The borderline: Basement membranes and the transition from premalignant to malignant neoplasia

Bosman, Fred T.

doi:10.1002/jemt.1070280306

Cited by 28 publications

(21 citation statements)

References 53 publications

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“…2A-D) demonstrated that neither raw soya diet nor the presence of developing tumours influenced the location and, perhaps, expression of laminin. And finally, our finding that BML was not expressed in invasive carcinomas is in agreement with the results of studies on several types of tumours (Barsky et al 1983;Bosman 1994). our observations argue for a direct correlation between BML and proliferation levels.…”

Section: Discussionsupporting

confidence: 93%

“…Since the early 1980s, it is a common observation that the basement membrane (BM) system is continuous in differentiated or benign epithelial tumours, whereas it is fragmented or missing in undifferentiated and invasive malignancies (Barsky et al 1983;Bosman 1994). In the 1990s, expression of laminin, a major structural molecule of BM, was shown in invasive areas of carcinomas in several cases (for references see Pyke et al 1995;Lohi 2001).…”

Section: Introductionmentioning

confidence: 99%

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Characterisation of the progression of azaserine-induced rat pancreatic adenocarcinoma by proliferative cell nuclear antigen, basement membrane laminin and trypsinogen immunohistochemistry

Nagy

Pálfia

Réz

2003

Histochem Cell Biol

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The progression of azaserine-induced rat pancreatic adenocarcinoma (AC) was characterised using quantitative and semiquantitative immunohistochemistry for proliferating cell nuclear antigen (PCNA), basement membrane laminin (BML) and trypsinogen (TG). Samples were taken 5-20 months after initiation. High PCNAlabelling indices (PCNA LIs) were measured 5 months after the induction of atypical acinar cell nodules (AACNs), which decreased later and stagnated until a further decline in the month 10 adenomas. Then a second premalignant proliferative wave was observed (month 13) within the adenoma stage. Later, in month 20 differentiated ACs PCNA LIs fell to the host tissue level but were found highest in the month 20 anaplastic ACs indicating a switch to malignant proliferation. Month 20 invasive ACs showed a number of separate proliferative foci. In early AACNs, BML decreased and remained low till the local maximum in the month 13 adenoma. Invasive ACs did not express BML. Month 5 AACN and differentiated AC were TG deficient but anaplastic AC regained its TG expression. However invasive AC was again TG negative. These results are discussed in combination with our previous data on progressional changes of autophagic capacity and microvessel densities.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Characterisation of the progression of azaserine-induced rat pancreatic adenocarcinoma by proliferative cell nuclear antigen, basement membrane laminin and trypsinogen immunohistochemistry

Nagy

Pálfia

Réz

2003

Histochem Cell Biol

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“…Based mostly on morphologic data, the loss of BM continuity has been associated with increasing malignancy. 51,52 Various proteolytic enzymes have an altered distribution and activity in malignant tissues 53 and it has been suggested that BM degradation is a prerequisite for invasion. 15,51 The expression and activity of proteolytic enzymes in carcinomas is regulated by an interaction between integrin and extracellular matrix and by endogenous growth factors, as well as by tissue inhibitors of metalloproteinase (TIMP).…”

