| 1. |
- Agathangelidis, Andreas, et al.
(author)
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High-Throughput immunogenetics for precision medicine in cancer
- 2022
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In: Seminars in Cancer Biology. - : Elsevier. - 1044-579X .- 1096-3650. ; 84, s. 80-88
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Journal article (peer-reviewed)abstract
- Cancer is characterized by an extremely complex biological background, which hinders personalized therapeutic interventions. Precision medicine promises to overcome this obstacle through integrating information from different 'subsystems', including the host, the external environment, the tumor itself and the tumor microenvironment. Immunogenetics is an essential tool that allows dissecting both lymphoid cancer ontogeny at both a cell-intrinsic and a cell-extrinsic level, i.e. through characterizing micro-environmental interactions, with a view to precision medicine. This is particularly thanks to the introduction of powerful, high-throughput approaches i.e. next generation sequencing, which allow the comprehensive characterization of immune repertoires. Indeed, NGS immunogenetic analysis (Immune-seq) has emerged as key to both understanding cancer pathogenesis and improving the accuracy of clinical decision making in oncology. Immune-seq has applications in lymphoid malignancies, assisting in the diagnosis e.g. through differentiating from reactive conditions, as well as in disease monitoring through accurate assessment of minimal residual disease. Moreover, Immune-seq facilitates the study of T cell receptor clonal dynamics in critical clinical contexts, including transplantation as well as innovative immunotherapy for solid cancers. The clinical utility of Immune-seq represents the focus of the present contribution, where we highlight what can be achieved but also what must be addressed in order to maximally realize the promise of Immune-seq in precision medicine in cancer.
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| 2. |
- Agathangelidis, Andreas, et al.
(author)
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Unlocking the secrets of immunoglobulin receptors in mantle cell lymphoma : Implications for the origin and selection of the malignant cells
- 2011
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1044-579X .- 1096-3650. ; 21:5, s. 299-307
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Research review (peer-reviewed)abstract
- Immunogenetic analysis of mantle cell lymphoma (MCL) has offered important evidence helping to decipher the immune pathways leading to its development and also prompting a reappraisal of the views about its ontogeny. In particular, older and more recent studies have demonstrated that MCL is characterized by a highly distinctive immunoglobulin gene repertoire with remarkable predominance of the IGHV3-21 and IGHV4-34 genes; restricted associations of IGHV,IGHD and IGHJ genes, culminating in the creation of quasi-identical ("stereotyped") heavy complementarity-determining region 3 sequences in roughly 10% of cases; and, very precisely targeted and, probably, functionally driven somatic hypermutation, ranging from minimal (in most cases) to pronounced. Furthermore, comparison to other entities, in particular CLL, revealed that several of these immunogenetic features are "MCL-biased". On these grounds, an antigen-driven origin of MCL could be envisaged, at least for subsets of cases.
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| 3. |
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| 4. |
- Alzrigat, Mohammad, et al.
(author)
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Epigenetics in multiple myeloma : From mechanisms to therapy
- 2018
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In: Seminars in Cancer Biology. - : ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD. - 1044-579X .- 1096-3650. ; 51, s. 101-115
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Research review (peer-reviewed)abstract
- Multiple myeloma (MM) is a tumor of antibody producing plasmablasts/plasma cells that resides within the bone marrow (BM). In addition to the well-established role of genetic lesions and tumor-microenvironment interactions in the development of MM, deregulated epigenetic mechanisms are emerging as important in MM pathogenesis. Recently, MM sequencing and expression projects have revealed that mutations and copy number variations as well as deregulation in the expression of epigenetic modifiers are characteristic features of MM. In the past decade, several studies have suggested epigenetic mechanisms via DNA methylation, histone modifications and non-coding RNAs as important contributing factors in MM with impacts on disease initiation, progression, clonal heterogeneity and response to treatment. Herein we review the present view and knowledge that has accumulated over the past decades on the role of epigenetics in MM, with focus on the interplay between epigenetic mechanisms and the potential use of epigenetic inhibitors as future treatment modalities for MM.
