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Article ; Online: Repurposed Drugs Trials for Ovarian Cancer.

DiFeo, Analisa

2019 Volume 25, Issue 2, Page(s) 149–152

MeSH term(s)	Clinical Trials as Topic ; Diabetes Mellitus, Type 2/drug therapy ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Hypoglycemic Agents/pharmacology ; Metformin/pharmacology ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/epidemiology ; Proportional Hazards Models
Chemical Substances	Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Hypoglycemic Agents ; Metformin (9100L32L2N)
Language	English
Publishing date	2019-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2018400-1
ISSN	1540-336X ; 1528-9117 ; 1081-4442
ISSN (online)	1540-336X
ISSN	1528-9117 ; 1081-4442
DOI	10.1097/PPO.0000000000000366
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Zs.A 4470: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The Molecular 'Myc-anisms' Behind Myc-Driven Tumorigenesis and the Relevant Myc-Directed Therapeutics.

McAnulty, Jessica / DiFeo, Analisa

International journal of molecular sciences

2020 Volume 21, Issue 24

Abstract: ... ...

Abstract	MYC
MeSH term(s)	Antineoplastic Agents/pharmacology ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Cell Cycle/drug effects ; Dimerization ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Molecular Targeted Therapy/methods ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Protein Stability/drug effects ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Synthetic Lethal Mutations/genetics ; Up-Regulation
Chemical Substances	Antineoplastic Agents ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; MAX protein, human ; Proto-Oncogene Proteins c-myc
Language	English
Publishing date	2020-12-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21249486
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Article ; Online: The Molecular ‘Myc-anisms’ Behind Myc-Driven Tumorigenesis and the Relevant Myc-Directed Therapeutics

Jessica McAnulty / Analisa DiFeo

International Journal of Molecular Sciences, Vol 21, Iss 9486, p

2020 Volume 9486

Abstract: MYC , a well-studied proto-oncogene that is overexpressed in >20% of tumors across all cancers, is classically known as “undruggable” due to its crucial roles in cell processes and its lack of a drug binding pocket. Four decades of research and ... ...

Abstract	MYC , a well-studied proto-oncogene that is overexpressed in >20% of tumors across all cancers, is classically known as “undruggable” due to its crucial roles in cell processes and its lack of a drug binding pocket. Four decades of research and creativity led to the discovery of a myriad of indirect (and now some direct!) therapeutic strategies targeting Myc. This review explores the various mechanisms in which Myc promotes cancer and highlights five key therapeutic approaches to disrupt Myc, including transcription, Myc-Max dimerization, protein stability, cell cycle regulation, and metabolism, in order to develop more specific Myc-directed therapies.
Keywords	myc ; cancer ; inhibitors ; transcription ; stability ; max ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2020-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Integrated stress response plasticity governs normal cell adaptation to chronic stress via the PP2A-TFE3-ATF4 pathway.

Avelar, Rita A / Gupta, Riya / Carvette, Gracie / da Veiga Leprevost, Felipe / Colina, Jose / Teitel, Jessica / Nesvizhskii, Alexey I / O'Connor, Caitlin M / Hatzoglou, Maria / Shenolikar, Shirish / Arvan, Peter / Narla, Goutham / DiFeo, Analisa

Research square

2024

Abstract: The integrated stress response (ISR) regulates cell fate during conditions of stress by leveraging the cell's capacity to endure sustainable and efficient adaptive stress responses. Protein phosphatase 2A (PP2A) activity modulation has been shown to be ... ...

