Relevant bibliographies by topics / Metastatic progression

Contents

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

Academic literature on the topic 'Metastatic progression'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Metastatic progression"

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Roda, Niccolo’, Valentina Gambino, and Marco Giorgio. "Metabolic Constrains Rule Metastasis Progression." Cells 9, no. 9 (2020): 2081. http://dx.doi.org/10.3390/cells9092081.

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Metastasis formation accounts for the majority of tumor-associated deaths and consists of different steps, each of them being characterized by a distinctive adaptive phenotype of the cancer cells. Metabolic reprogramming represents one of the main adaptive phenotypes exploited by cancer cells during all the main steps of tumor and metastatic progression. In particular, the metabolism of cancer cells evolves profoundly through all the main phases of metastasis formation, namely the metastatic dissemination, the metastatic colonization of distant organs, the metastatic dormancy, and ultimately t
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Morgans, Alicia K., Christopher Sweeney, Christopher J. D. Wallis, et al. "Progression patterns by types of metastatic spread, prostate-specific antigen (PSA), and clinical symptoms: Post-hoc analyses of ARAMIS." Journal of Clinical Oncology 40, no. 16_suppl (2022): 5044. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.5044.

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5044 Background: Darolutamide (DARO), a highly potent and structurally distinct androgen receptor inhibitor, prolonged metastasis-free survival by nearly 2 years and reduced the risk of death by 31% vs placebo (PBO) with a favorable tolerability profile in patients (pts) with nonmetastatic castration-resistant prostate cancer (nmCRPC) in ARAMIS. We present post-hoc analyses of ARAMIS to evaluate the association between metastatic progression with prostate-specific antigen (PSA) and clinical progression and to describe the distribution of metastatic progression between groups. Methods: Pts with
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Morgans, Alicia K., Christopher Sweeney, Christopher J. D. Wallis, et al. "Progression patterns by types of metastatic spread, prostate-specific antigen (PSA), and clinical symptoms: Post-hoc analyses of ARAMIS." Journal of Clinical Oncology 40, no. 16_suppl (2022): 5044. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.5044.

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5044 Background: Darolutamide (DARO), a highly potent and structurally distinct androgen receptor inhibitor, prolonged metastasis-free survival by nearly 2 years and reduced the risk of death by 31% vs placebo (PBO) with a favorable tolerability profile in patients (pts) with nonmetastatic castration-resistant prostate cancer (nmCRPC) in ARAMIS. We present post-hoc analyses of ARAMIS to evaluate the association between metastatic progression with prostate-specific antigen (PSA) and clinical progression and to describe the distribution of metastatic progression between groups. Methods: Pts with
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Park, Sun H., Shunsuke Tsuzuki, Kelly F. Contino, et al. "Crosstalk between bone metastatic cancer cells and sensory nerves in bone metastatic progression." Life Science Alliance 7, no. 12 (2024): e202302041. http://dx.doi.org/10.26508/lsa.202302041.

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Although the role of peripheral nerves in cancer progression has been appreciated, little is known regarding cancer/sensory nerve crosstalk and its contribution to bone metastasis and associated pain. In this study, we revealed that the cancer/sensory nerve crosstalk plays a crucial role in bone metastatic progression. We found that (i) periosteal sensory nerves expressing calcitonin gene–related peptide (CGRP) are enriched in mice with bone metastasis; (ii) cancer patients with bone metastasis have elevated CGRP serum levels; (iii) bone metastatic patient tumor samples express elevated calcit
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Seely, Kevin D., Amanda D. Morgan, Lauren D. Hagenstein, Garrett M. Florey, and James M. Small. "Bacterial Involvement in Progression and Metastasis of Colorectal Neoplasia." Cancers 14, no. 4 (2022): 1019. http://dx.doi.org/10.3390/cancers14041019.

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While the gut microbiome is composed of numerous bacteria, specific bacteria within the gut may play a significant role in carcinogenesis, progression, and metastasis of colorectal carcinoma (CRC). Certain microbial species are known to be associated with specific cancers; however, the interrelationship between bacteria and metastasis is still enigmatic. Mounting evidence suggests that bacteria participate in cancer organotropism during solid tumor metastasis. A critical review of the literature was conducted to better characterize what is known about bacteria populating a distant site and whe
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Albini, Adriana, and József Tímár. "Genomics of metastatic progression." Clinical & Experimental Metastasis 27, no. 6 (2010): 453. http://dx.doi.org/10.1007/s10585-010-9348-6.

