically aligned using Uniprot, and the corresponding genes were collated. The genes of different cancers were collated using CTD. Cytoscape 3.9.0 was used to create a map of the active ingredients and their corresponding targets. Finally, the results obtained were used to make predictions related to the treatment of cancer in lily. Results: The herb-compound-target network was obtained through screening. After cross-matching the active targets of the chemical components in lily with various cancers, 42 intersecting targets were obtained. Conclusion: The rank values (degree) of the intersecting targets were analysed and six targets with a degree greater than 5 were found to be PTGS2 (12), MMP1 (10), PPARG (8), HSP90AA1 (8), TP53 (8) and ESR2 (6); the diseases that were closely linked to the targets were Cancer, unspecific (The findings of this paper may provide a reference for the development of relevant targeted drugs and targeted therapeutic approaches in the future.
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Dissertations / Theses on the topic "Cancer molecular targets"

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Culp, W. David. "Identifying molecular targets for cancer therapy /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-188-3/.

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Ehsanian, Reza. "Molecular targets in head and neck cancer." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540135.

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Qureishi, Ali Akhtar Siddique. "Molecular targets in head and neck cancer." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/molecular-targets-in-head-and-neck-cancer(f4b44db3-7db7-4ed6-8b8d-77d3d446b116).html.

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Background: Head and neck cancer (HNSCC) affects 650,000 people annually. Laryngeal cancer (LSCC) and oropharyngeal cancer (OPSCC) are amongst the commonest sub-types. For other cancers e.g. breast cancer, personalised treatments based on tumour markers have improved patient survival. With the exception of human papilloma virus (HPV); there are no clinically utilised biomarkers in HNSCC. Insulin growth factor receptor 1 (IGF-1R) and HPV are promising molecular markers in LSCC and OPSCC respectively. This thesis investigates the use of IGF-1R as a marker of radiotherapy resistance in LSCC and evaluates HPV detection in patients with OPSCC. Aims: • To assess IGF-1R as a marker of radiotherapy resistance in LSCC. • To determine the diagnostic accuracy of salivary PCR to detect HPV in patients with OPSCC. Methods: Immunohistochemistry (IHC) was used to compare IGF-1R levels between patients with LSCC achieving long-term remission and experiencing recurrence after radiotherapy. LSCC cells were used to create and interrogate an in vitro model of radiation resistance. Following the completion of a systematic review on HPV testing in OPSCC, a diagnostic accuracy study was performed to determine the sensitivity and specificity of saliva testing for HPV in OPSCC. Results: IGF-1R levels are higher in radioresistant LSCC and increase following radiotherapy. IGF-1R inhibition appears to be more effective at limiting cell survival in cells with IGF-1R overexpression. The sensitivity and specificity of saliva testing when compared to p16 IHC and HPV DNA in situ hybridisation is 72.2% and 90%. Conclusions: Elevated IGF-1R appears to associate with previous radiotherapy and radiotherapy resistance in LSCC. Treatments accounting for IGF-1R status, or molecular therapies targeting this receptor, may have merit in patients whose tumours overexpress IGF-1R. Saliva testing for HPV is a promising alternative to p16 IHC performed on tumour tissue. In selected patients, this might avoid the need for surgical biopsies and expedite treatment.
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Campbell, Paul Michael. "DNA methylation machinery as molecular targets for cancer therapeutics." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82836.