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| 5. |
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| 6. |
- Axelson, Håkan, et al.
(author)
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Renal stem cells and their implications for kidney cancer.
- 2013
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 23:1, s. 56-61
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Research review (peer-reviewed)abstract
- The renal cell carcinomas (RCC) denote a diverse set of neoplasias with unique genetic and histological features. The RCCs emanate from the renal tubule, a highly heterogeneous epithelial structure, and depending on which cell is malignified the resulting cancer displays unique characteristics. Notwithstanding this, the cells of origin for the RCC forms are far from established, and only inferred by the accumulated weight of marker similarities, not always providing an unequivocal picture. The tubular epithelium is normally mitotically quiescent, but demonstrates a considerable regenerative capacity upon renal injury. Recently the hypothesis that regeneration is driven by adult stem cells has been added experimental support, providing further complexity to the issue of renal carcinogenesis. Whether these cells are linked to RCC is an open question. In the present review we therefore present the prevailing theories regarding kidney regeneration, since a better understanding of this process might be of relevance when considering the different malignancies that arise from kidney epithelium. Our own results show that papillary renal cell carcinoma displays considerable similarities to proximal tubular progenitor cells and we suggest that this tumor form may develop in a multi-step fashion via benign renal adenomas. The putative connection between renal stem cells and carcinomas is, however, not clarified, since the current understanding of the renal stem cell system is not complete. It is clear that the efforts to isolate and characterize renal progenitor/stem cells suffer from numerous technical limitations and that it remains likely that the kidney harbors different stem cell pools with a restricted differentiation potential.
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| 7. |
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| 8. |
- Baecklund, Eva, et al.
(author)
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Lymphoma development in patients with autoimmune and inflammatory disorders : What are the driving forces?
- 2014
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1044-579X .- 1096-3650. ; 24, s. 61-70
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Research review (peer-reviewed)abstract
- For decades, it has been known that patients with certain autoimmune and inflammatory disorders, such as rheumatoid arthritis (RA) and primary Sjogren's syndrome (pSS), have an increased risk of developing malignant lymphoma. Although the clinico-biological reasons for this association remain largely unknown, our knowledge has improved and new insights have been obtained. First, the direct link between autoimmunity and lymphomagenesis has been strengthened by large epidemiological studies showing a consistent risk increase of lymphoma associated with certain autoimmune/inflammatory conditions in independent cohorts from different countries. Second, a number of local and systemic disease-related risk factors in these diseases have been repeatedly linked to lymphoma development, with the prime examples being disease severity and the degree of inflammatory activity. Considering the key role of B- and T-cell activation in the pathogenesis of both autoimmunity and lymphoma, it is perhaps not surprising that longstanding chronic inflammation and/or antigen stimulation have emerged as major predisposing factors of lymphoma in patients with active autoimmune disease. Finally, increasing evidence suggests that lymphomas associated with autoimmunity constitute a different spectrum of entities compared to lymphomas arising in patients without any known autoimmune or inflammatory conditions, pointing to a different pathobiology. In this review, we summarize the recent literature that supports a direct or indirect link between immune-mediated disease and lymphoma and describe the characteristics of lymphomas developing in the different diseases. We also discuss molecular, genetic and microenvironmental factors that may come into play in the pathobiology of these disorders.
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| 9. |
- Berg, Tracy J, et al.
