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Article ; Online: Towards Understanding the Development of Breast Cancer: The Role of RhoJ in the Obesity Microenvironment.

Bou Malhab, Lara J / Nair, Vidhya A / Qaisar, Rizwan / Pintus, Gianfranco / Abdel-Rahman, Wael M

2024 Volume 13, Issue 2

Abstract: Obesity is a growing pandemic with an increasing risk of inducing different cancer types, including breast cancer. Adipose tissue is proposed to be a major player in the initiation and progression of breast cancer in obese people. However, the ... ...

Abstract	Obesity is a growing pandemic with an increasing risk of inducing different cancer types, including breast cancer. Adipose tissue is proposed to be a major player in the initiation and progression of breast cancer in obese people. However, the mechanistic link between adipogenicity and tumorigenicity in breast tissues is poorly understood. We used in vitro and in vivo approaches to investigate the mechanistic relationship between obesity and the onset and progression of breast cancer. In obesity, adipose tissue expansion and remodeling are associated with increased inflammatory mediator's release and anti-inflammatory mediators' reduction.. In order to mimic the obesity micro-environment, we cultured cells in an enriched pro-inflammatory cytokine medium to which we added a low concentration of beneficial adipokines. Epithelial cells exposed to the obesity micro-environment were phenotypically transformed into mesenchymal-like cells, characterized by an increase in different mesenchymal markers and the acquisition of the major hallmarks of cancerous cells; these include sustained DNA damage, the activation of the ATR-Chk2 pathway, an increase in proliferation rate, cell invasion, and resistance to conventional chemotherapy. Transcriptomic analysis revealed that several genes, including RhoJ, CCL7, and MMP9, acted as potential major players in the observed phenomenon. The transcriptomics findings were confirmed in vitro using qRT-PCR and in vivo using high-fat-diet-fed mice. Our data suggests RhoJ as a potential novel molecular driver of tumor development in breast tissues and a mediator of cell resistance to conventional chemotherapy through PAK1 activation. These data propose that RhoJ is a potential target for therapeutic interventions in obese breast cancer patients.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Adipokines ; Adiposity ; Breast Neoplasms/etiology ; Breast Neoplasms/genetics ; Obesity/complications ; Tumor Microenvironment ; rho GTP-Binding Proteins/genetics ; rho GTP-Binding Proteins/metabolism
Chemical Substances	Adipokines ; RHOJ protein, human (EC 3.6.1.-) ; Rhoj protein, mouse ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2024-01-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells13020174
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Article ; Online: Clinical and Radiographic Outcomes of Autogenous Inlay Graft vs Autogenous Onlay Graft for Anterior Maxillary Horizontal Ridge Augmentation: A Randomized Control Clinical Study.

Elsayed, Ahmed O / Abdel-Rahman, Fakhreldin H / Ahmed, Wael Mas / Tawfik, Mohamed A-M

The journal of contemporary dental practice

2024 Volume 25, Issue 2, Page(s) 107–113

Abstract: ... to cite this article: Elsayed AO, Abdel-Rahman FH, Ahmed WMAS, ...

