Of the deaths attributed to cancer, 90% are due to metastasis, and treatments that prevent or cure metastasis remain elusive. Emerging data indicate that hypoxia and the extracellular matrix (ECM) might have crucial roles in metastasis. During tumour evolution, changes in the composition and the overall content of the ECM reflect both its biophysical and biological properties and these strongly influence tumour and stromal cell properties, such as proliferation and motility. Originally thought of as independent contributors to metastatic spread, recent studies have established a direct link between hypoxia and the composition and the organization of the ECM, which suggests a new model in which multiple microenvironmental signals might converge to synergistically influence metastatic outcome.

/pdf/hypoxia-and-the-extracellular-matrix-drivers-of-tumour-7xig9u6nbf.pdf

Hypoxia and the extracellular matrix: drivers of tumour metastasis

Evidence for the potent influence of stromal organization and function on invasion and metastasis of breast tumors is ever growing. We have performed a rigorous examination of the relationship of a tumor-associated collagen signature-3 (TACS-3) to the long-term survival rate of human patients. TACS-3 is characterized by bundles of straightened and aligned collagen fibers that are oriented perpendicular to the tumor boundary. An evaluation of TACS-3 was performed in biopsied tissue sections from 196 patients by second harmonic generation imaging of the backscattered signal generated by collagen. Univariate analysis of a Cox proportional hazard model demonstrated that the presence of TACS-3 was associated with poor disease-specific and disease-free survival, resulting in hazard ratios between 3.0 and 3.9. Furthermore, TACS-3 was confirmed to be an independent prognostic indicator regardless of tumor grade and size, estrogen or progesterone receptor status, human epidermal growth factor receptor-2 status, node status, and tumor subtype. Interestingly, TACS-3 was positively correlated to expression of stromal syndecan-1, a receptor for several extracellular matrix proteins including collagens. Because of the strong statistical evidence for poor survival in patients with TACS, and because the assessment can be performed in routine histopathological samples imaged via second harmonic generation or using picrosirius, we propose that quantifying collagen alignment is a viable, novel paradigm for the prediction of human breast cancer survival.

Aligned collagen is a prognostic signature for survival in human breast carcinoma.

The relationship between lung liquid flow and fetal lung development has been studied at the cellular level using ultrastructural techniques. Continuous in utero tracheal ligation and drainage (over a period of 21-28 days) both result in malformations of the developing fetal lamb lung. Ligated lungs are larger, and drained lungs are smaller, than normal lungs at a similar gestational age. These changes are not merely due to altered lung liquid volume, but actual tissue growth thas been affected. Future alveolar wall thinning is enhanced in ligated lungs and inhibited in drained lungs, whilst the presence of differentiated alveolar type II cells (probably related to surfactant production) is decreased in ligated lungs and markedly enhanced in drained lungs. These results indicate the importance of fetal lung liquid in the regulation of pulmonary development in the fetus.

Morphological effects of chronic tracheal ligation and drainage in the fetal lamb lung.

Pseudoangiomatous hyperplasia of mammary stroma

The mammary gland consists of an extensively branched ductal network contained within a distinctive basement membrane and encompassed by a stromal compartment. During lactation, production of milk depends on the action of the two epithelial cell types that make up the ductal network: luminal cells, which secrete the milk components into the ductal lumen; and myoepithelial cells, which contract to aid in the ejection of milk. There is increasing evidence that the myoepithelial cells also play a key role in the organizational development of the mammary gland, and that the loss and/or change of myoepithelial cell function is a key step in the development of breast cancer. In this review we briefly address the characteristics of breast myoepithelial cells from human breast and mouse mammary gland, how they function in normal mammary gland development, and their recently appreciated role in tumor suppression.

https://link.springer.com/content/pdf/10.1186%2Fbcr1286.pdf

Myoepithelial cells: good fences make good neighbors.

Signature-based and Machine-Learning-based Web Application Firewalls: A Short Survey

Calcification in human breast carcinomas has been studied ultrastructurally. Multiple deposits of needle-shaped crystals intimately associated with electrondense material were observed among tumour cells. Similar deposits were present in intracytoplasmic lumina and the adjacent stroma. Cytoplasmic calcification was seen in membrane-bound vesicles and as partially membrane-bound clusters of crystals. It is suggested that the calcification is the result of an active secretory process rather than calcified necrotic or degenerate tumour cells. The possible mechanisms of calcification are discussed. Both electron diffraction and electron probe analysis show that the crystaline material is hydroxyapatite.

Calcification in human breast carcinomas: ultrastructural observations.

A histochemical and ultrastructural investigation of apocrine cells in the human breast has been carried out. These cells showed strong oxidative enzymatic activity, large numbers of mitochondria and numerous infoldings of the basal plasma membrane. In these features, such cells resemble the normal apocrine gland cells. These observations support the view that this lesion is a metaplastic change in normal breast epithelium.

Apocrine metaplasia in cystic hyperplastic mastopathy. Histochemical and ultrastructural observations.

The ultrastructure of four tubular carcinomas of the breast is described. The neoplastic tubules are single layered and lack a myo-epithelial component, an important feature in distinguishing tubular carcinoma from sclerosing adenosis. Numerous myo-fibroblasts are present in the stroma of all four tumours and, since cells of this type have been recorded only occasionally in the stroma of other types of breast carcinoma, it is suggested that they may be a characteristic feature of tubular carcinomas.

The ultrastructure of tubular carcinoma of the breast.

In a series of experiments, one rabbit fetus of a litter was decapitated in utero on day 24 of gestation and allowed to develop for a further 5 days. One effect of fetal decapitation was a reduction in the concentration of osmiophilic inclusion bodies in the type II pneumocytes of the lung. However, certain physical properties of the lung which depend on the presence of a surface active alveolar lining were normal. When 50 μg tetracosactrin was given to the fetus subcutaneously at the time of decapitation, there was no reduction in the concentration of inclusion bodies. It is suggested that though the production of surface active material in the pneumocyte is controlled at least in part by fetal adrenocortical hormones, the extrusion of this material into the alveolar space may be subject to other control. This may have important implications for the prophylactic treatment of the respiratory distress syndrome in premature babies by antepartum maternal glucocorticoid therapy.

https://adc.bmj.com/content/archdischild/48/9/709.full.pdf

Control of fetal lung development in the rabbit

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