Measurements of Cellular Proliferation and DNA in Breast Carcinoma

1989 ◽  
pp. 141-171 ◽  
Author(s):  
John Strauch Meyer
Keyword(s):  
Breast Carcinoma ◽  
Cellular Proliferation

scholarly journals The effects of chemotherapy on morphology, cellular proliferation, apoptosis and oncoprotein expression in primary breast carcinoma

1994 ◽  
Vol 70 (2) ◽  
pp. 335-341 ◽  
Author(s):  
SA Rasbridge ◽  
CE Gillett ◽  
A-M Seymour ◽  
K Patel ◽  
MA Richards ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Cellular Proliferation ◽  
Primary Breast Carcinoma

Effects of interferon-alpha on cellular proliferation and adhesion of breast carcinoma cells.

1999 ◽  
Author(s):  
M Maemura ◽  
Y Iino ◽  
J Horiguchi ◽  
H Takei ◽  
Y Horii ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Interferon Alpha ◽  
Cellular Proliferation ◽  
Carcinoma Cells ◽  
Breast Carcinoma Cells

scholarly journals Promyelocytic Leukemia (PML) gene regulation: implication towards curbing oncogenesis

2019 ◽  
Vol 10 (9) ◽  
Author(s):  
Neerajana Datta ◽  
Saimul Islam ◽  
Uttara Chatterjee ◽  
Sandip Chatterjee ◽  
Chinmay K. Panda ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Regulation ◽  
Breast Carcinoma ◽  
Cellular Proliferation ◽  
Critical Factor ◽  
Luciferase Reporter ◽  
Breast Cancer Cell Lines ◽  
Breast Cancers ◽  
Cellular Apoptosis ◽  
The Impact

Abstract Dysregulation of PML, a significant tumor suppressor is linked with cancers of different histological origins, with a decreased expression observed with a higher tumor grade. This necessitates studying the mechanisms to maintain a stable expression of PML. However much less is known about the transcriptional regulation of PML, more so in the context of breast carcinoma. ERβ has emerged as a critical factor in understanding breast cancer, especially since a huge proportion of breast cancers are ERα− and thus insensitive to tamoxifen therapy. This study aims to uncover an unidentified mechanism of PML gene regulation and its stabilization in breast cancer via ERβ signalling and the impact on cellular apoptosis. We found that clinical expression of PML positively correlates with that of ERβ both in normal and breast carcinoma samples and inversely correlates with markers of cellular proliferation, hinting towards a possible mechanistic interdependence. Both mRNA and protein expression of PML were increased in response to ERβ overexpression on multiple human breast cancer cell lines. Mechanistically, luciferase reporter assays and chromatin-immunoprecipitation assays demonstrated that ERβ can interact with the PML promoter via ERE and AP1 sites to enhance its transcription. ERβ induced stable PML expression causes a decline of its target protein Survivin and simultaneously provides a stable docking platform leading to stabilisation of its target Foxo3a, further causing transcriptional upregulation of pro-apoptotic factors p21 and p27. Immunohistochemical analyses of cancer and normal breast tissues and functional assays conducted corroborated the findings. Collectively, our study identifies ERβ signalling as a novel mechanism for PML gene regulation in ERα− breast cancer. It also reveals bi-directional downstream effect in which ‘ERβ-PML-(Foxo3a/Survivin)’ network acts as a therapeutic axis by suppressing cellular survival and promoting cellular apoptosis in breast carcinoma.

Clusterin in stool: A new diagnostic marker of colorectal cancer

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14561-14561
Author(s):  
S. Pucci ◽  
F. Sesti ◽  
P. Mazzarelli ◽  
E. Bonanno ◽  
L. G. Spagnoli
Keyword(s):  
Colorectal Cancer ◽  
Breast Carcinoma ◽  
Cellular Proliferation ◽  
Tumour Progression ◽  
Primary Tumour ◽  
Metastatic Potential ◽  
Early Screening ◽  
Number Of Patients ◽  
Incidence And Mortality

