The role of autologous hematopoietic progenitor and cell reinfusion for intensive chemotherapy in women with poor-prognosis breast cancer. Clinical studies with ex-vivo expanded cells produced with the Aastrom Replicell® technology

1999 ◽  
Vol 41 (2) ◽  
pp. 78-81 ◽  
Author(s):  
C. Chabannon ◽  
G. Novakovitch ◽  
J.-L. Blache ◽  
S. Olivero ◽  
J. Camerlo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Clinical Studies ◽  
Poor Prognosis ◽  
Ex Vivo ◽  
Intensive Chemotherapy ◽  
Hematopoietic Progenitor

scholarly journals Implications of TGFβ Signaling and CDK Inhibition for the Treatment of Breast Cancer

Cancers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 5343
Author(s):  
Joseph T. Decker ◽  
Jeffrey A. Ma ◽  
Lonnie D. Shea ◽  
Jacqueline S. Jeruss
Keyword(s):  
Breast Cancer ◽  
Poor Prognosis ◽  
Cell Cycle Control ◽  
Tgfβ Signaling ◽  
Cyclin Dependent Kinases ◽  
C Terminus ◽  
Smad3 Phosphorylation ◽  
Tumor Suppressive Function ◽  
Regulatory Actions

TGFβ signaling enacts tumor-suppressive functions in normal cells through promotion of several cell regulatory actions including cell-cycle control and apoptosis. Canonical TGFβ signaling proceeds through phosphorylation of the transcription factor, SMAD3, at the C-terminus of the protein. During oncogenic progression, this tumor suppressant phosphorylation of SMAD3 can be inhibited. Overexpression of cyclins D and E, and subsequent hyperactivation of cyclin-dependent kinases 2/4 (CDKs), are often observed in breast cancer, and have been associated with poor prognosis. The noncanonical phosphorylation of SMAD3 by CDKs 2 and 4 leads to the inhibition of tumor-suppressive function of SMAD3. As a result, CDK overactivation drives oncogenic progression, and can be targeted to improve clinical outcomes. This review focuses on breast cancer, and highlights advances in the understanding of CDK-mediated noncanonical SMAD3 phosphorylation. Specifically, the role of aberrant TGFβ signaling in oncogenic progression and treatment response will be examined to illustrate the potential for therapeutic discovery in the context of cyclins/CDKs and SMAD3.

scholarly journals Loss of HOXB3 promotes development of hormone receptor negative breast cancer

2020 ◽  
Author(s):  
Lizhe Zhu ◽  
Shibo Yu ◽  
Siyuan Jiang ◽  
Guanqun Ge ◽  
Yu Yan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Western Blot ◽  
Cell Line ◽  
Hormone Receptor ◽  
Poor Prognosis ◽  
Cancer Gene ◽  
Qrt Pcr ◽  
Lower Expression ◽  
Breast Cancer Gene

Abstract BackgroundThe homobox (HOX) gene family as a transcription factor encoding a specific nuclear protein is essential for embryonic development, differentiation, and homeostasis. The role of HOXB3 protein varies in different tumors. This study aims to explore the role of the HOXB3 gene in breast cancer.MethodDifferentiated expressed genes were screened by analyzing metastatic breast cancer gene chip data in TCGA and GEO database. The function of selected HOXB3 gene was also analyzed by GEPIA, Kaplan-Meier Plotter, Breast Cancer Gene-Expression Miner and metascape. Molecular biology methods such as qRT-PCR, western blot and IF was used to verify bio-informatics findings.ResultsBoth bio-informatics analyses and western blot showed that HOXB3 was lost in breast cancer compared to normal breast tissue. Survival analysis also showed that lower expression of HOXB3 was associated with poor prognosis. Bio-informatics analyses further showed that HOXB3 was positively correlated with hormone receptors. qRT-PCR, immunofluorescence and western blot also confirmed that HOXB3 had the highest expression in the immortalized breast epithelial cell line MCF-10A, lower in luminal breast cancer cell line T47D and the lowest in triple negative breast cancer (TNBC) cell line MDA-MB-231. Metascape for GO analysis of GEO data provided possible mechanism that HOXB3 could positively regulate cell adhesion, inhibit cell proliferation and activate immune response in breast cancer, and considered that HOXB3 might cause cell malignant transformation through the above pathways.ConclusionIn summary, HOXB3 expression was decreased in breast cancer, especially in hormone receptor-negative breast cancer. The lower expression of HOXB3 was associated with poor prognosis. It might become a new biomarker to predict prognosis of breast cancer.

High-dose paclitaxel, cyclophosphamide, and cisplatin with autologous hematopoietic progenitor-cell support: a phase I trial.