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Visentin, Sarah, Mirela Sedić, Sandra Kraljević Pavelić, and Krešimir Pavelić. "Targeting Tumour Metastasis: The Emerging Role of Nanotechnology." Current Medicinal Chemistry 27, no. 8 (2020): 1367–81. http://dx.doi.org/10.2174/0929867326666181220095343.

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The metastatic process has still not been completely elucidated, probably due to insufficient knowledge of the underlying mechanisms. Here, we provide an overview of the current findings that shed light on specific molecular alterations associated with metastasis and present novel concepts in the treatment of the metastatic process. In particular, we discuss novel pharmacological approaches in the clinical setting that target metastatic progression. New insights into the process of metastasis allow optimisation and design of new treatment strategies, especially in view of the fact that metasta
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Rupp, Kevin, Andreas Lösch, Yanren Linda Hu, et al. "Modeling metastatic progression from cross-sectional cancer genomics data." Bioinformatics 40, Supplement_1 (2024): i140—i150. http://dx.doi.org/10.1093/bioinformatics/btae250.

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Abstract Motivation Metastasis formation is a hallmark of cancer lethality. Yet, metastases are generally unobservable during their early stages of dissemination and spread to distant organs. Genomic datasets of matched primary tumors and metastases may offer insights into the underpinnings and the dynamics of metastasis formation. Results We present metMHN, a cancer progression model designed to deduce the joint progression of primary tumors and metastases using cross-sectional cancer genomics data. The model elucidates the statistical dependencies among genomic events, the formation of metas
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Mitra, Sumegha, Kartikeya Tiwari, Ram Podicheti, et al. "Transcriptome Profiling Reveals Matrisome Alteration as a Key Feature of Ovarian Cancer Progression." Cancers 11, no. 10 (2019): 1513. http://dx.doi.org/10.3390/cancers11101513.

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Background: Ovarian cancer is the most lethal gynecologic malignancy. There is a lack of comprehensive investigation of disease initiation and progression, including gene expression changes during early metastatic colonization. Methods: RNA-sequencing (RNA-seq) was done with matched primary tumors and fallopian tubes (n = 8 pairs) as well as matched metastatic and primary tumors (n = 11 pairs) from ovarian cancer patients. Since these are end point analyses, it was combined with RNA-seq using high-grade serous ovarian cancer cells seeded on an organotypic three-dimensional (3D) culture model o
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Eckhardt, Bedrich L., Belinda S. Parker, Ryan K. van Laar, et al. "Genomic Analysis of a Spontaneous Model of Breast Cancer Metastasis to Bone Reveals a Role for the Extracellular Matrix." Molecular Cancer Research 3, no. 1 (2005): 1–13. http://dx.doi.org/10.1158/1541-7786.1.3.1.

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Abstract A clinically relevant model of spontaneous breast cancer metastasis to multiple sites, including bone, was characterized and used to identify genes involved in metastatic progression. The metastatic potential of several genetically related tumor lines was assayed using a novel real-time quantitative RT-PCR assay of tumor burden. Based on this assay, the tumor lines were categorized as nonmetastatic (67NR), weakly metastatic to lymph node (168FARN) or lung (66cl4), or highly metastatic to lymph node, lung, and bone (4T1.2 and 4T1.13). In vitro assays that mimic stages of metastasis sho
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Dissertations / Theses on the topic "Metastatic progression"

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Wander, Seth A. "p27 and Metastatic Progression: Molecular Mechanisms Underlying Bone Metastasis." Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/690.

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The complex PI3K/mTOR pathway regulates tumor progression via effects on cellular proliferation, apoptosis, autophagy, and motility. New drugs that inhibit the catalytic site of both PI3K and mTOR have shown promise in clinical trials. Here, we report the first use of a novel, dual PI3K/mTOR catalytic site inhibitor (PF-04691502, PF1502) in a xenograft model of breast cancer metastasis to bone. Metastatic MDA-MB-1833 cells showed PI3K/mTOR activation relative to parental MDA-MB-231. Low-dose PF1502 significantly impaired tumor cell motility and invasion in vitro without causing cell cycle arre
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Li, Carman Man-Chung. "Transcriptional regulation of metastatic progression in lung adenocarcinoma." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/98545.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2015.<br>This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.<br>Cataloged from student-submitted PDF version of thesis.<br>Includes bibliographical references.<br>Lung cancer is the most prevalent cancer type, leading to more than one million deaths per year worldwide. The vast majority of these mortalities were attributed to metastasis, which is the dissemination of tumor cells from the lungs to other organs. The molecular
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Donald, Carlton Dewitt. "Metastatic characteristics of tumor progression in Prostate Cancer." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 1995. http://digitalcommons.auctr.edu/dissertations/3299.