14561 Background: Colon cancer is second only to lung cancer in men and to breast carcinoma in women, for incidence and mortality in western countries .The higher incidence per age is observed between the sixth and seventieth decade, while 60% of the patients survive up to five years. The most important reason for the low percentage of recoveries is due to the fact that when the primary tumour is removed, a high number of patients have already developed micro-metastases, principally at liver. Therefore, methods for early screening are requested. Molecular markers have emerged as an important strategy to evaluate the individual susceptibility for cancer insorgence and for clinical cancer therapy. Recent studies have demonstrated an increase in clusterin expression in breast carcinoma suggesting a possible role of this protein in tumour progression. Clusterin is an heterodimeric (a and β chains) ubiquitous glycoprotein implicated in a large number of physiological processes and in the control of cellular proliferation. Despite the original hypothesis that clusterin is a marker for programmed cell death, several experiments and clinical studies have demonstrated conflicting findings on its role in tumors. Methods: We have studied clusterin isoforms expression in tumour progression, in particular in the adenoma-carcinoma sequence of colorectal cancer. Results: the observation of 35 samples of human intestinal mucosa, such as endoscopic biopsies and surgical specimens, demonstrated that the progression towards high grade and metastatic colon carcinoma leads to a pattern shift of clusterin isoforms production, the complete loss of the proapoptotic nuclear form and an over expression of cytoplasmic secreted form correlateting to a phenotype with high metastatic potential. Moreover we observed in tumor biopsies the release of clusterin in the crypts lumen. The ELISA immuno-dosage of clusterin demonstrated that the sclusterin overexpression in tumours correlates to a significant increase of clusterin in the serum and stools of patients affected by tumoural pathologies and in particular by colorectal cancer. Conclusions: These data suggests a new role of secreted clusterin as a new diagnostic circulating marker and a potential new therapeutic target. No significant financial relationships to disclose.

Breast carcinoma in children

JAMA ◽  
1966 ◽  
Vol 195 (5) ◽  
pp. 388-390 ◽  
Author(s):  
R. W. McDivitt
Keyword(s):  
Breast Carcinoma

Correlation Between Cellular Functions and Morphological Changes of Human Trophoblast in Vitro

1975 ◽  
Vol 33 ◽  
pp. 600-601
Author(s):  
John C. Garancis ◽  
Robert O. Hussa ◽  
Michael T. Story ◽  
Donald Yorde ◽  
Roland A. Pattillo
Keyword(s):  
Electron Microscopy ◽  
Cellular Proliferation ◽  
Morphological Changes ◽  
Culture Fluid ◽  
Cellular Functions ◽  
Human Trophoblast ◽  
Transmission Electron ◽  
Marked Activity ◽  
Malignant Trophoblast

Human malignant trophoblast cells in continuous culture were incubated for 3 days in medium containing 1 mM N6-O2'-dibutyryl cyclic adenosine 3':5'-monophosphate (dibutyryl cyclic AMP) and 1 mM theophylline. The culture fluid was replenished daily. Stimulated cultures secreted many times more chorionic gonadotropin and estrogens than did control cultures in the absence of increased cellular proliferation. Scanning electron microscopy revealed remarkable surface changes of stimulated cells. Control cells (not stimulated) were smooth or provided with varying numbers of microvilli (Fig. 1). The latter, usually, were short and thin. The surface features of stimulated cells were considerably different. There was marked increase of microvilli which appeared elongated and thick. Many cells were covered with confluent polypoid projections (Fig. 2). Transmission electron microscopy demonstrated marked activity of cytoplasmic organelles. Mitochondria were increased in number and size; some giant forms with numerous cristae were observed.

Vascular adaptations to hypoxia: molecular and cellular mechanisms regulating vascular tone

2007 ◽  
Vol 43 ◽  
pp. 105-120 ◽  
Author(s):  
Michael L. Paffett ◽  
Benjimen R. Walker
Keyword(s):  
Vascular Tone ◽  
Cellular Proliferation ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Hypoxia Inducible Factor ◽  
Systemic Circulation ◽  
Cellular Mechanisms ◽  
Hypoxia Inducible Factor 1 ◽  
Pulmonary Vasoconstriction ◽  
Adaptive Mechanisms ◽  
Adaptive Processes

Several molecular and cellular adaptive mechanisms to hypoxia exist within the vasculature. Many of these processes involve oxygen sensing which is transduced into mediators of vasoconstriction in the pulmonary circulation and vasodilation in the systemic circulation. A variety of oxygen-responsive pathways, such as HIF (hypoxia-inducible factor)-1 and HOs (haem oxygenases), contribute to the overall adaptive process during hypoxia and are currently an area of intense research. Generation of ROS (reactive oxygen species) may also differentially regulate vascular tone in these circulations. Potential candidates underlying the divergent responses between the systemic and pulmonary circulations may include Nox (NADPH oxidase)-derived ROS and mitochondrial-derived ROS. In addition to alterations in ROS production governing vascular tone in the hypoxic setting, other vascular adaptations are likely to be involved. HPV (hypoxic pulmonary vasoconstriction) and CH (chronic hypoxia)-induced alterations in cellular proliferation, ionic conductances and changes in the contractile apparatus sensitivity to calcium, all occur as adaptive processes within the vasculature.

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