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One of the elements commonly seen in cancer is the change in methylation status of the genome. These aberrations in methylation appear to be critical for the neoplastic phenotype and manifest as changes to gene expression of oncogenes and tumour suppressors. In addition to epigenetic alterations, the proteins involved in maintaining the plastic methylation status of the genome, DNA methyltransferases and demethylases, also show methylation-independent protein-protein interactions that have effects on cell cycle progression and proliferation. As changes in gene expression and mitotic regulation are seminal elements of cancer, and because several methylated DNA binding proteins show differential expression in a wide variety of cancers, these proteins serve as prime targets for anticancer therapies. This thesis relates to exploring both current and forthcoming possibilities and mechanisms of utilizing the DNA methylation machinery for pharmacological intervention of cancer. Chapter two deals with an antisense drug, currently in clinical trials, targeted to reduction of DNA methyltransferase 1, the maintenance methylation enzyme in mammalian cells. Our data indicate that the existence of a common truncation mutation of the adenomatous polyposis coli gene seen in some forms of sporadic and familial colorectal cancer may lead to downstream upregulation of DNA methyltransferase 1, as reconstitution of the wildtype protein reduces DNA methyltransferase 1 mRNA and protein. Reduction of the transcripts of this methylation enzyme with an antisense oligonucleotide decreases the tumourigenicity of these colorectal cancer cells, and provides a rationale for use of this drug in colorectal cancer patients and prophylactic treatment of adenomatous polyposis coli mutation-bearing individuals. Chapter three describes the rationale, design, and in vitro and in vivo testing of antisense molecules against the methylated DNA binding protein MBD2. These drugs red
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Tarrado, Castellarnau Miriam. "Targeting metabolic reprogramming associated to cancer cells: search of novel targets and combined therapies in cancer treatment." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/385425.

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Cancer is characterised by the lost of physiological control and the malignant transformation of cells that acquire functional and genetic abnormalities, leading to tumour development and progression. Colon and lung cancer are two of the most common cancers worldwide. In early stages of the disease, surgery is the common choice while chemotherapy is the main treatment for advanced stage cancer. However, the currently available chemotherapeutic treatments exhibit modest efficacy due to their side effects and drug resistance. Therefore, the search for combined chemotherapies with low systemic toxicity and high efficiency holds great promise to decrease the morbidity and mortality of cancer. Tumour cells present common biological capabilities sequentially acquired during the development of cancer that are considered essential to drive malignancy. In particular, tumour cells switch their core metabolism to meet the increased requirements of cell growth and division. Indeed, oncogenic signals converge to reprogram tumour metabolism by enhancing key metabolic pathways such as glycolysis, pentose phosphate pathway (PPP), glutaminolysis and lipid, nucleic acid and amino acid metabolism. Several oncogenes including c-MYC, hypoxia inducible factor 1 (HIF1), phosphoinositide-3-kinase (PI3K), protein kinase B (PBK or Akt) and the mechanistic target of rapamycin (mTOR), have been known to be involved in the regulation of tumour metabolic reprogramming. Then, the study of the tumour metabolic reprogramming and its connection with oncogenic signalling is an essential strategy to identify new targets for cancer therapy. Thus, the main objective of this thesis was to explore new possibilities for cancer treatment and diagnosis. To this end, we have analysed the links between metabolism and tumour progression, the tumour metabolic reprogramming associated to the dysregulation of cell cycle, and the use of combination therapies for cancer treatment. In order to accomplish our main objective, the results of this thesis are divided in three chapters: 1. We have identified glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a potential predictive biomarker for tumour staging and prognosis of human colorectal cancer. In addition, our results clearly discourage the use of GAPDH as a housekeeping marker in colorectal cancer. 2. We have characterised the metabolic reprogramming associated to the inhibition of cyclin-dependent kinases 4 and 6 (CDK4/6) in colon cancer cells. CDK4/6 inhibition causes a shift towards enhanced metabolism of glucose, glutamine and amino acids by increasing mitochondrial metabolism and function as well as glycolytic flux. Fluxomics and transcriptomics integrated data analysis revealed that this metabolic reprogramming is directed by MYC, which is accumulated when CDK4/6 are inhibited. In fact, the identification of the tumour metabolic adaptations associated to CDK4/6 inhibition reveals potential metabolic vulnerabilities that can be exploited in combination therapies with CDK4/6 inhibitors. Accordingly, we have obtained synergistic and selective antiproliferative effects in vitro by inhibiting mTOR, PI3K/Akt axis or MYC target genes in combination with CDK4/6 inhibitors. Therefore, we propose new combination therapies that simultaneously target cell cycle and metabolism of cancer cells. 3. We have determined the molecular mechanism of action of the selenium compound methylseleninic acid (MSA) in cancer cells. MSA effects are associated with the inhibition of the Akt pathway, leading to dephosphorylation of FOXO transcription factors and their nuclear translocation which, in turn, activate the expression of FOXO target genes. By targeting the PI3K/Akt/FOXO pathway, MSA synergises with cisplatin in combination therapies to reduce the commonly observed toxicity and overcome the resistance of cisplatin-based chemotherapy. The completion of these objectives has shed new light on the understanding of tumour metabolic reprogramming as well as the mechanisms of action of compounds potentially useful as antitumour agents. We have used this information to develop new strategies complementing conventional and existing chemotherapies, providing new approaches for cancer treatment and diagnosis.
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Wong, Ka-wing, and 王家穎. "Study of potential targets of miR-143 in cervical cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206496.

