Relevant bibliographies by topics / Metastatic progression

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  2. Dissertations / Theses
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Academic literature on the topic 'Metastatic progression'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Metastatic progression"

1

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 the outgrowth into macroscopic lesions. However, the metabolic reprogramming of metastasizing cancer cells has only recently become the subject of intense study. From a clinical point of view, the latter steps of the metastatic process are very important, because patients often undergo surgical removal of the primary tumor when cancer cells have already left the primary tumor site, even though distant metastases are not clinically detectable yet. In this scenario, to precisely elucidate if and how metabolic reprogramming drives acquisition of cancer-specific adaptive phenotypes might pave the way to new therapeutic strategies by combining chemotherapy with metabolic drugs for better cancer eradication. In this review we discuss the latest evidence that claim the importance of metabolic adaptation for cancer progression.
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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 nmCRPC were randomized 2:1 to DARO (n=955) or PBO (n=554) while continuing androgen-deprivation therapy. Descriptive analyses were performed using the primary data cutoff (Sept 3, 2018) for the double-blind period. Post-baseline metastases were based on central review of conventional radiographic imaging every 16 weeks. PSA and pain progression were defined per primary analysis ( N Engl J Med. 2019;380:1235-46). Results: Metastatic progression was observed in 13.6% of DARO and 28.5% of PBO pts. Most pts had isolated progression as bone (DARO 46%, PBO 39%) or lymph node (32%; 40%) metastasis (Table). Pts with radiographic progression had shorter median time from initial diagnosis to study treatment (DARO 72.9, PBO 74.4 months) vs the overall ARAMIS population (86.2, 84.2 months). Of all pts with metastatic progression, baseline PSA levels (ng/mL) were similar in DARO (12.6) and PBO pts (15.1); DARO pts had lower median PSA before metastasis (16.7) vs PBO pts (48.0) and median absolute/relative PSA decrease from baseline of -0.7/-3.2% vs an increase for PBO pts of 29.5/181%. PSA progression before metastasis was observed in 55.6% (160/288) of pts, occurring in fewer DARO (45.4%) vs PBO pts (63.9%) (treatment difference 18.5%; nominal 95% CI 6.5%–30.6%). The median time between PSA progression and metastasis was 7.0 months with DARO vs 5.6 months with PBO. Pain progression before metastatic progression was rare and similar between groups (DARO 16.9%, PBO 17.7%). Conclusions: DARO significantly reduced risk of metastatic progression and improved overall survival vs PBO without changing the pattern of metastatic progression. Many pts with nmCRPC experienced metastatic progression without PSA progression, and pain progression was rare. These results support the use of imaging with PSA monitoring to properly identify disease progression in pts with nmCRPC. Clinical trial information: TBC. [Table: see text]
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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 nmCRPC were randomized 2:1 to DARO (n=955) or PBO (n=554) while continuing androgen-deprivation therapy. Descriptive analyses were performed using the primary data cutoff (Sept 3, 2018) for the double-blind period. Post-baseline metastases were based on central review of conventional radiographic imaging every 16 weeks. PSA and pain progression were defined per primary analysis ( N Engl J Med. 2019;380:1235-46). Results: Metastatic progression was observed in 13.6% of DARO and 28.5% of PBO pts. Most pts had isolated progression as bone (DARO 46%, PBO 39%) or lymph node (32%; 40%) metastasis (Table). Pts with radiographic progression had shorter median time from initial diagnosis to study treatment (DARO 72.9, PBO 74.4 months) vs the overall ARAMIS population (86.2, 84.2 months). Of all pts with metastatic progression, baseline PSA levels (ng/mL) were similar in DARO (12.6) and PBO pts (15.1); DARO pts had lower median PSA before metastasis (16.7) vs PBO pts (48.0) and median absolute/relative PSA decrease from baseline of -0.7/-3.2% vs an increase for PBO pts of 29.5/181%. PSA progression before metastasis was observed in 55.6% (160/288) of pts, occurring in fewer DARO (45.4%) vs PBO pts (63.9%) (treatment difference 18.5%; nominal 95% CI 6.5%–30.6%). The median time between PSA progression and metastasis was 7.0 months with DARO vs 5.6 months with PBO. Pain progression before metastatic progression was rare and similar between groups (DARO 16.9%, PBO 17.7%). Conclusions: DARO significantly reduced risk of metastatic progression and improved overall survival vs PBO without changing the pattern of metastatic progression. Many pts with nmCRPC experienced metastatic progression without PSA progression, and pain progression was rare. These results support the use of imaging with PSA monitoring to properly identify disease progression in pts with nmCRPC. Clinical trial information: TBC. [Table: see text]
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4