(author)
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Radiotherapy-induced remodeling of the tumor microenvironment by stromal cells
- 2022
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 86:Part 3, s. 846-856
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Research review (peer-reviewed)abstract
- Cancer cells reside amongst a complex milieu of stromal cells and structural features known as the tumor microenvironment. Often cancer cells divert and co-opt functions of stromal cells of the microenvironment to support tumor progression and treatment resistance. During therapy targeting cancer cells, the stromal cells of the microenvironment receive therapy to the same extent as cancer cells. Stromal cells therefore activate a variety of responses to the damage induced by these therapies, and some of those responses may support tumor progression and resistance. We review here the response of stromal cells to cancer therapy with a focus on radiotherapy in glioblastoma. We highlight the response of endothelial cells and the vasculature, macrophages and microglia, and astrocytes, as well as describing resulting changes in the extracellular matrix. We emphasize the complex interplay of these cellular factors in their dynamic responses. Finally, we discuss their resulting support of cancer cells in tumor progression and therapy resistance. Understanding the stromal cell response to therapy provides insight into complementary therapeutic targets to enhance tumor response to existing treatment options.
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| 10. |
- Bjerkvig, Rolf, et al.
(author)
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Cancer stem cells and angiogenesis
- 2009
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In: Seminars in Cancer Biology. - London : Academic Press. - 1044-579X .- 1096-3650. ; 19:5, s. 279-284
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Research review (peer-reviewed)abstract
- Most cancers contain tumor cells that display stem cell-like characteristics. How and when such cells appear in tumors are not clear, but may involve both stochastic as well as hierarchical events Most. likely, tumor cells that display stem cell-like characteristics can undergo asymmetric cell division giving rise to tumor cells that trigger angiogenic programs. As normal stem cells the cancer stem-like cells seem to adapt to hypoxic environments and will use metabolic pathways that involve increased conversion of glucose to pyruvate and lactate, and a concomitant decrease in mitochondrial metabolism and mitochondrial mass. The molecular pathways responsible for inducing glycolysis are now being explored. These pathways seem to mediate multiple metabolic functions in cancer stem-like cells, leading to a highly migratory and angiogenesis-independent phenotype. Future challenges will be to identify and validate molecular targets involved in anaerobic metabolic pathways active in cancer stem-like cells and to determine how these pathways differ from regulatory pathways involved in normal stem cell function.
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| 11. |
- Block, Keith I., et al.
(author)
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Designing a broad-spectrum integrative approach for cancer prevention and treatment
- 2015
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In: Seminars in Cancer Biology. - : Academic Press. - 1044-579X .- 1096-3650. ; 35, s. S276-S304
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Research review (peer-reviewed)abstract
- Targeted therapies and the consequent adoption of "personalized" oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are not reliant upon the same mechanisms as those which have been targeted). To address these limitations, an international task force of 180 scientists was assembled to explore the concept of a low-toxicity "broadspectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspects of relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a wide range of high-priority targets (74 in total) that could be modified to improve patient outcomes. For these targets, corresponding low-toxicity therapeutic approaches were then suggested, many of which were phytochemicals. Proposed actions on each target and all of the approaches were further reviewed for known effects on other hallmark areas and the tumor microenvironment Potential contrary or procarcinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixed evidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of the relationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. This novel approach has potential to be relatively inexpensive, it should help us address stages and types of cancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for future research is offered. (C) 2015 The Authors. Published by Elsevier Ltd.
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| 12. |
- Borg, Åke
(author)
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Molecular and pathological characterization of inherited breast cancer.
- 2001
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 11:5, s. 375-385
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Journal article (peer-reviewed)abstract
- The two major breast cancer susceptibility genes, BRCA1 and BRCA2, account for the majority of familial breast–ovarian cancer, but only a modest proportion of breast cancer families without ovarian or male breast cancer. Search for additional breast cancer genes with traditional linkage analysis has so far been unsuccessful, probably due to genetic heterogeneity. Pooling of families of different ethnical, cultural, and geographical origin proved to be a useful approach when identifying BRCA1 and BRCA2, but for genes mutated only in specific populations it is important not to introduce locus heterogeneity by pooling. Genetic heterogeneity can possibly be circumvented by using objective means, such as tumour histopathology or gene expression profiling, for subclassification of families prior to linkage analysis. Also, additional breast cancer genes can be identified by further characterization of the function of BRCA1 and BRCA2 and their interacting proteins.
