scholarly journals STAT Transcription Factors in Tumor Development and Targeted Therapy of Malignancies

10.5772/54893 ◽  
2013 ◽  
Author(s):  
Gordana Konjevic ◽  
Sandra Radenkovic ◽  
Ana Vuletic ◽  
Katarina Mirjacic ◽  
Vladimir Jurisic ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Targeted Therapy ◽  
Tumor Development

Transcription Factors in the Control of Tumor Development and Progression by TGF-β Signaling

2004 ◽  
pp. 167-207
Author(s):  
I. Timokhina ◽  
J. Lecanda ◽  
M. Kretzschmar
Keyword(s):  
Transcription Factors ◽  
Tumor Development

scholarly journals Familial Breast Cancer - Targeted Therapy in Secondary and Tertiary Prevention

Breast Care ◽  
2015 ◽  
Vol 10 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Karin Kast ◽  
Kerstin Rhiem
Keyword(s):  
Breast Cancer ◽  
Ovarian Cancer ◽  
Monoclonal Antibody ◽  
Targeted Therapy ◽  
Tumor Development ◽  
Treatment Decision ◽  
Standard Of Care ◽  
Breast And Ovarian Cancer ◽  
Treatment Decision Making ◽  
Receptor Modulator

The introduction of an increasing number of individualized molecular targeted therapies into clinical routine mirrors their importance in modern cancer prevention and treatment. Well-known examples for targeted agents are the monoclonal antibody trastuzumab and the selective estrogen receptor modulator tamoxifen. The identification of an unaltered gene in tumor tissue in colon cancer (KRAS) is a predictor for the patient's response to targeted therapy with a monoclonal antibody (cetuximab). Targeted therapy for hereditary breast and ovarian cancer has become a reality with the approval of olaparib for platin-sensitive late relapsed BRCA-associated ovarian cancer in December 2014. This manuscript reviews the status quo of poly-ADP-ribose polymerase inhibitors (PARPi) in the therapy of breast and ovarian cancer as well as the struggle for carboplatin as a potential standard of care for triple-negative and, in particular, BRCA-associated breast cancer. Details of the mechanism of action with information on tumor development are provided, and an outlook for further relevant research is given. The efficacy of agents against molecular targets together with the identification of an increasing number of cancer-associated genes will open the floodgates to a new era of treatment decision-making based on molecular tumor profiles. Current clinical trials involving patients with BRCA-associated cancer explore the efficacy of the molecular targeted therapeutics platinum and PARPi.

scholarly journals Discovery of Transcription Factors and Regulatory Regions Driving In Vivo Tumor Development by ATAC-seq and FAIRE-seq Open Chromatin Profiling

PLoS Genetics ◽  
2015 ◽  
Vol 11 (2) ◽  
pp. e1004994 ◽  
Author(s):  
Kristofer Davie ◽  
Jelle Jacobs ◽  
Mardelle Atkins ◽  
Delphine Potier ◽  
Valerie Christiaens ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Tumor Development ◽  
Open Chromatin ◽  
Regulatory Regions ◽  
Chromatin Profiling

scholarly journals Targeted Therapy of DNA Tumor Virus-Associated Cancers Using Virus-Activated Transcription Factors

2006 ◽  
Vol 13 (5) ◽  
pp. 899-909 ◽  
Author(s):  
Mi Jung Lim ◽  
Sang-Hyun Min ◽  
Jae-Jung Lee ◽  
Il Chul Kim ◽  
Ji Tae Kim ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Targeted Therapy ◽  
Tumor Virus

scholarly journals Conditional Deletion of Men1 in the Pancreatic β-Cell Leads to Glucagon-Expressing Tumor Development

Endocrinology ◽  
2015 ◽  
Vol 156 (1) ◽  
pp. 48-57 ◽  
Author(s):  
Feng Li ◽  
Yutong Su ◽  
Yulong Cheng ◽  
Xiuli Jiang ◽  
Ying Peng ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Tumor Development ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Pou Domain ◽  
Conditional Deletion ◽  
Cell Specificity ◽  
Insulin Promoter ◽  
Family Protein