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 whether a tumor depends upon the same microenvironment during or after metastasis. The processes of carcinogenesis, tumor growth and metastatic spread in the setting of bacterial infection were examined in detail. The literature was scrutinized to discover the role of the lymphatic and venous systems in tumor metastasis and how microbes affect these processes. Some bacteria have a potent ability to enhance epithelial–mesenchymal transition, a critical step in the metastatic cascade. Bacteria also can modify the microenvironment and the local immune profile at a metastatic site. Early targeted antibiotic therapy should be further investigated as a measure to prevent metastatic spread in the setting of bacterial infection.
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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 metastatic cells share common features with stem cells. Nano- and micro-technologies are herein elaborated in details as a promising therapeutic concept in targeted drug delivery for metastatic cancer. Progression in the field could provide a more efficient way to tackle metastasis and thus bring about advancements in the treatment and management of patients with advanced cancer.
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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 of the omentum, mimicking early metastasis. This comprehensive approach revealed key changes in gene expression occurring in ovarian cancer initiation and metastasis, including early metastatic colonization. Results: 2987 genes were significantly deregulated in primary tumors compared to fallopian tubes, 845 genes were differentially expressed in metastasis compared to primary tumors and 304 genes were common to both. An assessment of patient metastasis and 3D omental culture model of early metastatic colonization revealed 144 common genes that were altered during early colonization and remain deregulated even in the fully developed metastasis. Deregulation of the matrisome was a key process in early and late metastasis. Conclusion: These findings will help in understanding the key pathways involved in ovarian cancer progression and eventually targeting those pathways for therapeutic interventions.
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Entwistle, Susannah, Hannah K. Jackson, Ian Kerr, Beth Coyle, and Alistair Hume. "MEDB-64. Are Rab GTPases metastatic drivers in metastatic medulloblastoma?" Neuro-Oncology 24, Supplement_1 (2022): i121. http://dx.doi.org/10.1093/neuonc/noac079.438.

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Abstract Medulloblastoma is the most common malignant paediatric brain cancer with poorer prognosis related to the onset of metastasis. It has four molecular subgroups; Wingless (WNT), Sonic Hedgehog (SHH), group 3 and group 4, of which group 3 is the most likely to be metastatic and is therefore associated with the poorest prognosis. Exosomes are small membrane-bound extracellular vesicles of endosomal origin which contain a variety of cargo including RNA and proteins. Increased exosome release is connected with disease progression and metastasis in multiple cancers. Rabs are a family of small GTPases (70 in humans) which regulate vesicle trafficking. Several Rabs are known to regulate exosome biogenesis and secretion and may thereby contribute to cancer progression. The role of Rabs in metastatic medulloblastoma is unclear. We aim to explore whether Rabs contribute to the progression of metastatic medulloblastoma through the exosome biogenesis and secretion pathways. Through analysis of literature, databases such as ExoCarta.org, the R2: Genomics analysis and visualisation platform, and mRNA content of medulloblastoma exosomes, five novel Rab candidates were identified that may contribute to disease progression in group 3 medulloblastoma. Gene expression of these Rabs was then verified across SHH, group 3 and group 4 patient-derived cell lines using RT-qPCR, with candidate Rab expression confirmed in the three subgroups. Presence of Rab mRNA has also been found in exosomes derived from group 3 and group 4 patients, with an enrichment in group 3 exosomes. Current and future work aims to determine the potential roles of Rabs in medulloblastoma pathogenesis, and to determine whether Rabs contribute to increased exosome biogenesis which drives metastasis or are metastatic drivers in medulloblastoma themselves. Therefore, experiments to characterise Rab candidate protein expression within cells and assess their function after knockdown are necessary and timely.
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Chen, Jocelyn F., and Qin Yan. "The roles of epigenetics in cancer progression and metastasis." Biochemical Journal 478, no. 17 (2021): 3373–93. http://dx.doi.org/10.1042/bcj20210084.