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| 13. |
- Cao, YH
(author)
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Angiogenesis in malignancy
- 2009
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In: Seminars in cancer biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 19:5, s. 277-278
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Journal article (other academic/artistic)
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| 14. |
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| 15. |
- Cerezo-Magaña, M., et al.
(author)
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The pleiotropic role of proteoglycans in extracellular vesicle mediated communication in the tumor microenvironment
- 2020
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In: Seminars in Cancer Biology. - : ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD. - 1044-579X .- 1096-3650. ; 62, s. 99-107
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Research review (peer-reviewed)abstract
- Compartmental exchange between cells through extracellular vesicles (EVs), including exosomes and microvesicles, has emerged as a central mechanism that coordinates the complex communication between malignant and stromal cells during tumor initiation and evolution. Some of the most critical processes of EV-mediated communication, including EV biogenesis and EV uptake, can be mediated by heparan sulfate proteoglycans (HSPGs) that reside on the surface of producer and recipient cells as well as on EVs. With interestingly similar, HSPG-dependent, pathways as the ones exploited by some viruses, EVs may, in an evolutionary perspective, be viewed as endogenous counterparts of viral particles. Cancer cell-derived EVs exert their protumorigenic effects by direct interactions of biologically active surface molecules, by transfer of proteins and nucleic acids into recipient cells or by transfer of metabolites that can be utilized as an energy source by the recipient cell. Here, we discuss the pleiotropic role of the HSPG family in these different contexts of EV communication with a specific focus on tumor development. We propose EV-associated PGs as dynamic reservoirs and chaperones of signaling molecules with potential implications in ligand exchange between EVs and tumor target cells. The protumorigenic consequences of EV mediated communication through HSPG should motivate the development of therapeutic approaches targeting EV-HSPG interactions as a novel strategy in cancer treatment.
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| 16. |
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| 17. |
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| 18. |
- Christianson, Helena, et al.
(author)
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Exosome and microvesicle mediated phene transfer in mammalian cells.
- 2014
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 28:Apr 23, s. 31-38
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Research review (peer-reviewed)abstract
- Extracellular vesicles (EVs), e.g. exosomes and microvesicles, emerge as new signaling organelles in the exchange of information between cells at the paracrine and systemic level. It is clear that these virus like particles carry complex biological information that can elicit a pleiotropic response in recipient cells with potential relevance in physiology as well as in cancer and other pathological conditions. Numerous studies convincingly show that the molecular composition of EVs closely reflects their cell or tissue of origin. Thus, the signaling status of donor cells, more specifically their endosomal compartments, may largely determine the biological output in recipient cells, a process that we then may conceptualize as vesicle mediated phene transfer. Whereas more conventional modes of cell-cell communication mostly depend on extracellular ligand concentration and cell-surface receptor availability, the magnitude of the EV signaling response relies on the capture and uptake by target cells, allowing release of the EV content. Numerous reports point at the intriguing possibility that, among thousands of mRNAs, miRNAs, and proteins, single EV constituents effectuate the biological response, e.g. stimulation of angiogenesis and cancer cell metastasis, in recipient cells; however, we find it conceivable that strategies targeted at general mechanisms of EV function should provide more rational avenues for therapeutic intervention directed at the EV system. Such strategies include manipulation of EV formation in the endolysosomal system, EV stability in the extracellular milieu, and EV entry into target cells. Here, we provide important insights into potential mechanisms of EV transport in mammalian cells and how these may be targeted.
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| 19. |
- Cortez, Eliane, et al.
(author)
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Functional subsets of mesenchymal cell types in the tumor microenvironment.
