2 edition of Phenotypic switches in the malignant progression of human melanoma. found in the catalog.
Phenotypic switches in the malignant progression of human melanoma.
John R. MacDougall
|The Physical Object|
|Number of Pages||228|
Bröcker EB, Suter L, Brüggen J, Ruiter DJ, Macher E, Sorg C: Phenotypic dynamics of tumor progression in human malignant melanoma. Int J Cancer (36)–35 Google Scholar Abstract. The present-day concept of carcinogenesis includes three stages of development: first, the initiation stage in which a normal cell is affected by a carcinogenic initiator causing genetic damage but leaving the cell phenotypically unaltered: second, a promotion stage in which the genetic damage results in the growth of a visible tumor is essentially benign but has an increased.
In light of these evidences, not only the cancer cells can become CSCs but the reverse process can also happen. Our group investigated the possible factors involved in this phenotypic switching, demonstrating that human melanoma cells can switch their phenotype to the CSC state thanks to the activation of a complex miRNA network. The Basic Biology of Malignant Melanoma: Molecular Mechanisms of Disease Progression and Comparative Aspects Shola S. Sulaimon and Barbara E. Kitchell Malignant melanoma (MM) is a life-threatening disease characterized by a highly .
Rapid Communication Identification of a Melanoma Progression Antigen as Integrin VLA-2 C Eberhard Klein, Department of Dermatology, University of Ulm, West Germany Department of Dermatology, University of Ulm West Germany Thomas Steinmayer, Dieter Kaufmann, Department of Human Genetics, University of Ulm, West Germany Department of Human Genetics, University of . the ability to switch phenotype in various types of melanoma has been implicated in conferring a higher risk of death due to metas-tasis. The dynamic switch back and forth between proliferative and invasive states is the model that is biologically reﬂective of melanoma progression (35). Phenotype switching in melanoma can be initiated by mecha-.
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Introduction. Malignant melanoma accounts for 75% of deaths from all skin cancers in the U.S ().Women have higher survival than men and the Caucasian population has a fold greater risk than ethnic groups with deeply pigmented skin ().The 5-year survival rate is over 90% for localized melanoma but drops to 16% for distant-stage disease (), indicating that metastasis is the main reason for Cited by: The phenotypic changes in human melanoma cells during the course of tumor progression were studied with monoclonal antibodies (MAbs) against the melanoma Cited by: Introduction.
Malignant melanoma is an aggressive skin cancer arising from the melanocyte lineage. Despite extensive research efforts on the molecular aspects of malignant melanoma, no effective therapies exist and nearly all patients with advanced stage melanomas die due to its distant metastases after 6–10 months ().Melanoma is one of the most difficult cancers to treat successfully Cited by: Malignant melanoma is notorious for its inter- and intratumour heterogeneity, based on transcriptionally distinct melanoma cell phenotypes.
It is thought Cited by: Phenotypic plasticty and lineage switching in prostate cancer. Implications of non-genetic heterogeneity in cancer drug resistance and malignant progression. Phenotypic plasticity: the emergence of cancer stem cells and collective cell migration. Adaptive phenotypic switching in breast cancer in response to matric deprivation.
Clinical and histopathological evidence suggests that melanoma develops in a sequence of steps, progressing from benign proliferative lesions, to primary melanomas that do not show evidence for metastasis, to invasive primary lesions, and to metastases.
This review focuses on the experimental studies examining the phenotypic characteristics of cultured primary melanoma cells as they relate. Chapters discuss fundamental mechanisms of phenotypic switching, including transition states, cell fate decisions, epigenetic factors, stochasticity, protein-based inheritance, specific areas of human development and disease relevance, phenotypic plasticity in melanoma, prostate cancer, breast cancer, non-genetic heterogeneity in cancer.
Introduction. Melanoma, a malignant tumor of melanocytes, is considered to be the most aggressive of all skin cancers. 1 The genesis and progression of melanoma arise from complex changes in multiple signaling pathways that control cell proliferation and the ability to evade cell death processes.