Abstract	Aim: This study aimed to compare the efficacy of autogenous onlay and inlay grafts for anterior maxillary horizontal ridge augmentation. Materials and methods: This randomized clinical trial was performed on 14 patients with a deficient partially edentulous anterior maxillary ridge (3-5 mm in width). Patients were randomized and grouped into two equal groups: Group A was treated with symphyseal autogenous bone block, which was placed and fixed buccally as an onlay graft, and group B: was treated with symphyseal autogenous bone block, which was interpositioned and fixed in space created between buccal and lingual cortex as inlay graft. Patients were evaluated clinically and radiographically to evaluate the increase of bone width at [Baseline, immediate postoperative (T0)] and six months post-graft (T6). Results: A total of 14 patients (8 males and 6 females) with age range from 20 to 43 years old with a mean of 42.1 years were involved in our study. Radiographically, there was a significant statistical difference in comparing between two groups for the creation of a horizontal alveolar bone at T0. In the inlay group, the mean preoperative bone width was 3.9 ± 0.3 mm at T0 and 5.7 ± 0.5 mm at T6. While in the onlay group, the mean preoperative bone width was 3.7 ± 0.7 mm at T0 while at T6 the mean bone width was 6.1 ± 0.8 mm. This was statistically significant. Conclusion: Inlay block graft appears to be a successful treatment option for horizontal ridge augmentation in the maxillary arch. Clinical significance: both techniques are viable techniques for augmentation of atrophic alveolar ridge with uneventful healing. How to cite this article: Elsayed AO, Abdel-Rahman FH, Ahmed WMAS,
MeSH term(s)	Male ; Female ; Humans ; Young Adult ; Adult ; Inlays ; Bone Transplantation/methods ; Alveolar Ridge Augmentation/methods ; Alveolar Process/surgery ; Wound Healing ; Maxilla/surgery ; Dental Implantation, Endosseous
Language	English
Publishing date	2024-02-01
Publishing country	India
Document type	Randomized Controlled Trial ; Journal Article
ISSN	1526-3711
ISSN (online)	1526-3711
DOI	10.5005/jp-journals-10024-3634
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Article ; Online: Characterization of the Molecular Alterations Induced by the Prolonged Exposure of Normal Colon Mucosa and Colon Cancer Cells to Low-Dose Bisphenol A.

Nair, Vidhya A / Malhab, Lara J Bou / Abdel-Rahman, Wael M

International journal of molecular sciences

2022 Volume 23, Issue 19

Abstract: Colorectal cancer is a common cancer with a poor prognosis in both males and females. The influence of bisphenol A (BPA), a widely used environmental contaminant, in colon cancer development and progression is not well identified, in spite of the fact ... ...

Abstract	Colorectal cancer is a common cancer with a poor prognosis in both males and females. The influence of bisphenol A (BPA), a widely used environmental contaminant, in colon cancer development and progression is not well identified, in spite of the fact that the most common mode of exposure to BPA is ingestion. The aim of this work is to elucidate the carcinogenic effects of BPA in the colon in vitro. We analyzed BPA's effects on human colon epithelial (HCoEpiC) and colon cancer (HCT116) cells. BPA exerted cytotoxic effects and augmented the 5FU cytotoxicity on both cell lines at high doses, while it did not show this effect at low doses. Therefore, we focused on studying the effects of low-dose (0.0043 nM) exposure on normal colonic epithelial cells for a long period of time (two months), which is more consistent with environmental exposure levels and patterns. BPA increased cellular invasiveness through collagen and the ability to anchorage-independent cell growth, as measured by colony formation in soft agar, which could support oncogenicity. To gain insights into the mechanism of these actions, we performed transcriptomic analysis using next-generation sequencing, which revealed 340 differentially expressed transcripts by BPA in HCT116 and 75 in HCoEpiC. These transcripts belong in many cancer-related pathways such as apoptosis, cell proliferation, signal transduction, and angiogenesis. Some of the significant genes (
MeSH term(s)	Agar ; Benzhydryl Compounds/toxicity ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Fluorouracil ; HCT116 Cells ; HSP27 Heat-Shock Proteins/metabolism ; Humans ; Mucous Membrane/metabolism ; Phenols ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; Tumor Suppressor Protein p53/metabolism ; beta Catenin/metabolism
Chemical Substances	Benzhydryl Compounds ; FAM83H protein, human ; HSP27 Heat-Shock Proteins ; Phenols ; Tumor Suppressor Protein p53 ; beta Catenin ; Agar (9002-18-0) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; bisphenol A (MLT3645I99) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2022-10-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231911620
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Article ; Online: Obesity and Inflammation: Colorectal Cancer Engines.

Bou Malhab, Lara J / Abdel-Rahman, Wael M

Current molecular pharmacology

2021 Volume 15, Issue 4, Page(s) 620–646

Abstract: The prevalence of obesity continues to increase to the extent that it became a worldwide pandemic. An accumulating body of evidence has associated obesity with the development of different types of cancer, including colorectal cancer, which is a ... ...