Section: Laminin-5mentioning

confidence: 99%

Laminin-5 in the progression of carcinomas

Lohi¹

2001

Int. J. Cancer

112

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The basement membrane (BM) separates epithelial elements from the surrounding stroma. BM is dynamic in regulation of epithelial cells differentiation as well as their organization into 3-dimensional tissues. In these functions, among the molecules of the BM, laminins are especially dynamic. Laminins are distributed in a spatially and temporally regulated manner in various epithelial tissues. Various changes in the laminin distribution accompany the malignant transformation of epithelia. The role of the BM and laminins in the progression of carcinomas is not well understood. The BM has been suggested to act as a mechanical barrier against carcinoma cell invasion. BM laminins may play an active role in regulating the migration and proliferation of the carcinoma cells. Laminin isoform laminin-5 expression is typical for some invasive carcinomas and it may act as a ligand for invading carcinoma cells. Neoexpression of laminin-5 has also been associated to proliferative activity of the carcinoma cells. Integrins ␣ 3 ␤ 1 and ␣ 6 ␤ 4 are probable cell surface receptors acting with laminin-5 in the regulation of carcoma cell invasion and proliferation. © 2001 Wiley-Liss, Inc. Key words: laminin-5; carcinomas; invasion; integrin; basement membranesBasement membrane (BM) is a densified sheet of proteins of the extracellular matrix. The BM separates connective tissue from epithelium. In addition, endothelium, various types of muscle cell, lipocytes and Schwann cells are surrounded by BM. 1 Structural components of the BM are at least laminins, type IV collagens, nidogens, proteoglycans such as perlecan, fibulins as well as type VII collagen in the BMs containing lamina fibroreticularis layer. Additionally, fibronectin and tenascin are often located to the BM region, but they are not the structural components of the BMs. BM molecules are produced in cooperation between epithelial and mesenchymal cells. 2 Collagen type IV is a helical, trimeric protein. The most widely expressed type IV collagen trimer is composed of 2 ␣1(IV) chains and one ␣2(IV) chain. 3 The ␣3(IV)-␣6(IV) chains have a more restricted tissue distribution, present for example in the kidney. 4 -6 Nidogen-1 is a 150 kD glycoprotein consisting of three globular domains. 7 It binds collagen IV and laminin networks together. 8 Nidogen-1 binds also perlecan, fibulin-1 and fibulin-2. 9 Type VII collagen forms the anchoring fibrils and connects the BM lamina densa to the underlying connective tissue at least in BMs of stratified epithelium. 10,11 Type VII collagen binds, laminin-5 and type IV collagen. 12 The functions of BM in offering mechanical support are well known. 1 In addition to mechanical functions, the BM influences for cell proliferation, differentiation, adhesion, migration and gene expression. 13,14 BM acts as a factor in maintaining polarity and organization of epithelial cells 1,13,15,16 and it is an active regulator in epithelial-mesenchymal interactions during epithelial cell development. 17 BM molecules can regulate the activity of growth facto...

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“…Following the report that epithelial basement membrane (EBM) breaks are associated with the malignant phenotype in epithelial tumours , there has been intense interest in the diagnostic and prognostic significance of these breaks, and the literature on this subject is extensive [reviewed by D'Ardenne (1989) and Bosman (1994)]. Such studies on human colorectal (Forster et al, 1986;Havenith et al, 1988;Hewitt et al, 1991) and breast cancer (Albrechtsen et al, 1981;Barsky et al, 1983) have shown marked EBM deficiencies.…”

mentioning

confidence: 99%

Laminin and collagen IV subunit distribution in normal and neoplastic tissues of colorectum and breast

Hewitt

Powe²,

Morrell³

et al. 1997

Br J Cancer

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Summary To invade and metastasize, carcinomas must penetrate or lose their epithelial basement membrane (EBM), and then penetrate basement membranes (BMs) surrounding blood vessels, lymphatics, nerves and muscle cells. Knowledge of the composition of different BMs is necessary, so that appropriate antibodies and DNA probes are used to analyse these events. Laminin and type IV collagen are the principal BM components. However, recent studies show these two proteins exist in various isoforms, each of which is a heterotrimer of different subunit polypeptides. In this study, we analysed the distribution of laminin subunits, ax1 (lam), ax2(lam), f1 (lam), P2(lam) and yl (lam), and collagen IV subunits, cr1 (IV), a3(IV), ca4(IV) and c5(IV), in normal and neoplastic tissues of colorectum and breast. Subunits ca1 (IV), ca1 (lam), fl (lam) and yl (lam) were detected in all BMs, while the distribution of a3(IV), ax4(IV), a5(IV) and ax2(lam) was much more restricted. In carcinomas, EBM staining for all subunits was invariably discontinuous or absent, consistent with the presence of complete EBM breaks. Use of antibody to cr1 (lam) selectively stained the EBMs of carcinomas. Strong vascular staining for ac1 (lam), 1l (lam), yl (lam) and a1 (IV) suggests an abundance of BM proteins in vessel walls, which may aid tumour cell attachment before vascular invasion. Within carcinomas, vascular BM staining for 12(lam) was clearly weaker than in normal tissues, which may reflect incomplete maturation of these vessels.

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The borderline: Basement membranes and the transition from premalignant to malignant neoplasia

Cited by 28 publications

References 53 publications

Characterisation of the progression of azaserine-induced rat pancreatic adenocarcinoma by proliferative cell nuclear antigen, basement membrane laminin and trypsinogen immunohistochemistry

Characterisation of the progression of azaserine-induced rat pancreatic adenocarcinoma by proliferative cell nuclear antigen, basement membrane laminin and trypsinogen immunohistochemistry

Laminin-5 in the progression of carcinomas

Laminin and collagen IV subunit distribution in normal and neoplastic tissues of colorectum and breast

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