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Cervical cancer is a common gynaecological malignancy worldwide, with more than 450,000 incidences every year. Its etiology has been well documented to be associated with persistent infection with high-risk genotypes of human papillomavirus (HPV). The carcinoma can be screened by convention Pap smear and liquid-based cytology. Although preventable, cervical cancer remains a primary cause of death from cancer in developing countries where cytological screening is not so available. In the past decades, many studies have been carried out to explore molecular screening or diagnosis of cervical cancer, such as HPV DNA testing, histological or cytological biomarkers. Micro RNAs, small non-coding RNA molecules of 18-25 nucleotides in length, areaberrantly expressed in various cancers. MiR-143 was reported consistently downregulated in cervical cancer tissues and cell lines, but its functional roles in cervical carcinogenesis has not been clearly illustrated. Ten miR-143 downstream target genes were chosen and their expression levels in five cervical cancer cell lines (HeLa, SiHa, CaSki, C4-I and C33A) were investigated. In general, the gene expressions of candidates are upregulated in our cell lines with lowmiR-143 level. To further identify specific miR-143 targets in cervical cancer for biomarkers, protein expressions of TARDBP, ERK5, KRAS and PHF6were significantly downregulated upon miR-143 overexpression. Hence, miR-143 level is inversely correlated with the mRNA and protein expressions of these target genes. Immunohistochemical study of ERK5 and TARDBP on FFPE samples including normal cervix, CINs and SCC cases showed that both ERK5 and TARDBP were positively stained in SCC samples, whereas weaker staining was found in CINs (both LSILs and HSILs) for both antigens. Thus, the intensity of positive staining ascended with the histological grading: LSIL, HSIL and SCC samples. Such differential expression pattern supports ERK5 and TARDBP as specific markers for high grade cancerous lesions. In summary, two targets of miR-143, ERK5 and TARDBP, could be specific markers for high-grade lesion of cervical cancer. This is supported by their transcript and protein expressions inversely associated with miR-143 level, and that their strong immunohistochemical positivity in SCC samples. Their underlying molecular mechanisms involved in carcinogenesis and possible future applications require more in-depth researches.
published_or_final_version
Pathology
Master
Master of Medical Sciences
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Bachelor, Michael A. "Identification of molecular targets for the chemoprevention of non-melanoma skin cancer." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280585.