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Tumor biologist have long appreciated that both cell to cell and cell to extracellular matrix (ECM) interactions are involved in the invasive and metastatic events that are characteristic of malignancy. Cancer cell attachment to and invasion of an ECM has been associated with metastatic potential of cell lines of the Dunning rat prostate model. It was postulated that differences observed in the metastatic potential of four Dunning cell lines may correlate with cell-matrix interactions. Four cell lines, highly metastatic ML, MLL, AT-3 and non-metastatic AT-1 were studied. The adhesive, invasive
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Gooding, Alex Joseph. "Characterizing a Role for the lncRNA BORG during Breast Cancer Progression and Metastasis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1528462540265762.

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Usmani, Badar Alam. "Genomic instability and the metastatic potential of B16 murine melanomas." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238763.

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Mian, Shahid A. "Tissue transglutaminase and its relationship to cell cycle kinetics, apoptosis and tumour progression." Thesis, Nottingham Trent University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360772.

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Fiore, Leann S. "A Novel Link Between Abl Family Kinases and NM23-H1 During Metastatic Progression." UKnowledge, 2014. http://uknowledge.uky.edu/pharmacol_etds/5.

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Cancer patient mortality is caused by the ability of tumor cells to invade the extracellular matrix and metastasize. Our lab was the first to identify the role of Abl family of non-receptor tyrosine kinases (c-Abl and Arg) in the progression of solid tumor cancers. In our previous studies, we showed that high c-Abl/Arg activity promotes proliferation, invasion, and metastasis in melanoma and breast cancer cells lines. Here, we demonstrate that our previous findings are clinically relevant by showing increased c-Abl/Arg kinase activity in primary melanoma tumor tissue in comparison to low activ
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Fishel, Ben-Kenan Rotem. "Anatomic Patterns of Relapse and Progression Following Treatment with 131I-MIBG in Metastatic Neuroblastoma." Thesis, The University of Arizona, 2018. http://hdl.handle.net/10150/627159.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.<br>Purpose and Background: Neuroblastomais the most common pediatric extracranialsolid tumor •50% of patients present with metastatic disease typically involving bone and bone marrow •Despite intensive multimodality therapy, 40% of patients with high-risk neuroblastomawill experience relapse •131I-MIBG is an active salvage agent for relapsed and refractory MIBG-avid disease •It is unknown whether disease progression following 131I-MI
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Jones, Robert John. "A study of Src kinase in the regulation of metastatic progression in colorectal cancer." Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269495.

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Alcock, Helen Elizabeth. "The analysis of genetic change associated with metastatic progression in colorectal and other adenocarcinomas." Thesis, University of Sheffield, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392718.

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Books on the topic "Metastatic progression"

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1921-, Franks L. M., and Hart I, eds. Tumour progression and metastasis. Oxford University Press for the Imperial CancerResearch Fund, 1988.

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Imperial Cancer Research Fund (Great Britain). Tumour progression and metastasis. Edited by Hart I and Hart Ian. Published for the Imperial Cancer Research Fund by Oxford University Press, 1988.

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Károly, Lapis, Eckhardt S, and International Union Against Cancer, eds. Carcinogenesis and tumour progression. Akadémiai Kiadó, 1987.

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Kaiser, Hans E., and Aejaz Nasir, eds. Selected Aspects of Cancer Progression: Metastasis, Apoptosis and Immune Response. Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6729-7.

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1928-, Kaiser Hans E., Nasir Aejaz, and Nasir Nelly Adriana, eds. Selected aspects of cancer progression: Metastasis, apoptosis and immune response. Springer, 2008.

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

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L, Nicolson Garth, Fidler Isaiah J. 1936-, Triton Biosciences Inc, Smith, Kline & French Laboratories., and University of California, Los Angeles., eds. Tumor progression and metastasis: Proceedings of a Triton Biosciences-Smith, Kline & French-UCLA symposium held in Keystone, Colorado, April 6-12, 1987. A.R. Liss, 1988.