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Cancer metastasis remains a major clinical challenge for cancer treatment. It is therefore crucial to understand how cancer cells establish and maintain their metastatic traits. However, metastasis-specific genetic mutations have not been identified in most exome or genome sequencing studies. Emerging evidence suggests that key steps of metastasis are controlled by reversible epigenetic mechanisms, which can be targeted to prevent and treat the metastatic disease. A variety of epigenetic mechanisms were identified to regulate metastasis, including the well-studied DNA methylation and histone modifications. In the past few years, large scale chromatin structure alterations including reprogramming of the enhancers and chromatin accessibility to the transcription factors were shown to be potential driving force of cancer metastasis. To dissect the molecular mechanisms and functional output of these epigenetic changes, it is critical to use advanced techniques and alternative animal models for interdisciplinary and translational research on this topic. Here we summarize our current understanding of epigenetic aberrations in cancer progression and metastasis, and their implications in developing new effective metastasis-specific therapies.
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Shiraishi, Kenshiro, Keiichiro Tada, Jiro Kawamori, Atsushi Fukuuchi, and Tsunehiro Nishi. "Disease progression of metastatic breast cancer by first relapse site after definitive radiotherapy." Journal of Clinical Oncology 33, no. 28_suppl (2015): 36. http://dx.doi.org/10.1200/jco.2015.33.28_suppl.36.