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The ultraviolet (UV) component of sunlight has been identified as a major etiological factor in the development of non-melanoma skin cancer (NMSC). Upregulation of Activator Protein-1 (AP-1) and Cyclooxygenase-2 (COX-2) have clearly demonstrated a functional role in skin tumor promotion. The goal of this work was to contribute to the growing knowledge of UVA and UVB induced signaling events leading to increases in AP-1 and COX-2. We show that UVA induces COX-2 expression in the human keratinocyte cell line, HaCaT through a post-transcriptional mechanism involving the 3 ' untranslated region (3'UTR). Use of a pharmacological inhibitor of p38 MAPK, SB202190, decreased UVA-induced COX-2 steady-state mRNA and protein levels. The stability of COX-2 mRNA is increased in UVA-irradiated cells and dependent upon p38 MAPK activity. We further explored the role of UVA-induced p38 MAPK activity in apoptosis in both HaCaT cells and primary keratinocytes. Dramatic increases in apoptosis were observed in UVA-irradiated cells treated with SB202190 or through the use of a dominant-negative construct. UVA induced expression of Bcl-X L with abrogation of expression using SB202190. Overexpression of Bcl-X L prevented PARP (Poly ADP-ribose Polymerase) cleavage induced by the combination of UVA and p38 MAPK inhibition. We further demonstrated that UVA enhanced the stability of Bcl-XL mRNA through increases in p38 MAPK activity mediated through the 3' UTR. p38 MAPK and Bcl-XL expression play critical roles in the survival of UVA-irradiated keratinocytes. Previous investigations from the laboratory identified p38 MAPK and PI3-Kinase as the major mediators of UVB-induced AP-1 and COX-2 in the HaCaT cell line. To further validate p38 MAPK and PI3-Kinase as potential molecular targets we investigated whether an acute UVB dose activated the p38 MAPK and PI3-Kinase pathways in vivo. We observed rapid increases in both p38 MAPK and PI3-Kinase signaling in mouse epidermis. Activation of these pathways resulted in the phosphorylation of cyclic AMP response element binding protein (CREB). Topical treatment with SB202190 or LY294002 (a specific inhibitor of PI3-Kinase) significantly decreased UVB-induced COX-2 expression and AP-1 activation in vivo. Our data suggest that p38 MAPK and PI3-Kinase may serve as significant molecular targets for the chemoprevention of UVB-induced NMSC.
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Whetstone, Jennifer Lynn. "Identification of synthetic benzopyranones as selective agents for molecular targets in breast cancer /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486401895209686.

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Ong, Chee Wee. "Clinical and molecular characterisation of prognostic markers and therapeutic targets in prostate cancer." Thesis, Queen's University Belfast, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709689.

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The increasing advances in genomic technologies in the last decade have allowed us to understand the molecular mutational landscape of prostate cancer. However, validation of genomic profiles generated by high-throughput efforts is laborious and expensive. Therefore, there is a need for a systematic and streamlined assessment of high-throughput genomic data to prioritise genes for further detailed biological validation studies for which this thesis entailed. Through cluster analysis of a panel of carefully selected markers, such as AR, ERG, MYC, RB1, PTEN and TP53, we were able to align patients into individual subgroups based on their PTEN status. Subsequently, through an objective computer learning elastic net modelling, we identified a cluster of 35 genes that was defining the clusters in our cohort. The prognostic effect of this signature was conserved in three independent datasets, with prominent statistical power, in Gleason 7 prostate cancer. Notably, our study is the first to report a signature with prognostic value in Gleason 7 cases. Additionally, we were able to identify a putative actionable target, S1PR2, by overlapping PTEN-low expressing clinical cases with gene expression data available from a Pten-knockout mouse model. From our analysis, we have observed that the combined inhibition of S1PR2 and the S1P kinases, SPHK1/2 were able to reduce cell migration and viability. Through a series of molecular validation, we postulated that the inhibition of both S1PR2 and SPHK1/2 could decrease cell viability and migration essential for cancer cell survival. Collectively, our findings contributed to the better understanding of the genomic changes associated with the heterogeneity of prostate cancer. Furthermore, we have uncovered several possible avenues for novel therapeutic interventions for untreated Gleason 7 prostate cancer.
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Alfarsi, Halema. "In silico mutagenesis and 3D culture appraoch to define molecular targets in ovarian cancer." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS104.

