The vascular network of tumours — what is it not for?

Sivridis, Efthimios; Giatromanolaki, Alexandra; Koukourakis, Michael I.

doi:10.1002/path.1355

Cited by 60 publications

(47 citation statements)

References 99 publications

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“…Oxygen, nutrients, and metabolic wastes can simply diffuse in and out of small tumors, but growth beyond a critical size (1 mm 3 ) requires a vascular network (reviewed in [79]). Areas of hypoxia within tumors induce the expression of angiogenic factors, which prompt an influx of vessels from surrounding tissues.…”

Section: Igf2 and Angiogenesismentioning

confidence: 99%

IGF2: Epigenetic regulation and role in development and disease

Chao

D'Amore

2008

Cytokine & Growth Factor Reviews

281

221

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Insulin-like growth factor II (IGF2) is perhaps the most intricately regulated of all growth factors characterized to date. Its gene is imprinted-only one allele is active, depending on parental origin -and this pattern of expression is maintained epigenetically in almost all tissues. IGF2 activity is further controlled through differential expression of receptors and IGF-binding proteins (IGFBPs) that determine protein availability. This complex and multifaceted regulation emphasizes the importance of accurate IGF2 expression and activity. This review will examine the regulation of the IGF2 gene and what it has revealed about the phenomenon of imprinting, which is frequently disrupted in cancer. IGF2 protein function will be discussed, along with diseases that involve IGF2 overexpression. Roles for IGF2 in sonic hedgehog (Shh) signaling and angiogenesis will also be explored.

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Section: Igf2 and Angiogenesismentioning

confidence: 99%

IGF2: Epigenetic regulation and role in development and disease

Chao

D'Amore

2008

Cytokine & Growth Factor Reviews

281

221

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“…12,13 Although the proposed mechanisms of cancer cell invasion are all valid, they must have been incomplete. For a "second look" at malignant epithelial tumors stained simply with hematoxylin and eosin (H and E) will suffice to disclose it.…”

Section: Introductionmentioning

confidence: 99%

The pathology of tumor stromatogenesis

Giatromanolaki¹,

Sivridis²,

Koukourakis³

2007

Cancer Biology & Therapy

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Stromatogenesis is the formation of new, specific type, stroma at sites of active tumor cell invasion as an integral part of the invading process. The newly formed stroma by being wedged between tissue planes of least resistance disrupts the continuity of normal structures cleaving paths for the invading tumor cells-intramural stromatogenesis for endophytic tumors. Less frequently, the new stroma is formed towards a void space, i.e., at the free surfaces, whether internal or external (extramural stromatogenesis for exophytic tumors). It is postulated that the formation of this new stroma is generated and governed by the invading tumor cells with the tolerance and complicity of the adjacent activated fibroblasts. The spindle cells of the "neostroma" are intensely proliferating myofibroblasts, which are characterized by the frequent expression of a-smooth muscle actin and the particularly frequent expression of thymidine phosphorylase, PDGF-receptors and SPARC (secreted protein acidic rich in cysteine). The cellular and extracellular qualities, different as they are from those of reactive fibrosis, make stromatogenesis amenable to easy penetration by neoplastic cells and a prospective method for diagnosing early tumor invasion. Studies also suggest that the neostroma has complementary to cancer cell metabolic activity, important for buffering of cancer cell waste products and for the prevention of cancer cell acidic death. Thus, cancer cells and neostroma should not be seen as a mixture of heterogeneous uncoordinated cells but rather as a unified morphologic and metabolic domain with a harmonious collaboration between aerobic (myofibroblasts, endothelial cells) and anaerobic compartments (cancer cells).

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“…12,13 Experimental studies suggest that hypoxia is a potent stress stimulus triggering autophagy in normal and malignant cells.…”

mentioning

confidence: 99%

Autophagy patterns and prognosis in uveal melanomas

et al. 2011

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Autophagy is a self-degradation mechanism by which cells recycle their own cytoplasmic constituents. It has been claimed that, under certain conditions, such a process may be associated with tumor progression. In this study, the autophagic activity was investigated in a series of 99 uveal melanomas after immunohistochemical staining for the autophagy-associated proteins MAP1LC3A and BECN1, most commonly known as LC3A and Beclin 1, respectively. These were assessed in parallel with the hypoxia-inducible factor 1a (HIF1A) and its downstream protein lactate dehydrogenase 5 (composed by five LDHA subunits). Increased autophagic reactivity, detected by MAP1LC3A or BECN1, was associated with intense pigmentation and tumor hypoxia. Uveal melanomas with extensive overexpression of BECN1 or those with underexpression of this protein were associated with the worst prognosis, but the former manifested metastases much earlier than the latter; only 58% of patients with extensive BECN1 overexpression were alive at 4 years, compared with 80% of patients with underexpressed patterns. It is concluded that autophagy is commonly upregulated in uveal melanomas, and may be associated with hypoxia and intense pigmentation. There is a strong association between extensive BECN1 overexpression and early metastases/poor prognosis, and between underexpression of this protein and late metastases/better prognosis.

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The vascular network of tumours — what is it not for?

Cited by 60 publications

References 99 publications

IGF2: Epigenetic regulation and role in development and disease

IGF2: Epigenetic regulation and role in development and disease

The pathology of tumor stromatogenesis

Autophagy patterns and prognosis in uveal melanomas

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