- 2014
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 25:Jan 7, s. 3-9
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Research review (peer-reviewed)abstract
- In the field of tumor biology, increasing attention is now focused on the complex interactions between various constituent cell types within the tumor microenvironment as being functionally important for the etiology of the disease. The detailed description of tumor-promoting properties of cancer-associated fibroblasts, endothelial cells, pericytes, and immune cells, introduces novel potential drug targets for improved cancer treatments, as well as a rationale for exploring the tumor stroma as a previously unchartered source for prognostic or predictive biomarkers. However, recent work highlights the fact that cellular identity is perhaps too broadly defined and that subdivision of each cell type may reveal functionally distinct subsets of cells. Here, we will review our current understanding of the diversity of different subsets of mesenchymal cells, i.e., cancer-associated fibroblasts and pericytes, residing within the tumor parenchyma.
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| 20. |
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| 21. |
- Dalianis, T, et al.
(author)
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Welcome to the Polyomaviridae
- 2009
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In: Seminars in cancer biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 19:4, s. 209-210
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Journal article (other academic/artistic)
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| 22. |
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| 23. |
- Edsjö, Anders, et al.
(author)
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Neuroblastoma as an experimental model for neuronal differentiation and hypoxia-induced tumor cell dedifferentiation.
- 2007
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 17:3, s. 248-256
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Research review (peer-reviewed)abstract
- Neuroblastoma is a childhood tumor derived from precursor or immature cells of the sympathetic nervous system. Neuroblastomas show a tremendous clinical heterogeneity, encompassing truly benign as well as extremely aggressive forms. In vivo as well as in vitro data have shown that the degree of sympathetic neuronal tumor cell differentiation influences patient outcome. Unraveling mechanisms governing neuroblastoma cell differentiation is therefore a central issue in the neuroblastoma research field. In this communication, we discuss some of the in vitro models frequently used to study human neuroblastoma cell differentiation. We also review recent data demonstrating that oxygen shortage, hypoxia, shifts neuroblastoma cells toward an immature, stem cell-like phenotype and discuss the potential clinical impact of hypoxia on neuroblastoma behavior.
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| 24. |
- Fan, Xiaolong, et al.
(author)
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Glioma stem cells: Evidence and limitation.
- 2007
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 17:3, s. 214-218
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Research review (peer-reviewed)abstract
- Gliomas, in particular the high-grade anaplastic glioma and glioblastoma multiforme (GBM), are manifested by morphological, genetic and phenotypic heterogeneity. Most of the studies hitherto have been performed on bulk glioma cells, with limited understanding on the origin and the relative contribution of particular glioma cell populations to glioma growth and progression. Recent studies have demonstrated the existence of a small fraction of glioma cells endowed with features of primitive neural progenitor cells and tumor-initiating function. Such cells have been defined as glioma stem cells. However, questions remain as to whether the currently identified glioma stem cells are the cell-of-origin for glioma initiation and progression, or the results of such processes. In this review, we discuss the current evidence and limitation in identifying glioma stem cells and the potential origin of glioma stem cells in the context of post-natal neural cell regeneration and their transformation mechanisms. The implication of these findings for glioma diagnosis and treatment will also be reviewed.
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| 25. |
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| 26. |
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| 27. |
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| 28. |
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| 29. |
- Gerlee, Philip, 1980, et al.
(author)
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Bridging scales in cancer progression: Mapping genotype to phenotype using neural networks
- 2015
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 30, s. 30-41
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Journal article (peer-reviewed)abstract
- In this review we summarise our recent efforts in trying to understand the role of heterogeneity in cancer progression by using neural networks to characterise different aspects of the mapping from a cancer cells genotype and environment to its phenotype. Our central premise is that cancer is an evolving system subject to mutation and selection, and the primary conduit for these processes to occur is the cancer cell whose behaviour is regulated on multiple biological scales. The selection pressure is mainly driven by the microenvironment that the tumour is growing in and this acts directly upon the cell phenotype. In turn, the phenotype is driven by the intracellular pathways that are regulated by the genotype. Integrating all of these processes is a massive undertaking and requires bridging many biological scales (i.e. genotype, pathway, phenotype and environment) that we will only scratch the surface of in this review. We will focus on models that use neural networks as a means of connecting these different biological scales, since they allow us to easily create heterogeneity for selection to act upon and importantly this heterogeneity can be implemented at different biological scales. More specifically, we consider three different neural networks that bridge different aspects of these scales and the dialogue with the micro-environment, (i) the impact of the micro-environment on evolutionary dynamics, (ii) the mapping from genotype to phenotype under drug-induced perturbations and (iii) pathway activity in both normal and cancer cells under different micro-environmental conditions.