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36 Background: Bone metastasis as initial distant relapse is commonly considered to have better prognosis than other sites in metastatic breast cancer. To elucidate true clinical course of metastatic disease, it is essential that we prospectively manage patients since primary setting. Methods: Overall, 3,417 patients with breast cancer treated with mastectomy (n = 379, 11.1%) or breast-conserving surgery (n = 3,029, 88.6%) followed by definitive radiotherapy at two institutions in Center of Tokyo between 1980 and 2014 were included in the study. Information on all patients was prospectively collected and rigorously-controlled. Initial metastatic relapse sites included bone, brain, and other (mainly visceral). Intrinsic subtypes of tumor were classified as luminal A, luminal-human epidermal growth factor receptor 2 (HER2), luminal B, triple negative, and HER2 identified by routine immunohistochemistry and histological grade. Cumulative incidence rates of overall survival (OS) for each affected site after metastatic relapse were estimated according to Kaplan-Meier method. Results: Median follow-up time for living patients was 113 months. A total of 370 patients experienced metastatic progression as first relapse event. Median duration of OS after initial metastatic relapse was 69 month in all subtypes. No difference was seen in OS among five subtypes after initial bone or brain relapse. Meanwhile, OS of luminal subtypes after initial other-site relapse was better than that of triple negative and HER2 subtypes (P = .003). Notably, OS rates of bone and non-bone/brain metastasis groups as initial relapse site were almost identical (P= .626). Conclusions: We find no difference in mortality after metastatic relapse between bone and other site except for brain metastasis as initial relapse in breast cancer patients following definitive radiotherapy in our cohort without primary metastatic setting. Careful consideration is needed for initial distant relapse regardless of which site is involved. However, prognosis of metastatic breast cancer after definitive radiotherapy is favorable based on real world data, attributable mainly to improved systemic therapy and modern multidisciplinary approach.
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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 arrest, apoptosis, or reduced proliferation. Pre-treatment of tumor cells at this dose reduced bone metastatic outgrowth in vivo. The atypical tumor suppressor, p27KIP1, is phosphorylated in its C-terminal region by multiple AGC kinases downstream of PI3K/mTOR. These phosphorylation events promote cytoplasmic mislocalzation of p27 which, in turn, facilitates inhibition of the RhoA cytoskeletal regulatory protein. The resulting turnover of the actin cytoskeleton is thought to underlie the increased cellular motility attributed to cytoplasmic p27. In MDA-MB-1833 cells, PI3K/mTOR inhibition reduced p27 C-terminal phosphorylation at T157 and T198 and reduced cytoplasmic p27 levels. Overexpression of a p27T157D/T198D phospho-mimetic mutant conferred resistance to the anti-motility effects of PF1502 in vitro. MDA-MB-1833 cells demonstrate p27-dependent inhibition of RhoA-ROCK signaling, as well as p27-dependent motility and invasion in vitro, however, RhoA knockdown did not confer resistance to the anti-motility effects of PF1502. p27shRNA dramatically impaired the bone metastatic outgrowth of MDA-MB-1833 in vivo. In an effort to explore potentially novel RhoA-independent mechanisms whereby cytoplasmic p27 might drive tumor cell motility and metastasis, we turned to the process known as epithelial-to-mesenchymal transition (EMT). The EMT program has been implicated as a critical driver of tumor metastasis in a variety of cancer models. PI3K/mTOR inhibition and shRNA p27 treatment both reversed expression of EMT markers in MDA-MB-1833. Thus, PI3K/mTOR appears to drive p27-dependent motility and metastasis at least in part by induction of an EMT-like phenotype, a novel mechanism through which p27 might act to promote tumor progression. These results provide an important new clinical rationale supporting the use of PI3K/mTOR inhibitors as anticancer agents via their inhibition of tumor invasion and metastasis.
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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 mechanisms for metastasis is complex and not well understood. In this thesis, I investigated the gene expression changes in tumor cells that contribute to metastasis of lung adenocarcinoma, the major subtype of lung cancer. Using a genetically-engineered mouse model and derivative cell lines, we showed that metastatic lung adenocarcinoma cells are capable of forming proteolytic membrane protrusions known as invadopodia to degrade the extracellular matrix. The formation and function of invadopodia are dependent on an isoform switch of the adaptor protein Tks5. The Tks5long isoform, which is upregulated in metastatic cells, is capable of localizing to the cell membrane and activating invadopodia formation. In contrast, the Tks5short isoform, which is transcribed from a promoter independent of Tks5long, is the predominant isoform in non-metastatic cells, and functions to inhibit invadopodia-mediated matrix degradation by destabilizing these protrusions. We demonstrated that an increased ratio of Tks5long-to- Tks5short promoted invadopodia activity in vitro and metastasis in vivo. Furthermore, a high Tks5long-to-Tks5short ratio in human tumors correlated with advanced stage and worse survival. These data strongly suggest that a balance between Tks5long and Tks5short expression is critical for metastasis. In addition, we found that the expression of the pro-metastatic Tks5long isoform is synergistically inhibited by three transcription factors - Nkx2-1, Foxa2, and Cdx2. These three factors were highly expressed in non-metastatic cells, and downregulated in metastatic cells. Altered expression of these factors led to commensurate changes in Tks5long levels. Finally, we demonstrated that Nkx2-1, Foxa2, and Cdx2 function cooperatively to inhibit metastasis by suppressing a network of target genes. Silencing of all three factors in non-metastatic cells activated a program of metastasis-related genes, and increased metastasis in a transplantation model. Furthermore, the expression patterns of these factors strongly correlated with tumor progression in an autochthonous model of lung adenocarcinoma, and were closely associated with disease stage and survival outcomes of human patients. Collectively, these findings strongly argue that Nkx2-1, Foxa2, and Cdx2 synergize to restrain metastatic progression. Taken together, this study provides insights on some of the key molecular regulators of lung cancer metastasis. Our findings contribute to a better understanding of metastasis, and potentially to the development of better therapeutic strategies in the future.<br>by Carman Man-Chung Li.<br>Ph. D.
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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 and chemoinvasive capability of each cell line was compared. Cell adhesion was examined by plating the cells on plastic dishes coated with various components of the ECM (fibronectin, laminin and collagen) as well as EHS Natrix (a natural ECM) . Invasion was determined by examining cells ability to traverse a matrigel barrier. Correlations were found between the cells' adhesive and invasive abilities in response to the ECM. These observations suggest that ECM components are highly involved in prostate cancer cell activities and loss may contribute to tumor progression and metastasis.
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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 activity as compared to benign nevi. Additionally, in breast cancer tissue, we found aggressive tumor subtypes (triple-negative and high-grade breast cancer) had increased c-Abl/Arg activity as compared to less aggressive subtypes. To define the mechanism by which c-Abl and Arg promote melanoma and breast cancer metastasis, we searched for novel pathways by which c-Abl and Arg promote invasion, a key step in metastasis. Significantly, we found that c-Abl and Arg decrease the expression of non-metastatic protein, NM23-H1, a metastasis suppressor that is lost during metastatic progression. We demonstrate that NM23-H1 is localized and degraded within the lysosome via proteases, cathepsins L and B. Moreover, we show that c-Abl and Arg upregulate cathepsin mRNA levels and activate the cathepsins, which in-turn degrade NM23-H1. We demonstrate that this pathway is functionally significant as c-Abl and Arg require the downregulation of NM23-H1 to promote invasion in melanoma and breast cancer cell lines. We show that the pathway is clinically significant as c-Abl/Arg activity is inversely correlated with NM23-H1 expression in mouse lung metastases, as well as in human primary melanoma and primary breast cancer tissue. In summary, we are the first to demonstrate novel crosstalk between oncogenic and metastasis suppressor signaling pathways, and provide evidence that pharmacological inhibition of Abl family kinases in melanoma and breast cancer patients may prevent metastatic progression by stabilizing a metastasis suppressor.
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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-MIBG treatment occurs in previously involved vs. new sites of disease •A better understanding of this pattern may inform the use of consolidative focal therapies following 131I-MIBG administration
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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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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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1928-, Kaiser Hans E., ed. Cancer growth and progression. Kluwer Academic Publishers, 1989.

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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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S, El-Deiry Wafik, ed. Tumor progression and therapeutic resistance. New York Academy of Sciences, 2005.