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Le cancer de l’ovaire est la première cause de décès par cancer gynécologique chez la femme. La survie globale à 5 ans est inférieur à 40% due à un diagnostique tardif et une haute fréquence des récidives malgré une chimiosensibilité initiale. Les caractéristiques cliniques et anatomopathologiques ne prédisent pas de façon précise le pronostic des patients et il est urgent de trouver de nouvelles cibles moléculaires. Ces dernières années plusieurs nouvelles stratégies ont émergé. De nombreux consortium ont analysé de façon exhaustive le génome des cancers ovariens établissant ainsi une carte d ‘identité précise des cancers avancés. Par ailleurs plusieurs groupes ont montré le rôle primordial du stroma tumoral dans la progression des tumeurs ovariens.Dans ce travail de thèse nous avons d’abord mis en place un modèle de culture tridimensionnel des cancers de l’ovaire en utilisant la membrane amniotique comme substitut au péritoine. Nous avons pu ainsi quantifier les premières étapes de l’invasion tumorale et montrer le rôle primordial des MSCs via la sécrétion de l’Interleukin IL6. Notre deuxième travail a consisté en une analyse des données de génomiques du TCGA. Nous avons utilisé les concepts de Background mutation rate et mis en place un système de mutagenèse in silico avec des boucles de réitération (Bootstrap). Cette stratégie nous a permis d’obtenir une liste des gènes qui auraient du être retrouvé muté. En posant l ‘hypothèse que les gènes protégés des mutations étaient primordiales au développement tumoral nous avons mis en place une plateforme de screening basé sur l’inhibition par siRNA pour démontrer la validité de notre stratégie. Ainsi nous avons pu montrer le rôle primordial de gène dont la fonction n’était pas décrite dans le cancer de l’ovaire (ANKLE2, MAB1-Beta).Au total utilisant deux stratégies différentes de recherche nous avons pu mettre ne évidence le rôle d’IL6 dans l’invasion initiale du péritoine par les cellules tumorales ovariennes et déterminer le rôle de gènes non muté dans la progression tumorale
Ovarian cancer causes more deaths in the United States than any other type of female reproductive tract cancer, with an estimated 21,980 new cases and 14,270 deaths in 2014. Approximately 70% of ovarian cancers are diagnosed at advanced stage and only 30% of women with such cancers can expect to survive 5 years. This low survival rate is due to the frequent diagnosis of epithelial ovarian cancer at an advanced stage, and to intrinsic and acquired resistance to platinum-based chemotherapy. Clinical and pathological classification methods, including tumor grade and the extent of surgical debulking, still fail to fully predict disease progression and patient outcome. Clinical profile of initial response to chemotherapy in the majority of patients followed by recurrence in high proportion of patients suggests the presence of a subpopulation of cells that survives and leads to chemoresistance. Only by treating this subpopulation we can achieve durable response rates.Genomic instability is a hallmark of malignant tumors, causing disturbed integrity of the genome, numerical alterations, and structural changes. For various cancer types greater genomic instability has been associated with poor prognosis, suggesting that genomic instability may confer growth advantage of cancer cells. With the recent development of next-generation sequencing (NGS) technology, the Cancer Genome Atlas (TCGA) researchers have identified molecular abnormalities related to the pathophysiology, clinical outcome, and potential therapeutic targets in high-grade serous ovarian cancer (HGSC). The TCGA study provides a large-scale integrative view of the aberration in HGSC with extensive heterogeneity between individual tumorsOur research protocols enabled us to combine computational biology approach and gene knock down in the first part to identify genes that play an important role in ovarian cancer biology. we carried out in silico mutagenesis of the human genome corresponding to the regions sequenced by publically available ovarian cancer sequencing data from the TCGA. We compared the simulated mutations to the observed mutations in the TCGA cohort. We found genes that were observed to be mutated less than expected from the simulation data.Our approach allowed us to identify therefore a set of genes that we think are selected and remain unmutated for their potential role in tumor progression. Silencing of un-mutated genes impacted growth, morphology, migration, invasion and chemotherapeutic. This is the first study depicting that inhibition of a specific non-mutated gene by its single targeting siRNA can be utilized to obtain improved therapeutic efficiency
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Books on the topic "Cancer molecular targets"

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E, Steele Vernon, ed. Cellular and molecular targets for chemoprevention. Boca Raton, Fla: CRC Press, 1992.