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| 30. |
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| 31. |
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| 32. |
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| 33. |
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| 34. |
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| 35. |
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| 36. |
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| 37. |
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| 38. |
- He, Fei, et al.
(author)
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Sex dimorphism in the tumor microenvironment : From bench to bedside and back
- 2022
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In: Seminars in Cancer Biology. - : Elsevier. - 1044-579X .- 1096-3650. ; 86:3, s. 166-179
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Research review (peer-reviewed)abstract
- Cancer represents a significant cause of death and suffering in both the developed and developing countries. Key underlying issues in the mortality of cancer are delayed diagnosis and resistance to treatments. However, improvements in biomarkers represent one important step that can be taken for alleviating the suffering caused by malignancy. Precision-based medicine is promising for revolutionizing diagnostic and treatment strategies for cancer patients worldwide. Contemporary methods, including various omics and systems biology approaches, as well as advanced digital imaging and artificial intelligence, allow more accurate assessment of tumor characteristics at the patient level. As a result, treatment strategies can be specifically tailored and adapted for individual and/or groups of patients that carry certain tumor characteristics. This includes immunotherapy, which is based on characterization of the immunosuppressive tumor microenvironment (TME) and, more specifically, the presence and activity of immune cell subsets. Unfortunately, while it is increasingly clear that gender strongly affects immune regulation and response, there is a knowledge gap concerning differences in sex-specific immune responses and how these contribute to the immunosuppressive TME and the response to immunotherapy. In fact, sex dimorphism is poorly understood in cancer progression and is typically ignored in current clinical practice. In this review, we aim to survey the available literature and highlight the existing knowledge gap in order to encourage further studies that would contribute to understanding both gender-biased immunosuppression in the TME and the driver of tumor progression towards invasive and metastatic disease. The review highlights the need to include sex optimized/genderized medicine as a new concept in future medicine cancer diagnostics and treatments.
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| 39. |
- Hemminki, Kari, et al.
(author)
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Autoimmune diseases and hematological malignancies : exploring the underlying mechanisms from epidemiological evidence
- 2020
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 64, s. 114-121
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Research review (peer-reviewed)abstract
- Autoimmune diseases are characterized by the irregular functioning of the immune system that leads to the loss of tolerance to self-antigens. The underlying nature of autoimmune diseases has led to speculation that the risk of malignancy might be higher or lower in patients with such diseases. However, the rarity and heterogeneity of both autoimmune diseases and malignancies is the main challenge for systematic exploration of associations between autoimmune diseases and cancer. The nationwide usages of electronic health records in Sweden and other countries has created longitudinal clinical datasets of large populations, which are ideal for quantifying the associations as well as possible guidance concerning the underlying mechanisms. In this report, we firstly summarize the population-based epidemiological association studies between autoimmune diseases and subsequent hematological malignancies using data derived mainly from Swedish nationwide data. These include over one million cancer cases and approximately 500,000 patients with medically diagnosed autoimmune disease. We further discuss the underlying mechanisms that contribute to the observed association between autoimmune diseases and hematological malignancies, including shared genetics, environmental factors, medical treatments of autoimmune diseases as well as dysregulated immune function.
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| 40. |
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| 41. |
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| 42. |
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| 43. |
- Höglund, Mattias
(author)
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Bladder cancer, a two phased disease?