Aberrant behavior of key signaling pathways, such as RAS/RAF/MAPK, JNK, PI3K/Akt. A high degree of phenotypic plasticity is a hallmark of malignant melanoma (MM), a most aggressive skin cancer originating from neural crest-derived melanocytes. In MM, phenotypic plasticity is controlled by a master regulator of melanocyte development, the microphthalmia-associated transcription factor (MITF) (Cheli et al.,Bell and.
Here, using genetic target modulation, we report the identification of GLO1 as a novel molecular determinant of invasion and metastasis in malignant melanoma. First, A human malignant melanoma. Co-expression modules and hubs associated with melanoma progression, EMT, and metastasis in the cellular model of melanoma progression.
a, b Matrices containing the module-trait relationships for each cell line (a) or for tumor state, progression, EMT, and metastasis (b).Module names are shown on the y-axis, and correlation coefficients are displayed at the top of each row.
Melanoma progression has been described as a step-wise transformation of melanocytes to malignant melanoma triggered by a phenotypic switch toward a more aggressive status. 24 To determine whether. Phenotypic plasticity and subsequent generation of intratumoral heterogeneity underly key traits in malignant melanoma such as drug resistance and metastasis.
Melanoma plasticity promotes a switch. Abstract. Human malignant melanoma is a spontaneous tumor, which progresses from the initial premalignant lesion to highly metastatic forms. Tumor progression seems to be a complex multistage process, during which several distinct properties have to be aquired by the tumor cells either sequentially or in parallel (1,2).
The vast majority of primary human cutaneous melanomas undergo a slow and gradual progression from a clinically indolent, curable radial growth phase (RGP) to a malignant vertical growth phase. We sought to develop a way of isolating genetically related malignant variants from a benign RGP human melanoma, called WM The parent and variants were then used as a model system to examine to.
INTRODUCTION. While overall cancer incidence rates have decreased in the United States, the incidence rate of human malignant melanoma continues to increase .As the most malignant skin cancer, melanoma is the sixth most common cancer in men and the seventh in women in the United States .When diagnosed before the cancer has spread, melanoma can be cured by surgical.
Epithelial ovarian cancer is a devastating disease responsible for the deaths of ∼15, Americans per year, even more than melanoma or brain tumors (Jemal et al., ).Independent studies have demonstrated that in the ovarian carcinoma microenvironment, T cells (and only they) can spontaneously exert clinically relevant pressure against tumor progression (Zhang et al., ; Sato.
Cutaneous malignant melanoma (CMM) begins in the epidermis as the clonal emergence of melanocytes having a deregulated mitotic cycle.
In a manner not yet understood, some descendents of these cells loosen their adhesions in situ and migrate into the dermis, thus initiating the processes of invasion and metastasis. These cells look and act much like macrophage-melanoma hybrids created.
Microarray gene expression profiling is a powerful tool for generating molecular cancer classifications. However, elucidating biological insights from these large data sets has been challenging. Previously, we identified a gene expression-based classification of primary uveal melanomas that accurately predicts metastatic death.
Class 1 tumors have a low risk and class 2 tumors a high risk for. Integrins are transmembrane adhesion receptors that provide the physical link between the actin cytoskeleton and the extracellular matrix. It has been well established that integrins play a major role in various cancer stages, such as tumor growth, progression, invasion and metastasis.
In breast cancer, integrin alphavbeta3 has been associated with high malignant potential in cancer cells. In a coculture system, adipocytes secreted the cytokines IL-6 and TNF-α, which induced a proliferative-to-invasive phenotypic switch in melanoma cells by repressing the expression of the microRNA miR In a xenograft model, miR exhibited a dual role in melanoma progression, promoting cell proliferation while inhibiting metastatic spread.
The malignant potential of small congenital nevocellular nevi J Am Acad Dermatol 6: () 6. BrÃcker, E.B. Suter, L. BrÃ¼ggen, J. Ruiter, D.J. Macher, E. Sorg, C. Phenotypic dynamics of tumor progression in human malignant melanoma Int J Cancer () 7.In this regard, human malignant melanoma provides a particularly good model for studying progressive etiologically relevant events, since clinical and pathological observations have defined cutaneous lesions that represent sequential steps in the progression to melanoma [4, 5, 6].
Moreover, cells representing these stages (e.g., normal.