Targeted Therapy of Human Breast Cancer by 2-5A-Antisense Directed Against Telomerase RNA

1999 ◽  
Author(s):  
John K. Cowell
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Human Breast Cancer ◽  
Telomerase Rna ◽  
Human Breast

scholarly journals Expression and Function of Phosphodiesterase Type 5 in Human Breast Cancer Cell Lines and Tissues: Implications for Targeted Therapy

2015 ◽  
Vol 22 (9) ◽  
pp. 2271-2282 ◽  
Author(s):  
Stefania Catalano ◽  
Antonella Campana ◽  
Cinzia Giordano ◽  
Balázs Győrffy ◽  
Roberta Tarallo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Phosphodiesterase Type ◽  
And Function

scholarly journals Cellular dormancy in minimal residual disease following targeted therapy

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Jason R. Ruth ◽  
Dhruv K. Pant ◽  
Tien-chi Pan ◽  
Hans E. Seidel ◽  
Sanjeethan C. Baksh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Tumor Cells ◽  
Human Breast Cancer ◽  
Residual Disease ◽  
Residual Tumor ◽  
Human Breast ◽  
Primary Tumors ◽  
Oncogenic Pathway ◽  
Recurrent Tumors

Abstract Background Breast cancer mortality is principally due to tumor recurrence, which can occur following extended periods of clinical remission that may last decades. While clinical latency has been postulated to reflect the ability of residual tumor cells to persist in a dormant state, this hypothesis remains unproven since little is known about the biology of these cells. Consequently, defining the properties of residual tumor cells is an essential goal with important clinical implications for preventing recurrence and improving cancer outcomes. Methods To identify conserved features of residual tumor cells, we modeled minimal residual disease using inducible transgenic mouse models for HER2/neu and Wnt1-driven tumorigenesis that recapitulate cardinal features of human breast cancer progression, as well as human breast cancer cell xenografts subjected to targeted therapy. Fluorescence-activated cell sorting was used to isolate tumor cells from primary tumors, residual lesions following oncogene blockade, and recurrent tumors to analyze gene expression signatures and evaluate tumor-initiating cell properties. Results We demonstrate that residual tumor cells surviving oncogenic pathway inhibition at both local and distant sites exist in a state of cellular dormancy, despite adequate vascularization and the absence of adaptive immunity, and retain the ability to re-enter the cell cycle and give rise to recurrent tumors after extended latency periods. Compared to primary or recurrent tumor cells, dormant residual tumor cells possess unique features that are conserved across mouse models for human breast cancer driven by different oncogenes, and express a gene signature that is strongly associated with recurrence-free survival in breast cancer patients and similar to that of tumor cells in which dormancy is induced by the microenvironment. Although residual tumor cells in both the HER2/neu and Wnt1 models are enriched for phenotypic features associated with tumor-initiating cells, limiting dilution experiments revealed that residual tumor cells are not enriched for cells capable of giving rise to primary tumors, but are enriched for cells capable of giving rise to recurrent tumors, suggesting that tumor-initiating populations underlying primary tumorigenesis may be distinct from those that give rise to recurrence following therapy. Conclusions Residual cancer cells surviving targeted therapy reside in a well-vascularized, desmoplastic microenvironment at both local and distant sites. These cells exist in a state of cellular dormancy that bears little resemblance to primary or recurrent tumor cells, but shares similarities with cells in which dormancy is induced by microenvironmental cues. Our observations suggest that dormancy may be a conserved response to targeted therapy independent of the oncogenic pathway inhibited or properties of the primary tumor, that the mechanisms underlying dormancy at local and distant sites may be related, and that the dormant state represents a potential therapeutic target for preventing cancer recurrence.

scholarly journals Human Breast Cancer Tumor Models: Molecular Imaging of Drug Susceptibility and Dosing during HER2/neu-targeted Therapy

Radiology ◽  
2008 ◽  
Vol 248 (3) ◽  
pp. 925-935 ◽  
Author(s):  
Michael S. Gee ◽  
Rabi Upadhyay ◽  
Henry Bergquist ◽  
Herlen Alencar ◽  
Fred Reynolds ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Molecular Imaging ◽  
Human Breast Cancer ◽  
Drug Susceptibility ◽  
Human Breast ◽  
Tumor Models ◽  
Cancer Tumor

Mechanisms of Disease: understanding resistance to HER2-targeted therapy in human breast cancer

2006 ◽  
Vol 3 (5) ◽  
pp. 269-280 ◽  
Author(s):  
Rita Nahta ◽  
Dihua Yu ◽  
Mien-Chie Hung ◽  
Gabriel N Hortobagyi ◽  
Francisco J Esteva
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Disease Understanding

Dyskerin expression influences the level of ribosomal RNA pseudo-uridylation and telomerase RNA component in human breast cancer

2006 ◽  
Vol 210 (1) ◽  
pp. 10-18 ◽  
Author(s):  
L Montanaro ◽  
M Brigotti ◽  
J Clohessy ◽  
S Barbieri ◽  
C Ceccarelli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ribosomal Rna ◽  
Human Breast Cancer ◽  
Telomerase Rna ◽  
Human Breast

scholarly journals Advancements in Human Breast Cancer Targeted Therapy and Immunotherapy

2021 ◽  
Vol 12 (23) ◽  
pp. 6949-6963
Author(s):  
Mayassa J. Bou-Dargham ◽  
Sophia Draughon ◽  
Vance Cantrell ◽  
Zahraa I. Khamis ◽  
Qing-Xiang Amy Sang
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Cancer Targeted Therapy
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