Abstract	The prevalence of obesity continues to increase to the extent that it became a worldwide pandemic. An accumulating body of evidence has associated obesity with the development of different types of cancer, including colorectal cancer, which is a notorious disease with a high mortality rate. At the molecular level, colorectal cancer is a heterogenous disease characterized by a myriad of genetic and epigenetic alterations associated with various forms of genomic instability (detailed in Supplementary Materials). Recently, the microenvironment has emerged as a major factor in carcinogenesis. Our aim is to define the different molecular alterations leading to the development of colorectal cancer in obese patients with a focus on the role of the microenvironment in carcinogenesis. We also highlight all existent molecules in clinical trials that target the activated pathways in obesity-associated colorectal cancer, whether used as single treatments or in combination. Obesity predisposes to colorectal cancer via creating a state of chronic inflammation with dysregulated adipokines, inflammatory mediators, and other factors such as immune cell infiltration. A unifying theme in obesity-mediated colorectal cancer is the activation of the PI3K/AKT, mTOR/MAPK, and STAT3 signaling pathways. Different inhibitory molecules towards these pathways exist, increasing the therapeutic choice of obesity-associated colon cancer. However, obese patients are more likely to suffer from chemotherapy overdosing. Preventing obesity through maintaining a healthy and active lifestyle remains to be the best remedy.
MeSH term(s)	Carcinogenesis ; Colonic Neoplasms ; Humans ; Inflammation/complications ; Inflammation/metabolism ; Obesity/complications ; Obesity/metabolism ; Phosphatidylinositol 3-Kinases ; Tumor Microenvironment
Language	English
Publishing date	2021-09-01
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1874-4702
ISSN (online)	1874-4702
DOI	10.2174/1874467214666210906122054
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Article ; Online: Highlights on the Role of

Hafezi, Shirin / Saber-Ayad, Maha / Abdel-Rahman, Wael M

International journal of molecular sciences

2021 Volume 22, Issue 19

Abstract: The most frequent mutated oncogene family in the history of human cancer is the RAS gene family, ... ...

Abstract	The most frequent mutated oncogene family in the history of human cancer is the RAS gene family, including
MeSH term(s)	Animals ; Carcinoma, Pancreatic Ductal/complications ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/immunology ; Carcinoma, Pancreatic Ductal/metabolism ; Diabetes Complications/genetics ; Humans ; Pancreatic Neoplasms/complications ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Tumor Microenvironment
Chemical Substances	Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2021-09-23
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/ijms221910219
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Article: Comprehensive analysis of the role of ubiquitin-specific peptidases in colorectal cancer: A systematic review.

Al-Balushi, Eman / Al Marzouqi, Amina / Tavoosi, Shima / Baghsheikhi, Amir Hossein / Sadri, Arash / Aliabadi, Leyla Sharifi / Salarabedi, Mohammad-Mahdi / Rahman, Syed Azizur / Al-Yateem, Nabeel / Jarrahi, Alireza Mosavi / Halimi, Aram / Ahmadvand, Mohammad / Abdel-Rahman, Wael M

World journal of gastrointestinal oncology

2024 Volume 16, Issue 1, Page(s) 197–213

Abstract: Background: Colorectal cancer (CRC) is the third most frequent and the second most fatal cancer. The search for more effective drugs to treat this disease is ongoing. A better understanding of the mechanisms of CRC development and progression may reveal ...

Abstract	Background: Colorectal cancer (CRC) is the third most frequent and the second most fatal cancer. The search for more effective drugs to treat this disease is ongoing. A better understanding of the mechanisms of CRC development and progression may reveal new therapeutic strategies. Ubiquitin-specific peptidases (USPs), the largest group of the deubiquitinase protein family, have long been implicated in various cancers. There have been numerous studies on the role of USPs in CRC; however, a comprehensive view of this role is lacking. Aim: To provide a systematic review of the studies investigating the roles and functions of USPs in CRC. Methods: We systematically queried the MEDLINE ( Results: Our study highlights the pivotal role of various USPs in several processes implicated in CRC: Regulation of the cell cycle, apoptosis, cancer stemness, epithelial-mesenchymal transition, metastasis, DNA repair, and drug resistance. The findings of this study suggest that USPs have great potential as drug targets and noninvasive biomarkers in CRC. The dysregulation of USPs in CRC contributes to drug resistance through multiple mechanisms. Conclusion: Targeting specific USPs involved in drug resistance pathways could provide a novel therapeutic strategy for overcoming resistance to current treatment regimens in CRC.
Language	English
Publishing date	2024-01-16
Publishing country	China
Document type	Journal Article
ZDB-ID	2573696-6
ISSN	1948-5204
ISSN	1948-5204
DOI	10.4251/wjgo.v16.i1.197
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Article ; Online: The Endocrine Disruptor Bisphenol A (BPA) Exerts a Wide Range of Effects in Carcinogenesis and Response to Therapy.

