Prostate cancer stem cells

Lang, Shona; Frame, Fiona M.; Collins, Anne T.

doi:10.1002/path.2478

Cited by 118 publications

(111 citation statements)

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“…Proposed prostate stem cell niche genes, such as Fzd6, Wnt2 and Wnt4, are also differentially expressed by other primitive niches such as embryonic dermis and epidermis 61 . Epigenetic or genetic alterations of stem cell related genes, give rise to cancer stem cells 56,62 . Although basal stem/progenitor cells have been proposed to represent a cell type of cancer origin, human prostate cancer has a markedly luminal phenotype 56 .…”

Section: Role Of Wnt Signaling In Prostate Developmentmentioning

confidence: 99%

WNT Signaling in Prostate Development and Carcinogenesis

Kharaishvili¹,

Simkova²,

Makharoblidze³

et al. 2011

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. The Wnt signaling pathway is crucial for cell fate decisions, stem cell renewal, regulation of cell proliferation and differentiation. Deregulated Wnt signaling is also implicated in a number of hereditary and degenerative diseases and cancer.Methods and results. This review highlights the role of the Wnt pathway in the regulation of stem/progenitor cell renewal and prostate gland development and how this signaling is altered in prostate cancer. Recent evidence suggests that Wnt signaling regulates androgen activity in prostate cancer cells, enhances androgen receptor expression and promotes the growth of prostate cancer even after androgen ablation therapy. There is also strong evidence that Wnt signaling is enhanced in androgen-ablation resistant tumors and bone metastases.Conclusions. Further study of the modulators of this pathway will be of therapeutic relevance as inhibition of Wnt signaling may have the potential to reduce the self-renewal and aggressive behaviour of prostate cancer while Wnt signaling activation might enhance stem cell activity when tissue regeneration is required.

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Section: Role Of Wnt Signaling In Prostate Developmentmentioning

confidence: 99%

WNT Signaling in Prostate Development and Carcinogenesis

Kharaishvili¹,

Simkova²,

Makharoblidze³

et al. 2011

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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“…Cancer stem cells have also been found only in certain types of cancer. Furthermore, the origin of cancer stem cells is ambiguous: some suggest they do come from mutated stem cells ( [28]), others that they are mutated progenitor or differentiated cells. The model heavily relies on the assumption that stem cells mutate into cancer stem cells.…”

Section: Discussionmentioning

confidence: 99%

A Mathematical Model of Cancer Stem Cell Lineage Population Dynamics with Mutation Accumulation and Telomere Length Hierarchies

Kapitanov

2012

Math. Model. Nat. Phenom.

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Abstract. There is evidence that cancer develops when cells acquire a sequence of mutations that alter normal cell characteristics. This sequence determines a hierarchy among the cells, based on how many more mutations they need to accumulate in order to become cancerous. When cells divide, they exhibit telomere loss and differentiate, which defines another cell hierarchy, on top of which is the stem cell. We propose a mutation-generation model, which combines the mutation-accumulation hierarchy with the differentiation hierarchy of the cells, allowing us to take a step further in examining cancer development and growth. The results of the model support the hypothesis of the cancer stem cell's role in cancer pathogenesis: a very small fraction of the cancer cell population is responsible for the cancer growth and development. Also, according to the model, the nature of mutation accumulation is sufficient to explain the faster growth of the cancer cell population. However, numerical results show that in order for a cancer to develop within a reasonable time frame, cancer cells need to exhibit a higher proliferation rate than normal cells.

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“…Stem-like functions of CSCs inherited from their normal stem cells counterparts may be critical for survival during long periods of time in tissues (Hsieh et al, 2007;O'Brien et al, 2010;Rajan et al, 2009;Rosen & Jordan, 2009;Vermeulen et al, 2008;Witte, 2009). In this regard, the generation of cancer cells and their success in tumor growth are probably dependent on dysregulations affecting cells with stem-like characteristics and have the ability to promote tumor and support tumor development (Dalerba et al, 2007;Lang et al, 2009;Weissman et al, 2001). In www.intechopen.com fact, malignant tumors, like normal tissue, frequently contain cells at various stages of differentiation, a mechanism that mimics dedifferentiation of mature cell types and presumes a hierarchical organization (Clarke et al, 2006;Clevers, 2005 …”

Section: Stem Cells In the Prostatementioning

confidence: 99%

“…Therefore, the recognition of markers for CSC and cell proliferation during the processes of prostate tumor initiation and progression is of vital importance to track CSCs for the development and improvement of therapies. It is also important to remark that subpopulations of prostate tumor cells with cancer progenitor properties are thought to support refractory response to a given treatment, leading to prostate tumor recurrence; therefore, new approaches to identifying and targeting these cancer subpopulations might provide an avenue to managing metastatic and recurrent disease refractive to treatment (Chaffer & Weinberg, 2011;Lang et al, 2009;Polyak & Hahn, 2006). This chapter will discuss the potential applications of CSC markers that may predict risk of clinical outcome and provide a guide for appropriate therapy of prostate neoplasias.…”

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confidence: 99%