Abstract	The integrated stress response (ISR) regulates cell fate during conditions of stress by leveraging the cell's capacity to endure sustainable and efficient adaptive stress responses. Protein phosphatase 2A (PP2A) activity modulation has been shown to be successful in achieving both therapeutic efficacy and safety across various cancer models; however, the molecular mechanisms driving its selective antitumor effects remain unclear. Here, we show for the first time that ISR plasticity relies on PP2A activation to regulate drug response and dictate cellular fate under conditions of chronic stress. We demonstrate that genetic and chemical modulation of the PP2A leads to chronic proteolytic stress and triggers an ISR to dictate cell fate. More specifically, we uncovered that the PP2A-TFE3-ATF4 pathway governs ISR cell plasticity during endoplasmic reticular and cellular stress independent of the unfolded protein response. We further show that normal cells reprogram their genetic signatures to undergo ISR-mediated adaptation and homeostatic recovery thereby successfully avoiding toxicity following PP2A-mediated stress. Conversely, oncogenic specific cytotoxicity induced by chemical modulation of PP2A is achieved by activating chronic and irreversible ISR in cancer cells. Our findings propose that a differential response to chemical modulation of PP2A is determined by intrinsic ISR plasticity, providing a novel biological vulnerability to selectively induce cancer cell death and improve targeted therapeutic efficacy.
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-4013396/v1
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Article: Cooperativity of c-MYC with Krüppel-Like Factor 6 Splice Variant 1 induces phenotypic plasticity and promotes prostate cancer progression and metastasis.

Izadmehr, Sudeh / Fernandez-Hernandez, Heriberto / Wiredja, Danica / Kirschenbaum, Alexander / Lee-Poturalski, Christine / Tavassoli, Peyman / Yao, Shen / Schlatzer, Daniela / Hoon, Divya / Difeo, Analisa / Levine, Alice C / Mosquera, Juan-Miguel / Galsky, Matthew D / Cordon-Cardo, Carlos / Narla, Goutham

bioRxiv : the preprint server for biology

2024

Abstract: Metastasis remains a major cause of morbidity and mortality in men with prostate cancer, and the functional impact of the genetic alterations, alone or in combination, driving metastatic disease remains incompletely understood. The proto-oncogene c-MYC, ... ...

Abstract	Metastasis remains a major cause of morbidity and mortality in men with prostate cancer, and the functional impact of the genetic alterations, alone or in combination, driving metastatic disease remains incompletely understood. The proto-oncogene c-MYC, commonly deregulated in prostate cancer. Transgenic expression of c-MYC is sufficient to drive the progression to prostatic intraepithelial neoplasia and ultimately to moderately differentiated localized primary tumors, however, c-MYC-driven tumors are unable to progress through the metastatic cascade, suggesting that a "second-hit" is necessary in the milieu of aberrant c-MYC-driven signaling. Here, we identified cooperativity between c-MYC and KLF6-SV1, an oncogenic splice variant of the KLF6 gene. Transgenic mice that co-expressed KLF6-SV1 and c-MYC developed progressive and metastatic prostate cancer with a histological and molecular phenotype like human prostate cancer. Silencing c-MYC expression significantly reduced tumor burden in these mice supporting the necessity for c-MYC in tumor maintenance. Unbiased global proteomic analysis of tumors from these mice revealed significantly enriched vimentin, a dedifferentiation and pro-metastatic marker, induced by KLF6-SV1. c-MYC-positive tumors were also significantly enriched for KLF6-SV1 in human prostate cancer specimens. Our findings provide evidence that KLF6-SV1 is an enhancer of c-MYC-driven prostate cancer progression and metastasis, and a correlated genetic event in human prostate cancer with potential translational significance.
Language	English
Publishing date	2024-02-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.30.577982
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Article ; Online: Effects of Metformin on Cellular Proliferation and Steroid Hormone Receptors in Patient-Derived, Low-Grade Endometrial Cancer Cell Lines.

Collins, Gretchen / Mesiano, Sam / DiFeo, Analisa

Reproductive sciences (Thousand Oaks, Calif.)

2018 Volume 26, Issue 5, Page(s) 609–618

Abstract: Endometrial cancer (EC) is the most common gynecologic malignancy and is the result of disruption of the balance between estrogen-stimulated growth and progesterone-induced growth modulation. Metformin has been shown to inhibit EC proliferation; however, ...

