Hyperplasia: The spread of abnormal cells through a plane lattice

1971 ◽  
Vol 3 (2) ◽  
pp. 210-211 ◽  
Author(s):  
Trevor Williams ◽  
Rolf Bjerknes

When a basal cell divides, both daughter cells remain in the basal layer of the epithelium, with one of the neighbouring cells being pushed out to make room. This fact opens the possibility that a cell with a heritable advantage over the normal cells may gradually produce a clone covering more and more of the basal layer. The advantage in question may consist in a faster rate of division than normal, or a more tenacious hold on the basement membrane; we shall limit consideration to the former situation.

1971 ◽  
Vol 3 (02) ◽  
pp. 210-211 ◽  
Author(s):  
Trevor Williams ◽  
Rolf Bjerknes

When a basal cell divides, both daughter cells remain in the basal layer of the epithelium, with one of the neighbouring cells being pushed out to make room. This fact opens the possibility that a cell with a heritable advantage over the normal cells may gradually produce a clone covering more and more of the basal layer. The advantage in question may consist in a faster rate of division than normal, or a more tenacious hold on the basement membrane; we shall limit consideration to the former situation.


1981 ◽  
Vol 18 (03) ◽  
pp. 732-737
Author(s):  
D. Y. Downham ◽  
S. B. Fotopoulos

Normal and abnormal cells are positioned at the vertices of a regular two-dimensional lattice. Abnormal cells divide k times as fast as normal cells. Whenever a cell divides, the daughter is the same type as the parent and replaces an adjacent cell. The Kolmogorov forwards and backwards equations are derived, and then used to obtain bounds for the distribution function of the time when all the abnormal cells are forced from the plane. These bounds are used to comment on the non-asymptotic variance of the number of abnormal cells at a given time and on a method of estimating k.


1981 ◽  
Vol 18 (3) ◽  
pp. 732-737 ◽  
Author(s):  
D. Y. Downham ◽  
S. B. Fotopoulos

Normal and abnormal cells are positioned at the vertices of a regular two-dimensional lattice. Abnormal cells divide k times as fast as normal cells. Whenever a cell divides, the daughter is the same type as the parent and replaces an adjacent cell. The Kolmogorov forwards and backwards equations are derived, and then used to obtain bounds for the distribution function of the time when all the abnormal cells are forced from the plane. These bounds are used to comment on the non-asymptotic variance of the number of abnormal cells at a given time and on a method of estimating k.


Hand Surgery ◽  
2002 ◽  
Vol 07 (02) ◽  
pp. 295-298 ◽  
Author(s):  
M. Galeano ◽  
M. Colonna ◽  
M. Lentini ◽  
F. Stagno D'Alcontres

Basal cell carcinoma (BCC) is the most common skin malignancy arising from cells of the basal layer of the epithelium or from the external root sheath of the hair follicle. BCC of the digit is a rare entity. The article presents one such case of bowenoid BCC of the thumb which required amputation at the MP joint.


Small groups of two to four fibroblasts at the periphery of outgrowths from cultured explants of chick embryo heart were isolated from their neighbours by sweeping away the nearby cells. The groups and the explants were left attached to the glass substrate, undisturbed. The behaviour of the isolated cells was photographically recorded during about 8 h of further culture. The cells of these groups dispersed, though not as a rule so far as to lose all mutual contacts, the dispersal being counterbalanced by the addition of new cells through mitosis. The accompanying changes in speed of locomotion, and the non-random nature of the spreading, are interpreted in terms of the effects of contacts between the cells. During the first four hours after isolation, but not thereafter, the cells of the groups on the average moved slowly away from the explant. Control groups in an intact outgrowth moved away faster and with no diminution of speed during the period of observation. The movement of the isolated groups can be partly accounted for by the tendency of cells to conserve for a time the direction of their movement before isolation; and by a strong reluctance of the isolated cells to move across the area, from which cells had been scraped away, that lay between the group and the explant. A new outgrowth of the residual sheet of cells still connected to the explant, however, advanced across this area, approaching and in most cases overhauling the isolated group. It is concluded that a chemotactic gradient around the explant is unlikely to play any significant part in the outward movement of fibroblasts from an explant in tissue culture. The cells of the isolated groups underwent an outburst of mitosis about 3 h after isolation. Mitoses in these relatively free cells are oriented in relation to the polarity of the cell before division. Locomotion of the daughter-cells tends to be faster than usual for at least 2 h after a cell divides.


2014 ◽  
Vol 369 (1652) ◽  
pp. 20130502 ◽  
Author(s):  
Mu Li ◽  
Emily Zeringer ◽  
Timothy Barta ◽  
Jeoffrey Schageman ◽  
Angie Cheng ◽  
...  

Exosomes are tiny vesicles (30–150 nm) constantly secreted by all healthy and abnormal cells, and found in abundance in all body fluids. These vesicles, loaded with unique RNA and protein cargo, have a wide range of biological functions, including cell-to-cell communication and signalling. As such, exosomes hold tremendous potential as biomarkers and could lead to the development of minimally invasive diagnostics and next generation therapies within the next few years. Here, we describe the strategies for isolation of exosomes from human blood serum and urine, characterization of their RNA cargo by sequencing, and present the initial data on exosome labelling and uptake tracing in a cell culture model. The value of exosomes for clinical applications is discussed with an emphasis on their potential for diagnosing and treating neurodegenerative diseases and brain cancer.


Langmuir ◽  
2014 ◽  
Vol 30 (8) ◽  
pp. 2101-2108 ◽  
Author(s):  
Shaun P. Garland ◽  
Clayton T. McKee ◽  
Yow-Ren Chang ◽  
Vijay Krishna Raghunathan ◽  
Paul Russell ◽  
...  

2021 ◽  
Author(s):  
Moataz Dowaidar

Autophagy is a double-edged sword in cancer, and numerous aspects should be taken into account before deciding on the most effective strategy to target the process. The fact that several clinical studies are now ongoing does not mean that the patient group that may benefit from autophagy-targeting medicines has been identified. Autophagy inhibitors that are more potent and specialized, as well as autophagy indicators, are also desperately required. The fact that these inhibitors only work against tumors that rely on autophagy for survival (RAS mutants) makes it difficult to distinguish them from tumors that continue to develop even when autophagy is absent. Furthermore, mutations such as BRAF have been shown to make tumors more susceptible to autophagy suppression, suggesting that targeting such tumours may be a viable strategy for overcoming their chemotherapy resistance. In the meantime, we are unable to identify if autophagy regulation works in vivo or whether it selectively targets a disease while inflicting injury to other healthy organs and tissues. A cell-type-specific impact appears to be observed with such therapy. As a result, it is just as important to consider the differences between tumors that originate in different organs as it is to consider the signaling pathways that are similar across them. For a therapy or cure to be effective, the proposed intervention must be tailored to the specific needs of each patient.Over the last several years, a growing amount of data has implicated autophagy in a variety of disorders, including cancer. In normal cells, this catabolic process is also required for cell survival and homeostasis. Despite the fact that medications targeting intermediates in the autophagy signaling pathway are being created and evaluated at both the preclinical and clinical levels, given the complicated function of autophagy in cancer, we still have a long way to go in terms of establishing an effective therapeutic approach. This article discusses current tactics for exploiting cancer cells' autophagy dependency, as well as obstacles in the area. We believe that the unanswered concerns raised in this work will stimulate researchers to investigate previously unknown connections between autophagy and other signaling pathways, which might lead to the development of novel, highly specialized autophagy therapies.


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