1996 ◽  
Vol 14 (5) ◽  
pp. 1463-1472 ◽  
Author(s):  
S M Stemmer ◽  
P J Cagnoni ◽  
E J Shpall ◽  
S I Bearman ◽  
S Matthes ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ovarian Cancer ◽  
Poor Prognosis ◽  
Progenitor Cell ◽  
Multiorgan Failure ◽  
Metastatic Breast ◽  
Hematopoietic Progenitor Cell ◽  
High Dose ◽  
Hematopoietic Progenitor ◽  
Cell Support

PURPOSE To determine the maximal-tolerated dose (MTD) of paclitaxel in combination with high-dose cyclophosphamide (CPA) and cisplatin (cDDP) followed by autologous hematopoietic progenitor-cell support (AHPCS). PATIENTS AND METHODS Forty-nine patients with poor-prognosis breast cancer, non-Hodgkin's lymphoma (NHL), or ovarian cancer were treated with escalating doses of paclitaxel infused over 24 hours, followed by CPA (5,625 mg/m2 intravenously over 1 hour in three divided doses) and cDDP (165 mg/m2 intravenously as a continuous infusion over 72 hours) and AHPCS. Pharmacokinetic measurements for each drug were performed. RESULTS Dose-limiting toxicities were encountered in two patients at 825 mg/m2 of paclitaxel; one patient died of multiorgan failure that involved the lung, CNS, and kidneys, and the other developed grade 3 respiratory, CNS, and renal toxicity, which resolved. The MTD of this combination was determined to be paclitaxel 775 mg/m2, CPA 5,625 mg/m2, and cDDP 165 mg/m2 followed by AHPCS. Sensory polyneuropathy and mucositis were prominent toxicities, but both were reversible and tolerable. The pharmacokinetics of paclitaxel correlated significantly with the severity of mucositis (P < .001) and peripheral neuropathy (P < .00004). Eighteen of 33 patients (54%) with measurable, heavily pretreated metastatic breast cancer achieved a partial response (PR). Responses were also observed in patients with NHL (four of five patients) and ovarian cancer (two of two). CONCLUSION It is possible to escalate the dose of paclitaxel to 775 mg/m2 in combination with 5,625 mg/m2 of CPA, 165 mg/m2 of cDDP, and AHPCS. An encouraging response rate in poor-prognosis patients with breast cancer, NHL, and ovarian cancer warrants further study.

1215 Role of cooperative groups and funding source in clinical studies that support approved therapy for breast cancer

2015 ◽  
Vol 51 ◽  
pp. S176-S177 ◽  
Author(s):  
G. Anguera ◽  
A. Tibau ◽  
F. Andrés-Pretel ◽  
M. Andrés ◽  
B. Seruga ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Clinical Studies ◽  
Funding Source ◽  
Cooperative Groups

scholarly journals The Role of PPARγ Ligands in Breast Cancer: From Basic Research to Clinical Studies

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2623
Author(s):  
Giuseppina Augimeri ◽  
Cinzia Giordano ◽  
Luca Gelsomino ◽  
Pierluigi Plastina ◽  
Ines Barone ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Clinical Studies ◽  
Molecular Mechanisms ◽  
Basic Research ◽  
Therapeutic Effects ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Natural And Synthetic

Peroxisome proliferator-activated receptor gamma (PPARγ), belonging to the nuclear receptor superfamily, is a ligand-dependent transcription factor involved in a variety of pathophysiological conditions such as inflammation, metabolic disorders, cardiovascular disease, and cancers. In this latter context, PPARγ is expressed in many tumors including breast cancer, and its function upon binding of ligands has been linked to the tumor development, progression, and metastasis. Over the last decade, much research has focused on the potential of natural agonists for PPARγ including fatty acids and prostanoids that act as weak ligands compared to the strong and synthetic PPARγ agonists such as thiazolidinedione drugs. Both natural and synthetic compounds have been implicated in the negative regulation of breast cancer growth and progression. The aim of the present review is to summarize the role of PPARγ activation in breast cancer focusing on the underlying cellular and molecular mechanisms involved in the regulation of cell proliferation, cell cycle, and cell death, in the modulation of motility and invasion as well as in the cross-talk with other different signaling pathways. Besides, we also provide an overview of the in vivo breast cancer models and clinical studies. The therapeutic effects of natural and synthetic PPARγ ligands, as antineoplastic agents, represent a fascinating and clinically a potential translatable area of research with regards to the battle against cancer.

Ex-vivo expansion of hematopoietic progenitor cells: preliminary results in breast cancer

1999 ◽  
Vol 41 (2) ◽  
pp. 82-86 ◽  
Author(s):  
I. McNiece ◽  
R. Jones ◽  
P. Cagnoni ◽  
S. Bearman ◽  
Y. Nieto ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Progenitor Cells ◽  
Ex Vivo ◽  
Ex Vivo Expansion ◽  
Hematopoietic Progenitor Cells ◽  
Hematopoietic Progenitor ◽  
Preliminary Results

scholarly journals Frailty syndrome. What physicians and cardiologists need to know?

2020 ◽  
Vol 92 (1) ◽  
pp. 62-68
Author(s):  
K E Krivoshapova ◽  
E A Vegner ◽  
O L Barbarash
Keyword(s):  
Clinical Studies ◽  
Poor Prognosis ◽  
Independent Predictor ◽  
Treatment Strategies ◽  
Frailty Syndrome ◽  
Primary And Secondary Prevention ◽  
The Poor ◽  
Clinical Syndromes ◽  
Complicated Course

The review presents the data and evidences from recent clinical studies on the frailty syndrome - one of the most relevant clinical syndromes, though not studied well yet. The latest data on the prevalence of frailty and various factors contributing to its onset are reported. The presence of frailty is considered as an independent predictor of poor prognosis and high mortality rate. The role of frailty in the development of cardiovascular diseases, their progression and complicated course has been analyzed using the latest studies. In addition, the tendency towards higher incidence of frailty among the population of different countries and the poor prognosis of frail patients requires a series of clinical studies aimed at developing measures for primary and secondary prevention, as well as effective treatment strategies for frailty. The PubMed was used for a literature review.

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