Abstract	Endometrial cancer (EC) is the most common gynecologic malignancy and is the result of disruption of the balance between estrogen-stimulated growth and progesterone-induced growth modulation. Metformin has been shown to inhibit EC proliferation; however, its role in early-stage EC and its effects on steroid hormone receptors have not been adequately explored. Our aim was to examine the effects of metformin on cellular proliferation in patient-derived, low-grade EC cell lines and to determine whether it directly modulates steroid hormone receptor expression. Two novel EC cell lines were produced (EM2 and 3) from endometrial tumor tissue obtained from women undergoing surgery. Cellular proliferation was determined by the 3-(4,5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide assay, and in both cell lines, metformin decreased cell proliferation in a dose-dependent (10-200 µmol/L) manner and induced apoptosis as measured by cleaved PARP. Furthermore, metformin abrogated the effects of E2 on cell proliferation. Using quantitative real-time polymerase chain reaction and Western immunoblotting, metformin significantly decreased estrogen receptor (ER) α messenger RNA abundance but did not consistently affect the expression of progesterone receptor. Estrogen receptor α protein levels significantly decreased across all metformin doses tested, which resulted in a significant decrease in the expression of the ER targets genes Keratin-19 and Wnt-1 inducible signaling pathway 2. In addition, metformin increased phosphorylation of AMPK in a dose-dependent manner (10-200 µmol/L) indicating an effect on mammalian target of rapamycin (mTOR) signaling. Our data suggest that metformin therapy represents a potential fertility-sparing option for women with early-stage EC, given its capacity to inhibit EC cell proliferation, ERα expression, and the mTOR cell proliferation pathway.
MeSH term(s)	Aged ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Dose-Response Relationship, Drug ; Endometrial Neoplasms/metabolism ; Estrogen Receptor alpha/metabolism ; Female ; Humans ; Metformin/administration & dosage ; Neoplasm Grading ; RNA, Messenger/metabolism ; Receptors, Progesterone/metabolism ; Signal Transduction/drug effects
Chemical Substances	ESR1 protein, human ; Estrogen Receptor alpha ; RNA, Messenger ; Receptors, Progesterone ; Metformin (9100L32L2N)
Language	English
Publishing date	2018-05-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2276411-2
ISSN	1933-7205 ; 1933-7191
ISSN (online)	1933-7205
ISSN	1933-7191
DOI	10.1177/1933719118779734
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Zs.A 4113: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: miR-181a modulates circadian rhythm in immortalized bone marrow and adipose derived stromal cells and promotes differentiation through the regulation of PER3.

Knarr, Matthew / Nagaraj, Anil Belur / Kwiatkowski, Lily J / DiFeo, Analisa

Scientific reports

2019 Volume 9, Issue 1, Page(s) 307

Abstract: miRNAs are important regulators of diverse cellular processes including proliferation, apoptosis, and differentiation. In the context of bone marrow derived stromal cell and adipose derived stromal cell differentiation, miRNAs are established regulators ... ...

Abstract	miRNAs are important regulators of diverse cellular processes including proliferation, apoptosis, and differentiation. In the context of bone marrow derived stromal cell and adipose derived stromal cell differentiation, miRNAs are established regulators of both differentiation or stemness depending on their target. Furthermore, miRNA dysregulation can play a key role in various disease states. Here we show that miR-181a is regulated in a circadian manner and is induced during both immortalized bone marrow derived stromal cell (iBMSC) as well as primary patient adipose derived stromal cell (PASC) adipogenesis. Enhanced expression of miR-181a in iBMSCs and PASCs produced a robust increase in adipogenesis through the direct targeting of the circadian factor period circadian regulator 3 (PER3). Furthermore, we show that knocking down endogenous miR-181a expression in iBMSC has a profound inhibitory effect on iBMSC adipogenesis through its regulation of PER3. Additionally, we found that miR-181a regulates the circadian dependency of the adipogenesis master regulator PPARγ. Taken together, our data identify a previously unknown functional link between miR-181a and the circadian machinery in immortalized bone marrow stromal cells and adipose derived stromal cells highlighting its importance in iBMSC and ASC adipogenesis and circadian biology.
MeSH term(s)	Adipogenesis ; Adipose Tissue/cytology ; Animals ; Bone Marrow Cells/cytology ; Cell Differentiation/drug effects ; Cell Line ; Cells, Cultured ; Circadian Rhythm/drug effects ; Humans ; MicroRNAs/pharmacology ; MicroRNAs/physiology ; Period Circadian Proteins/drug effects ; Period Circadian Proteins/physiology ; Stromal Cells/metabolism
Chemical Substances	MIrn181 microRNA, human ; MicroRNAs ; PER3 protein, human ; Period Circadian Proteins
Language	English
Publishing date	2019-01-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-36425-w
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Mistletoe Extract Viscum Fraxini-2 for Treatment of Advanced Hepatocellular Carcinoma: A Case Series.