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

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1952-, Dickson Robert B., and Lippman Marc E. 1945-, eds. Mammary tumorigenesis and malignant progression: Advances in cellular and molecular biology of breast cancer. Kluwer Academic Publishers, 1994.

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1943-, Harris Curtis C., Liotta L. A, Genentech Inc, and University of California, Los Angeles., eds. Genetic mechanisms in carcinogenesis and tumor progression: Proceedings of a Genentech-UCLA symposium held at Keystone, Colorado, January 21-27, 1989. Wiley-Liss, 1990.

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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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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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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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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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Poupon, Marie-France, Nicole Hanania, Maria-Dolores Boyano, et al. "Metastatic Process Does Not Select Cells for Metastatic Ability But Metastatic Cells Are Selected for by Drug Resistance. Implications for Tumor Progression." In New Concepts in Cancer. Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-10671-4_9.

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Lorger, Mihaela, and Brunhilde Felding-Habermann. "Integrin Signaling in Angiogenesis and Metastatic Cancer Progression in the Brain." In Signaling Pathways and Molecular Mediators in Metastasis. Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2558-4_13.

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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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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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Lawlor, Elizabeth R. "Abstract IA26: Cell plasticity and metastatic progression of Ewing sarcoma." In Abstracts: Advances in Sarcomas: From Basic Science to Clinical Translation; May 16-19, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.sarcomas17-ia26.

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Silva, Gabriela Calado, Denise Sobral Viana, Cecilia Souza Avila Pessoa, and Erich Roberto Santos da Costa Filho. "DESCRIPTIVE EPIDEMIOLOGICAL PROFILE OF PATIENTS WITH HER2-POSITIVE METASTATIC BREAST CANCER SUBMITTED TO PERTUZUMAB AND TRASTUZUMAB AT THE CANCER HOSPITAL OF PERNAMBUCO." In XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1024.

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Abstract:
Introduction: HER2-positive breast cancer is characterized by a hyperexpression or gene amplification of human epidermal growth factor receptor 2, a tyrosine kinase membrane receptor that has a profile with major aggressiveness and worse prognosis among all molecular subtypes. The metastatic pattern of this disease is one of the greatest challenges in mastology and requires an urgency and effective therapeutics to control this disease. Advances in therapy have allowed more specific treatments for anti-HER2 treatment that allowed improvement in the overall survival and disease-free survival of patients. Double-block therapy, performed by using Trastuzumabe and Pertuzumabe, is the first-line treatment for metastatic HER2-positive breast cancer. This kind of therapy was initially adopted effectively by SUS in 2019. Therefore, it is advisable to consider the use of this therapy at the Cancer Hospital of Pernambuco (HCP) to analyze the current results in patients and assess the local results. Objective: The goal of this study was to understand the epidemiological profile of patients with HER2-positive metastatic breast cancer treated at the HCP and submitted to double-block therapy with Trastuzumab and Pertuzumab, analyzing progression-free survival and overall survival. Methods: This is a retrospective descriptive study conducted in November 2021. Relevant aspects of treatment, analysis of disease-free survival, and overall survival were analyzed in the medical records of patients with metastatic HER2-positive breast cancer who used Trastuzumab and Pertuzumab. The survey of the analyzed data was carried out by completing a specific form created by the researcher especially for this study. Anonymity and clarity of the information were ensured. Results: From 124 selected medical records, this study selected 78 patients with metastatic HER2 breast cancer, with a mean age of 50.4 years; 62.34% had positive hormone receptors and 44.87% had metastasis de novo. About 36% of patients had been using double-block for up to 6 months, which made it difficult to assess the behavior of the disease from medical examinations and images, given the short time; but it was found that of all patients, 15.4% have disease stability, 32.1% had regression, and 28.2% had disease progression. There was a median of 12 months for disease progression, but with a median of 11 months of use of double-block therapy with Trastuzumab and Pertuzumab. As for the overall survival, it is estimated, based on statistical data from the current sample, that an accumulated probability of death of up to 16.7% in up to 5 years. Women older than 60 years and those who had disease progression had a higher risk of death. Conclusion: This study evaluated metastatic HER2-positive breast cancer as a particular behavior tumor. The patients selected from the HCP submitted to the use of Trastuzumab and Pertuzumab in the metastatic scenario have a follow-up time still recent, which causes incipient data for the evaluation of specific outcomes that depend on the temporal component. Follow-up and updates of the analysis of outcomes are suggested, in the near future, to enrich the treatments proposed for the target population. Ethical aspect: This study was conducted strictly based on the Resolutions 510/16 and 416/12 of the Health National Council and was only conducted after HCP Research Ethics Committee approval.
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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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