Hafezi, Shirin A / Abdel-Rahman, Wael M

Current molecular pharmacology

2019 Volume 12, Issue 3, Page(s) 230–238

Abstract: Background: Bisphenol A (BPA) is a synthetic plasticizer that is commonly used in the production of polycarbonate plastics and epoxy resins. Human exposure occurs when BPA migrates from food and beverage containers into the contents when heated or even ... ...

Abstract	Background: Bisphenol A (BPA) is a synthetic plasticizer that is commonly used in the production of polycarbonate plastics and epoxy resins. Human exposure occurs when BPA migrates from food and beverage containers into the contents when heated or even under normal conditions of use. BPA exerts endocrine disruptor action due to its weak binding affinity for the estrogen receptors ERα and ERβ. BPA exerts other effects by activating the membrane receptor GPER (GPR30) and/or other receptors such as the estrogen-related receptors (ERRs). Objective: This review summarizes emerging data on BPA and cancer. These include data linking exposure to BPA with an increased risk of hormone-related cancers such as those of the ovary, breast, prostate, and even colon cancer. BPA can also induce resistance to various chemotherapeutics such as doxorubicin, cisplatin, and vinblastine in vitro. The development of chemoresistance to available therapeutics is an emerging significant aspect of BPA toxicity because it worsens the prognosis of many tumors. Conclusion: Recent findings support a causal role of BPA at low levels in the development of cancers and in dictating their response to cytotoxic therapy. Accurate knowledge and consideration of these issues would be highly beneficial to cancer prevention and management.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Benzhydryl Compounds/adverse effects ; Carcinogenesis/chemically induced ; Carcinogenesis/drug effects ; Drug Resistance, Neoplasm/drug effects ; Endocrine Disruptors/adverse effects ; Humans ; Neoplasms/chemically induced ; Neoplasms/diagnosis ; Neoplasms/drug therapy ; Phenols/adverse effects ; Prognosis
Chemical Substances	Antineoplastic Agents ; Benzhydryl Compounds ; Endocrine Disruptors ; Phenols ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2019-03-08
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1874-4702
ISSN (online)	1874-4702
DOI	10.2174/1874467212666190306164507
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Article ; Online: Highlights on the Role of KRAS Mutations in Reshaping the Microenvironment of Pancreatic Adenocarcinoma

Shirin Hafezi / Maha Saber-Ayad / Wael M. Abdel-Rahman

International Journal of Molecular Sciences, Vol 22, Iss 10219, p

2021 Volume 10219

Abstract: The most frequent mutated oncogene family in the history of human cancer is the RAS gene family, including NRAS , HRAS , and, most importantly, KRAS . A hallmark of pancreatic cancer, recalcitrant cancer with a very low survival rate, is the prevalence ... ...

Abstract	The most frequent mutated oncogene family in the history of human cancer is the RAS gene family, including NRAS , HRAS , and, most importantly, KRAS . A hallmark of pancreatic cancer, recalcitrant cancer with a very low survival rate, is the prevalence of oncogenic mutations in the KRAS gene. Due to this fact, studying the function of KRAS and the impact of its mutations on the tumor microenvironment (TME) is a priority for understanding pancreatic cancer progression and designing novel therapeutic strategies for the treatment of the dismal disease. Despite some recent enlightening studies, there is still a wide gap in our knowledge regarding the impact of KRAS mutations on different components of the pancreatic TME. In this review, we will present an updated summary of mutant KRAS role in the initiation, progression, and modulation of the TME of pancreatic ductal adenocarcinoma (PDAC). This review will highlight the intriguing link between diabetes mellitus and PDAC, as well as vitamin D as an adjuvant effective therapy via TME modulation of PDAC. We will also discuss different ongoing clinical trials that use KRAS oncogene signaling network as therapeutic targets.
Keywords	RAS ; adenocarcinoma ; pancreas ; tumor microenvironment ; stellate cells ; cancer-associated fibroblast ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Ramadan Diurnal Intermittent Fasting Is Associated With Attenuated FTO Gene Expression in Subjects With Overweight and Obesity: A Prospective Cohort Study.