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Chatterjee, Malay, ed. Molecular Targets and Strategies in Cancer Prevention. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31254-5.

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Chatterjee, Malay, and Khosrow Kashfi, eds. Cell Signaling & Molecular Targets in Cancer. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-0730-0.

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Pecorino, Lauren. Molecular biology of cancer: Mechanisms, targets, and therapeutics. Oxford: Oxford University Press, 2005.

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Pecorino, Lauren. Molecular biology of cancer: Mechanisms, targets, and therapeutics. 2nd ed. Oxford: Oxford University Press, 2008.

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Pecorino, Lauren. Molecular biology of cancer: Mechanisms, targets, and therapeutics. 2nd ed. Oxford: Oxford University Press, 2008.

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Pecorino, Lauren. Molecular biology of cancer: Mechanisms, targets, and therapeutics. 2nd ed. Oxford: Oxford University Press, 2008.

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Pecorino, Lauren. Molecular biology of cancer: Mechanisms, targets, and therapeutics. 2nd ed. Oxford: Oxford University Press, 2008.

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Kelley, Mark Richard. DNA repair in cancer therapy: Molecular targets and clinical applications. London: Elsevier/Academic Press, 2012.

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DNA repair in cancer therapy: Molecular targets and clinical applications. London: Elsevier/Academic Press, 2012.

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Book chapters on the topic "Cancer molecular targets"

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Annunziata, Christina M., and Phillip A. Dennis. "Molecular Targets." In Cancer Drug Discovery and Development, 1–21. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9135-4_1.

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Dumitrescu, Ramona G. "Epigenetic Targets in Cancer Epidemiology." In Methods in Molecular Biology, 457–67. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-416-2_23.

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Hochwald, Steven N., William G. Cance, and Elena Kurenova. "Pancreatic Cancer: Molecular Targets for Therapy." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_4358-4.

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Hochwald, Steven N., William G. Cance, and Elena Kurenova. "Pancreatic Cancer Molecular Targets for Therapy." In Encyclopedia of Cancer, 3421–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_4358.

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Hochwald, Steven N., Elena Kurenova, and William G. Cance. "Pancreas Cancer Molecular Targets for Therapy." In Encyclopedia of Cancer, 2770–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4358.

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Unver, Nese, and Chirayu Mohindroo. "Targets and Strategies for Cancer Immunoprevention." In Methods in Molecular Biology, 7–17. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2014-4_2.

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Cappello, Paola, Sara Bulfamante, Giorgia Mandili, and Francesco Novelli. "Discovery of Targets for Cancer Immunoprevention." In Methods in Molecular Biology, 19–33. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2014-4_3.

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Ayriss, Joanne E., Chien-Tsun Kuan, Susan T. Boulton, David A. Reardon, and Darell D. Bigner. "Molecular Targets for Antibody-Mediated Immunotherapy of Malignant Glioma." In CNS Cancer, 865–98. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-553-8_36.

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Bronchud, Miguel H. "Selecting the Right Targets for Cancer Therapy." In Principles of Molecular Oncology, 1–26. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-470-4_1.

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Bronchud, Miguel H. "Selecting the Right Targets for Cancer Therapy." In Principles of Molecular Oncology, 3–49. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-664-5_1.

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Conference papers on the topic "Cancer molecular targets"

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Brown, Powel H. "Abstract ED02-01: Molecular targets of cancer preventive agents." 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-ed02-01.

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Kobayashi, Hisataka. "Near infrared photoimmunotherapy for cancer; New targets on cancer and immune-suppressive cells." In Reporters, Markers, Dyes, Nanoparticles, and Molecular Probes for Biomedical Applications XIII, edited by Samuel Achilefu and Ramesh Raghavachari. SPIE, 2021. http://dx.doi.org/10.1117/12.2577639.