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Metastatic Progression and Tumour Heterogeneity. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03928-854-0.

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Zannetti, Antonella, Gennaro Ilardi, and Wolfgang Link, eds. Tumor Microenvironment: Molecular Mechanisms and Signaling Pathways Involved in Metastatic Progression. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-448-3.

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Healey, John H., and David McKeown. Orthopaedic surgery in the palliation of cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0125.

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Metastatic spread of cancer to bone is frequent and causes pain, disability, and functional limitation. New understanding of the homing method of cancer cells to bone and the mechanism of cancer production of pain raise possible new treatment strategies. Non-surgical treatments such as chemotherapy and hormone therapy are effective in early disease. Bisphosphonates and inhibition of osteoprotegerin prevent progression of bone lesions and avoid pain, radiation, and surgery. Radiotherapy arrests disease and relieves pain in many cases. Surgery is needed when the bone is weak or fractured. It eff
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Book chapters on the topic "Metastatic progression"

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Roskelley, Calvin D. "Microenvironmental Control of Metastatic Progression." In Cancer Metastasis - Biology and Treatment. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12136-9_6.

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Spiegel, David, and Susan H. Sands. "Psychological Influences on Metastatic Disease Progression." In Metastasis / Dissemination. Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2534-2_23.

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Venna, Suraj S., and Mohammed Kashani-Sabet. "Molecular Signatures in Melanoma Progression." In From Local Invasion to Metastatic Cancer. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-087-8_41.

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Rambaldi, Pier Francesco. "Metastatic Gastric Adenocarcinoma: Progression of Disease." In Whole-Body FDG PET Imaging in Oncology. Springer Milan, 2013. http://dx.doi.org/10.1007/978-88-470-5295-6_76.

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Wedemann, Gero, Anja Bethge, Volker Haustein, and Udo Schumacher. "Computer Simulation of the Metastatic Progression." In Methods in Molecular Biology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8244-4_8.

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Bozkurt, Yunus Erol, and Turgay Turan. "Enzalutamide Therapy for Metastatic Prostate Cancer." In Current Management of Metastatic Prostate Cancer. Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359142.7.

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Enzalutamide (ENZ), a potent androgen receptor pathway inhibitor, gained FDA approval in 2012 for metastatic castration-resistant prostate cancer (mCRPC) post-docetaxel chemotherapy. It exhibits high affinity to the androgen receptor (AR), disrupting AR signaling crucial for prostate cancer growth. Notably, ENZ’s mechanism inhibits AR nuclear translocation and exerts apoptotic effects, distinct from older antiandrogens like bicalutamide. Clinical trials demonstrate ENZ’s efficacy across various stages of prostate cancer, from metastatic hormone-sensitive disease to non-metastatic CRPC, prolong
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Banys-Paluchowski, Malgorzata, Florian Reinhardt, and Tanja Fehm. "Disseminated Tumor Cells and Dormancy in Breast Cancer Progression." In Circulating Tumor Cells in Breast Cancer Metastatic Disease. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-35805-1_3.

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Podolanczuk, Anna, Bethan Psaila, and David Lyden. "Role of Bone Microenvironment/Metastatic Niche in Cancer Progression." In Bone and Cancer. Springer London, 2009. http://dx.doi.org/10.1007/978-1-84882-019-7_6.

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Akalin, Mustafa Kaan, and Eyyup Sabri Pelit. "Apalutamide Therapy for Metastatic Prostate Cancer." In Current Management of Metastatic Prostate Cancer. Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359142.9.

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In this section, apalutamide and androgen Deprivation Therapy (ADT) are recommended for the treatment of hormone-sensitive metastatic prostate cancer (mHSPC). Apalutamide, as a second-generation androgen receptor inhibitor, extends progression-free survival and overall survival when used in combination with ADT. Clinical trials have demonstrated that the combination of apalutamide and ADT is more effective and better tolerated compared to ADT alone. As an innovative non-steroidal anti-androgen, apalutamide exhibits higher affinity to the androgen receptor and prevents androgen receptor translo
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Muller, Anja, Bernhard Homey, and Robert L. Ferris. "Head and Neck Cancer: An Example for the Role of Chemokine Receptors in Tumor Progression and Metastasis." In From Local Invasion to Metastatic Cancer. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-087-8_22.