Madkour, Mohamed I / Malhab, Lara J Bou / Abdel-Rahman, Wael M / Abdelrahim, Dana N / Saber-Ayad, Maha / Faris, MoezAlIslam E

Frontiers in nutrition

2022 Volume 8, Page(s) 741811

Abstract: ... females, mean age 38.4 ± 11.2 years) subjects with overweight and obesity (BMI = 29.89 ± 5.02 kg/m ...

Abstract	Aim and background: A growing body of evidence supports the impact of intermittent fasting (IF) on normalizing body weight and that the interaction between body genes and environmental factors shapes human susceptibility to developing obesity. Methods: Sixty-three (63) subjects were recruited, of which 57 (17 males and 40 females, mean age 38.4 ± 11.2 years) subjects with overweight and obesity (BMI = 29.89 ± 5.02 kg/m Results: In contrast to normal BMI subjects, the relative gene expressions in overweight/obese were significantly decreased at the end of Ramadan (-32.30%, 95% CI-0.052 -0.981) in comparison with the pre-fasting state. Significant reductions were found in body weight, BMI, fat mass, body fat percent, hip circumference, LDL, IL-6, TNF-α ( Conclusions: RIF is associated with the downregulation of the
Language	English
Publishing date	2022-03-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2776676-7
ISSN	2296-861X
ISSN	2296-861X
DOI	10.3389/fnut.2021.741811
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Article ; Online: The role of Aquaporins in tumorigenesis: implications for therapeutic development.

Bhattacharjee, Arkadyuti / Jana, Ankit / Bhattacharjee, Swagato / Mitra, Sankalan / De, Swagata / Alghamdi, Badrah S / Alam, Mohammad Zubair / Mahmoud, Ahmad Bakur / Al Shareef, Zainab / Abdel-Rahman, Wael M / Woon-Khiong, Chan / Alexiou, Athanasios / Papadakis, Marios / Ashraf, Ghulam Md

Cell communication and signaling : CCS

2024 Volume 22, Issue 1, Page(s) 106

Abstract: Aquaporins (AQPs) are ubiquitous channel proteins that play a critical role in the homeostasis of the cellular environment by allowing the transit of water, chemicals, and ions. They can be found in many different types of cells and organs, including the ...

Abstract	Aquaporins (AQPs) are ubiquitous channel proteins that play a critical role in the homeostasis of the cellular environment by allowing the transit of water, chemicals, and ions. They can be found in many different types of cells and organs, including the lungs, eyes, brain, glands, and blood vessels. By controlling the osmotic water flux in processes like cell growth, energy metabolism, migration, adhesion, and proliferation, AQPs are capable of exerting their regulatory influence over a wide range of cellular processes. Tumour cells of varying sources express AQPs significantly, especially in malignant tumours with a high propensity for metastasis. New insights into the roles of AQPs in cell migration and proliferation reinforce the notion that AQPs are crucial players in tumour biology. AQPs have recently been shown to be a powerful tool in the fight against pathogenic antibodies and metastatic cell migration, despite the fact that the molecular processes of aquaporins in pathology are not entirely established. In this review, we shall discuss the several ways in which AQPs are expressed in the body, the unique roles they play in tumorigenesis, and the novel therapeutic approaches that could be adopted to treat carcinoma.
MeSH term(s)	Humans ; Neoplasms/pathology ; Carcinogenesis ; Cell Transformation, Neoplastic ; Water/metabolism ; Aquaporins/chemistry ; Aquaporins/metabolism
Chemical Substances	Water (059QF0KO0R) ; Aquaporins
Language	English
Publishing date	2024-02-09
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2126315-2
ISSN	1478-811X ; 1478-811X
ISSN (online)	1478-811X
ISSN	1478-811X
DOI	10.1186/s12964-023-01459-9
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