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Komseli, Eirini-Stavroula, Fabiola Sesti, Konstantinos Evangelou, Christina Cheimonidou, Athanassios Kotsinas, Vassilis Gorgoulis, and Ioannis P. Trougakos. "Abstract B73: Proteostasis network modules as molecular targets for cancer therapeutics." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b73.

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Merchant, Kendra T., Appu Rathinavelu, James Kumi‐Diaka, Nwadiuto Esiobu, Robert Zoeller, James Hartmann, and Michelle Johnson. "Abstract C85: Novel molecular targets for genistein in prostate cancer cells." 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-c85.

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Stangeland, Biljana, Mrinal Joel, Awais Mughal, Zanina Grieg, Ingunn Ramsnes, Staale Nygaard, Cecilie Sandberg, et al. "Abstract B202: Identification of new molecular targets in glioblastoma." 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-b202.

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Kolev, Vihren, Yan Wang, Kam Sprott, Irina Shapiro, Jennifer Ring, Jonathan Pachter, and David Weaver. "Abstract C29: FAK inhibition targets cancer stem cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-c29.

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Toyoshima, Masafumi, Heather Howie, Maki Imakura, Ryan Walsh, Julie Park, and Carla Grandori. "Abstract C135: Therapeutic targets for MYC-driven cancer." 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-c135.

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Edgren, Henrik, Kalle Ojala, and Anja Ruusulehto. "Abstract A75: Pan-cancer identification of fusion genes as therapeutic targets in cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-a75.

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Yoshino, Hirofumi, Hideki Enokida, Takeshi Yamasaki, Hideo Hidaka, Takeshi Chiyomaru, Nijiro Nohata, Naohiko Seki, and Masayuki Nakagawa. "Abstract 1103: Molecular targets regulated by tumor suppressivemicroRNA-1andmicroRNA-133ain bladder cancer." 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.am2012-1103.

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Li, Rick, Shenshen Lai, Allan Mah, Hong Zhang, Jun Yan, Anthony Marotta, and Zaihui Zhang. "Abstract A152: Emerging indications for kinase-targeted therapies: screening for new targets." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a152.

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Reports on the topic "Cancer molecular targets"

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Verma, Ajit K. Molecular Targets for Prevention of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2009. http://dx.doi.org/10.21236/ada538690.

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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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Verma, Ajit K. Molecular Targets for the Prevention of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada497253.

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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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Roper, Justin R. Onboard SPECT for Localizing Functional and Molecular Targets in Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada509347.

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Hong, Waun K., and Roy Herbst. Imaging and Molecular Markers for Patients with Lung Cancer: Approaches with Molecular Targets, Complementary/Innovative Treatment, and Therapeutic Modalities. Fort Belvoir, VA: Defense Technical Information Center, February 2011. http://dx.doi.org/10.21236/ada548594.

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Hong, Waun Ki, and Roy Herbst. IMPACT (Imaging and Molecular Markers for Patients with Lung Cancer: Approaches with Molecular Targets and Complementary, Innovative and Therapeutic Modalities). Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada485809.

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Hong, Waun K., and Roy Herbst. IMPACT (Imaging and Molecular Markers for Patients with Lung Cancer: Approaches with Molecular Targets and Complementary, Innovative and Therapeutic Modalities). Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada504658.

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Hong, Waun K. IMPACT: Imaging and Molecular Markers for Patients with Lung Cancer: Approaches with Molecular Targets, Complementary/Innovative Treatments, and Therapeutic Modalities. Fort Belvoir, VA: Defense Technical Information Center, February 2013. http://dx.doi.org/10.21236/ada579142.

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Hong, Waun K. IMPACT: Imaging and Molecular Markers for Patients with Lung Cancer: Approaches with Molecular Targets, Complementary/Innovative Treatments, and Therapeutic Modalities. Fort Belvoir, VA: Defense Technical Information Center, February 2014. http://dx.doi.org/10.21236/ada602577.

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