- 2007
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 17:3, s. 225-232
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Research review (peer-reviewed)abstract
- The processes of intraepithelial migration, intraluminal seeding, and field cancerization as models for initiation, spread, and recurrences of urothelial cell carcinoma (UCC) are reviewed in light of recent molecular investigations. The accumulated molecular data on synchronous and metachronous tumors indicate that the majority of recurrent and multiple tumors are monoclonal. Molecular data has also shown the presence of chromosomal and genetic changes in precursor lesions as well as in normal urothelial cells. Genetic-histological mapping of cystectomized bladders has shown that overt tumors occur as local events in areas of genetically altered urothelium. A model is put forward in which the tumor process is initiated by genetically altered but histologically normal cells that produce fields of altered cells by intraepithelial displacement. By the accumulation of further genetic changes the fields of altered urothelium reaches a state of criticality, which locally may produce frank tumors.
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| 44. |
- Johansson, Martin, et al.
(author)
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Kidney cancer.
- 2013
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 23:1, s. 1-2
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Journal article (peer-reviewed)
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| 45. |
- Kajitani, Naoko, et al.
(author)
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The role of RNA-binding proteins in the processing of mRNAs produced by carcinogenic papillomaviruses
- 2022
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1044-579X .- 1096-3650. ; 86, s. 482-496
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Research review (peer-reviewed)abstract
- Human papillomaviruses (HPV) are epitheliotropic DNA tumor viruses that are prevalent in the human population. A subset of the HPVs termed high-risk HPVs (HR-HPVs) are causative agents of anogenital cancers and head-and-neck cancers. Cancer is the result of persistent high-risk HPV infections that have not been cleared by the immune system of the host. These infections are characterized by dysregulated HPV gene expression, in particular constitutive high expression of the HPV E6 and E7 oncogenes and absence of the highly immunogenic viral L1 and L2 capsid proteins. HPVs make extensive use of alternative mRNA splicing to express its genes and are therefore highly dependent on cellular RNA-binding proteins for proper gene expression. Levels of RNA-binding proteins are altered in HPV-containing premalignant cervical lesions and in cervical cancer. Here we review our current knowledge of RNA-binding proteins that control HPV gene expression. We focus on RNA-binding proteins that control expression of the E6 and E7 oncogenes since they initiate and drive development of cancer and on the immunogenic L1 and L2 proteins as there silencing may contribute to immune evasion during carcinogenesis. Furthermore, cellular RNA-binding proteins are essential for HPV gene expression and as such may be targets for therapy to HPV infections and HPV-driven cancers.
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| 46. |
- Kimbung, Siker, et al.
(author)
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Clinical and molecular complexity of breast cancer metastases.
- 2015
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In: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 35, s. 85-95
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Research review (peer-reviewed)abstract
- Clinical oncology is advancing toward a more personalized treatment orientation, making the need to understand the biology of metastasis increasingly acute. Dissecting the complex molecular, genetic and clinical phenotypes underlying the processes involved in the development of metastatic disease, which remains the principal cause of cancer-related deaths, could lead to the identification of more effective prognostication and targeted approaches to prevent and treat metastases. The past decade has witnessed significant progress in the field of cancer metastasis research. Clinical and technological milestones have been reached which have tremendously enriched our understanding of the complex pathways undertaken by primary tumors to progress into lethal metastases and how some of these processes might be amenable to therapy. The aim of this review article is to highlight the recent advances toward unraveling the clinical and molecular complexity of breast cancer metastases. We focus on genes mediating breast cancer metastases and organ-specific tropism, and discuss gene signatures for prediction of metastatic disease. The challenges of translating this information into clinically applicable tools for improving the prognostication of the metastatic potential of a primary breast tumor, as well as for therapeutic interventions against latent and active metastatic disease are addressed.
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| 47. |
- Klein, E, et al.
(author)
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Burkitt lymphoma
- 2009
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In: Seminars in cancer biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 19:6, s. 345-346
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Journal article (other academic/artistic)
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| 48. |
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| 49. |
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| 50. |
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