Lee, Richard T / Yang, Peiying / Alahmadi, Asrar / McQuade, Jennifer / Yuan, Eric / Difeo, Analisa / Narla, Goutham / Kaseb, Ahmed

Case reports in oncology

2021 Volume 14, Issue 1, Page(s) 224–231

Abstract: Background: Hepatocellular carcinoma (HCC) is the fourth leading cause of death from cancer worldwide, and for advanced HCC the prognosis is poor. Preliminary studies indicate mistletoe extracts may have anticancer activity for HCC.: Methods: A ... ...

Abstract	Background: Hepatocellular carcinoma (HCC) is the fourth leading cause of death from cancer worldwide, and for advanced HCC the prognosis is poor. Preliminary studies indicate mistletoe extracts may have anticancer activity for HCC. Methods: A prospective observational case series of advanced HCC patients that chose to take a mistletoe extract called viscum fraxini-2 (VF-2) alone for treatment. Time on treatment, imaging, and laboratory values were collected for descriptive analyses. Results: A total of 12 patients with advanced HCC enrolled onto the protocol, and 10 patients had data available for evaluation. The majority were male (10/12) with a median age of 64 (SD 11). Most patients had received sorafenib therapy (9/12) and had varying Child-Pugh classes (A-4, B-6, C-2). Treatment with VF-2 ranged from 1 to 36 weeks with a mean of 12.3 weeks (SD 12). Six patients received 8 weeks of treatment, and 3 patients received 12 or more weeks of treatment. For patients that received at least 4 weeks of treatment, the average AFP value stabilized during the first 4 weeks of treatment. Two patients experienced an AFP decrease of >30%, approximately 37 and 40% decreases at the nadir. One patient had stable disease of 9 months. Major side effects were fever, fatigue, rash, and local injection site reaction of swelling, redness, and tenderness. Conclusion: This case series of advanced HCC indicates that mistletoe extract VF-2 may have potential biological activity against HCC for selected patients. Research is needed to identify the active compound and predictive markers of response.
Language	English
Publishing date	2021-03-01
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2458961-5
ISSN	1662-6575
ISSN	1662-6575
DOI	10.1159/000511566
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Article: Detection of Tumor-Specific PTPmu in Gynecological Cancer and Patient Derived Xenografts.

Vincent, Jason / Craig, Sonya E L / Johansen, Mette L / Narla, Jyosthna / Avril, Stefanie / DiFeo, Analisa / Brady-Kalnay, Susann M

Diagnostics (Basel, Switzerland)

2021 Volume 11, Issue 2

Abstract: Background: We developed a fluorophore-conjugated peptide agent, SBK4, that detects a tumor-specific proteolyzed form of the cell adhesion molecule, PTPmu, found in the tumor microenvironment. We previously demonstrated its tissue specific distribution ... ...