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Conference papers on the topic "Metastatic progression"

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Eleswarapu, Ananth, Sung-Hyeok Hong, Arnulfo Mendoza, and Chand Khanna. "Abstract 2359: Modeling the kinetics of metastatic progression." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2359.

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Tavazoie, Sohail F. "Abstract IA20: Post-transcriptional regulation of metastatic progression." In Abstracts: AACR Special Conference: Computational and Systems Biology of Cancer; February 8-11, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.compsysbio-ia20.

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Nickerson, Michael L., Sudipto Das, Hong Lou, et al. "Abstract 454:TET2alterations facilitate progression of metastatic prostate 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.am2014-454.

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Wang, Wang, and Michael G. Brattain. "Abstract 3296: Cell survival in colon cancer metastatic progression." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3296.

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Kabir, M., S. Hassan, V. Kata, D. Joshi, S. Khanna, and M. Phillips. "Disseminated Nocardiosis: Mimicking Metastatic Progression With Post-obstructive Pneumonia." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5653.

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Camargo, Luana Cristina, Joao Paulo Figueiro Longo, Karen Letycia Rodrigues de Paiva, Marina Mesquita Simões, Thais Bergmann, and Victor Carlos Mello da Silva. "Immunotherapy vaccines for triple-negative breast cancer and its influence on the tumor microenvironment." In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1024.

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Objective: Cancer is still a complex and debilitating disease even though advances in treatment have occurred. Triplenegative breast cancer (TNBC) is an aggressive subtype of breast cancer with a poor prognosis and occurs more frequently in young women. Due to its metastatic features and unique tumor microenvironment, TNBC treatment is limited. In this study, we evaluated how three chemotherapy drugs could be used to produce vaccines with cells under immunogenic cell death. Methodology: For that, 4T1-luc2 cells were treated with cisplatin (100 μM), mitoxantrone (MTX) (15 μM), and doxorubicin (
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Tavazoie, Sohail. "Abstract SY05-02: Novel roles for microRNAs in metastatic progression." 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-sy05-02.

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Evans, Justin, Amber J. Giles, Meera Murgai, Miki Kasai, Caitlin Reid, and Rosandra Natasha Kaplan. "Abstract 5139: Adjuvant immunotherapy targeting CSF1R to limit metastatic progression." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5139.

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Aiello, Nicole M., David L. Bajor, Minh N. Pham, Robert H. Vonderheide, and Ben Z. Stanger. "Abstract 5176: Chemotherapy alters the natural history of metastatic progression." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5176.

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Casal, Ignacio, Marta Jaén та Rubén A. Bartolomé. "Abstract 4177: An IL13Rα2 peptide inhibits colorectal cancer metastatic progression". У Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4177.

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Reports on the topic "Metastatic progression"

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Flanagan, Louise A. Molecular Mechanisms of Metastatic Progression in Breast Cancer. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada434588.

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Flanagan, Louise. Molecular Mechanisms of Metastatic Progression in Breast Cancer. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada540994.

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Vadlamudi, Ratna K. A Molecular Approach for Metastatic Progression of Breast Cancer. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada407418.

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Thiagalingam, Sam. Metastatic Progression of Breast Cancer by Allelic Loss on Chromosome 18q21. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada442805.

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Oursler, Merry J. Transforming Growth Factor B Regulation of Tumor Progression in Metastatic Cancer. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada395849.

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Selvamurugan, Nagarajan. Collagenases in Breast Cancer Cell-Induced Metastatic Tumor Growth and Progression. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada407462.

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Oursler, Merry Jo. Transforming Growth Factor Beta Regulation of Tumor Progression in Metastatic Cancer. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada427069.

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Thiagalingam, Sam. Metastatic Progression of Breast Cancer by Allelic Loss on Chromosome 18q21. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada430065.

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Thiagalingam, Sam. Metastatic Progression of Breast Cancer by Allelic Loss on Chromosome 18q21. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada410792.

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Antich, Peter P., Anca Constantinescu, Matthew Lewis, Ralph Mason, and Edmond Richer. Investigation of Metastatic Breast Tumor Heterogeneity and Progression Using Dual Optical/SPECT Imaging. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada471735.

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You might also be interested in the extended bibliographies on the topic 'Metastatic progression' for particular source types:
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