Abstract The tumor suppressor menin is recognized as a key regulator of β-cell proliferation. To induce tumorigenesis within the pancreatic β-cells, floxed alleles of Men1 were selectively ablated using Cre-recombinase driven by the insulin promoter. Despite the β-cell specificity of the RipCre, glucagon-expressing tumors as well as insulinomas developed in old mutant mice. These glucagon-expressing tumor cells were menin deficient and expressed the mature α-cell-specific transcription factors Brain-specific homeobox POU domain protein 4 (Brn4) and v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B (MafB). Moreover, the inactivation of β-cell-specific transcription factors was observed in mutant β-cells. Our work shows that Men1 ablation in the pancreatic β-cells leads to the inactivation of specific transcription factors, resulting in glucagon-expressing tumor development, which sheds light on the mechanisms of islet tumorigenesis.

scholarly journals Control of Oxidative Stress in Cancer Chemoresistance: Spotlight on Nrf2 Role

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 510
Author(s):  
Giuseppina Barrera ◽  
Marie Angele Cucci ◽  
Margherita Grattarola ◽  
Chiara Dianzani ◽  
Giuliana Muzio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Antioxidant Response ◽  
Redox Status ◽  
Antioxidant Systems ◽  
Drug Induced ◽  
Transcriptional Coactivators ◽  
Metabolic Remodeling

Chemoresistance represents the main obstacle to cancer treatment with both conventional and targeted therapy. Beyond specific molecular alterations, which can lead to targeted therapy, metabolic remodeling, including the control of redox status, plays an important role in cancer cell survival following therapy. Although cancer cells generally have a high basal reactive oxygen species (ROS) level, which makes them more susceptible than normal cells to a further increase of ROS, chemoresistant cancer cells become highly adapted to intrinsic or drug-induced oxidative stress by upregulating their antioxidant systems. The antioxidant response is principally mediated by the transcription factor Nrf2, which has been considered the master regulator of antioxidant and cytoprotective genes. Nrf2 expression is often increased in several types of chemoresistant cancer cells, and its expression is mediated by diverse mechanisms. In addition to Nrf2, other transcription factors and transcriptional coactivators can participate to maintain the high antioxidant levels in chemo and radio-resistant cancer cells. The control of expression and function of these molecules has been recently deepened to identify which of these could be used as a new therapeutic target in the treatment of tumors resistant to conventional therapy. In this review, we report the more recent advances in the study of Nrf2 regulation in chemoresistant cancers and the role played by other transcription factors and transcriptional coactivators in the control of antioxidant responses in chemoresistant cancer cells.

scholarly journals p63 and p53: Collaborative Partners or Dueling Rivals?

2021 ◽  
Vol 9 ◽  
Author(s):  
Dana L. Woodstock ◽  
Morgan A. Sammons ◽  
Martin Fischer
Keyword(s):  
Transcription Factors ◽  
Cell Fate ◽  
Chromatin Structure ◽  
Paradigm Shift ◽  
Target Genes ◽  
Tumor Development ◽  
Dominant Negative ◽  
Tumor Suppressor P53 ◽  
Common Goal ◽  
Direct Cell

The tumor suppressor p53 and its oncogenic sibling p63 (ΔNp63) direct opposing fates in tumor development. These paralog proteins are transcription factors that elicit their tumor suppressive and oncogenic capacity through the regulation of both shared and unique target genes. Both proteins predominantly function as activators of transcription, leading to a paradigm shift away from ΔNp63 as a dominant negative to p53 activity. The discovery of p53 and p63 as pioneer transcription factors regulating chromatin structure revealed new insights into how these paralogs can both positively and negatively influence each other to direct cell fate. The previous view of a strict rivalry between the siblings needs to be revisited, as p53 and p63 can also work together toward a common goal.

scholarly journals NFAT transcription factors: from cell cycle to tumor development

2005 ◽  
Vol 38 (3) ◽  
pp. 335-344 ◽  
Author(s):  
J.P.B. Viola ◽  
L.D.S. Carvalho ◽  
B.P.F. Fonseca ◽  
L.K. Teixeira
Keyword(s):  
Cell Cycle ◽  
Transcription Factors ◽  
Tumor Development
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