Abstract	Background: We developed a fluorophore-conjugated peptide agent, SBK4, that detects a tumor-specific proteolyzed form of the cell adhesion molecule, PTPmu, found in the tumor microenvironment. We previously demonstrated its tissue specific distribution in high-grade brain tumors. To extend those studies to other aggressive solid tumor types, we assessed the tissue distribution of PTPmu/SBK4 in a set of matched gynecologic cancer patient derived xenografts (PDXs) and primary patient tumors, as well as a limited cohort of tumors from gynecological cancer patients. PDXs isolated from the tissues of cancer patients have been shown to yield experimentally manipulatable models that replicate the clinical characteristics of individual patients' tumors. In this study, gynecological cancer PDXs and patient biopsies were examined to determine if tumor-specific proteolyzed PTPmu was present. Methods: We used the peptide agent SBK4 conjugated to the fluorophore Texas Red (TR) to label tumor tissue microarrays (TMAs) containing patient and/or PDX samples from several high-grade gynecologic cancer types, and quantified the level of staining with Image J. In one TMA, we were able to directly compare the patient and the matched PDX tissue on the same slide. Results: While normal tissue had very little SBK4-TR staining, both primary tumor tissue and PDXs have higher labeling with SBK4-TR. Matched PDXs and patient samples from high-grade endometrial and ovarian cancers demonstrated higher levels of PTPmu by staining with SBK4 than normal tissue. Conclusion: In this sample set, all PDXs and high-grade ovarian cancer samples had increased labeling by SBK4-TR compared with the normal controls. Our results indicate that proteolyzed PTPmu and its novel peptide detection agent, SBK4, allow for the visualization of tumor-specific changes in cell adhesion molecules by tissue-based staining, providing a rationale for further development as an imaging agent in aggressive solid tumors, including gynecological cancers.
Language	English
Publishing date	2021-01-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662336-5
ISSN	2075-4418
ISSN	2075-4418
DOI	10.3390/diagnostics11020181
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Article ; Online: Detection of Tumor-Specific PTPmu in Gynecological Cancer and Patient Derived Xenografts

Jason Vincent / Sonya E. L. Craig / Mette L. Johansen / Jyosthna Narla / Stefanie Avril / Analisa DiFeo / Susann M. Brady-Kalnay

Diagnostics, Vol 11, Iss 2, p

2021 Volume 181

Abstract	Background: We developed a fluorophore-conjugated peptide agent, SBK4, that detects a tumor-specific proteolyzed form of the cell adhesion molecule, PTPmu, found in the tumor microenvironment. We previously demonstrated its tissue specific distribution in high-grade brain tumors. To extend those studies to other aggressive solid tumor types, we assessed the tissue distribution of PTPmu/SBK4 in a set of matched gynecologic cancer patient derived xenografts (PDXs) and primary patient tumors, as well as a limited cohort of tumors from gynecological cancer patients. PDXs isolated from the tissues of cancer patients have been shown to yield experimentally manipulatable models that replicate the clinical characteristics of individual patients’ tumors. In this study, gynecological cancer PDXs and patient biopsies were examined to determine if tumor-specific proteolyzed PTPmu was present. Methods: We used the peptide agent SBK4 conjugated to the fluorophore Texas Red (TR) to label tumor tissue microarrays (TMAs) containing patient and/or PDX samples from several high-grade gynecologic cancer types, and quantified the level of staining with Image J. In one TMA, we were able to directly compare the patient and the matched PDX tissue on the same slide. Results: While normal tissue had very little SBK4-TR staining, both primary tumor tissue and PDXs have higher labeling with SBK4-TR. Matched PDXs and patient samples from high-grade endometrial and ovarian cancers demonstrated higher levels of PTPmu by staining with SBK4 than normal tissue. Conclusion: In this sample set, all PDXs and high-grade ovarian cancer samples had increased labeling by SBK4-TR compared with the normal controls. Our results indicate that proteolyzed PTPmu and its novel peptide detection agent, SBK4, allow for the visualization of tumor-specific changes in cell adhesion molecules by tissue-based staining, providing a rationale for further development as an imaging agent in aggressive solid tumors, including gynecological cancers.
Keywords	cancer ; ovarian cancer ; endometrial cancer ; biomarker ; protein tyrosine phosphatase ; PTP ; Medicine (General) ; R5-920
Subject code	616 ; 610
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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