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313 results on '"Ouhtit, Allal"'

53. Visualization of gene expression of short and long forms of prolactin receptor in rat digestive tissues

Author

Ouhtit, Allal, Kelly, Paul A., and Morel, Gerard

Subjects
Prolactin -- Physiological aspects, Gene expression -- Analysis, Messenger RNA -- Physiological aspects, Biological sciences
Abstract

The short-form prolactin receptor transcript is expressed mainly in the liver and the long-form predominates in the pancreas and esophagus. Remaining parts of the gastrointestinal tract have an equal distribution of short and long-form transcripts. Prolactin receptors are localized in various regions of the gastrointestinal tract and stomach and colon. The transcripts are localized to lamina propria rather than epithelial tissues.

Published
1994

54. Unmasking the interplay between mTOR and Nox4: novel insights into the mechanism connecting diabetes and cancer

Author

Mroueh, Fatima Mohsen, primary, Noureldein, Mohamed, additional, Zeidan, Youssef H., additional, Boutary, Suzan, additional, Irani, Sara Abou Merhi, additional, Eid, Stéphanie, additional, Haddad, Mary, additional, Barakat, Rasha, additional, Harb, Frederic, additional, Costantine, Joseph, additional, Kanj, Rouwaida, additional, Sauleau, Erik‐Andre, additional, Ouhtit, Allal, additional, Azar, Sami T., additional, Eid, Ali H., additional, and Eid, Assaad A., additional

Published
2019
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57. UV-radiation-specific p53 mutation frequency in normal skin as a predictor of risk of basal cell carcinoma

Author

Ouhtit, Allal, Nakazawa, Hisayoshi, Armstrong, Bruce K., Kricker, Anne, Tan, Ernest, Yamasaki, Hiroshi, and English, Dallas R.

Subjects
Tumor suppressor genes -- Health aspects, Gene mutations -- Health aspects, Basal cell carcinoma -- Genetic aspects, Skin, Effect of radiation on the -- Research, Health
Abstract

Background: A strong association has been found between skin cancer and exposure to UV radiation. The p53 tumor suppressor gene (also known as TP53), which is frequently mutated in human cancers, is believed to be an early target in UV radiation-associated skin carcinogenesis. We have previously developed a sensitive, polymerase chain reaction-based method capable of detecting and quantifying a UV radiation-specific mutation in the p53 gene (codons 247 and 248: AACCGG [right arrow] AATTGG) in normal skin. We have used this method to examine whether UV radiation-specific mutation frequency is associated with risk of basal cell carcinoma (BCC) and with sun exposure. Methods: This case-control study in Australia involved 53 case subjects with BCC and 75 control subjects. DNA was isolated from normal skin (mirror-image anatomic site to the cancer site for case subjects and a randomly selected site for control subjects) and assayed for p53 mutation. Relationships between p53 mutation frequency and risk of BCC, sun sensitivity, or sun exposure were estimated by use of odds ratios (ORs) and 95% confidence intervals (95% CIs). Results: Case subjects were more likely to have a p53 mutation than control subjects (OR = 3.1; 95% CI = 1.3-7.1). In addition, the odds of BCC increased monotonically with increasing frequency of p53 mutation. No statistically significant associations could be demonstrated between p53 mutation frequency and age, sex, sensitivity to the sun, pigmentary characteristics, total lifetime sun exposure, or sun exposure to the biopsy site. Conclusions: Our results indicate that tandem CC [right arrow] TT mutations involving codons 247 and 248 of the p53 gene are associated with an increased risk of BCC but cannot be used as an accurate measure of total UV-radiation exposure. [J Natl Cancer Inst 1998;90:523-31]

Published
1998

58. List of contributors

Author

Alam, Asrar, Arukha, Ananta P., Bandichhor, Rakeshwar, Bawankule, Dnyaneshwar Umrao, Bhatt, Divya, Fatima, Kaynat, Gade, Neeta, Gorki, Varun, Gupta, Ankit, Gupta, Shefali, Imam, Maryam, Islahi, Sana, Kapoor, Neha, Kaushik, Naveen Kumar, Kothapalli, Yugandhar, Mishra, Anushree, Ouhtit, Allal, Pai, Somnath Srinivas, Pandey, Abhay Kumar, Prakash, Shantanu, Qidwai, Tabish, Shukla, Suruchi, Siddiqui, Faiza Amber, Singh, Shiv Vardan, Singh, Uma S., Srivsatava, Sanchita, Tasleem Raza, Syed, Tripathi, Ujjwal K., and Yadav, Gaya P.

Published
2024
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59. Inositol 1,4,5-Trisphosphate Receptors in Hypertension

Author

Eid, Ali H., primary, El-Yazbi, Ahmed F., additional, Zouein, Fouad, additional, Arredouani, Abdelilah, additional, Ouhtit, Allal, additional, Rahman, Md M., additional, Zayed, Hatem, additional, Pintus, Gianfranco, additional, and Abou-Saleh, Haissam, additional

Published
2018
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63. Differential effects of leptin on the invasive potential of androgen-dependent and -independent prostate carcinoma cells

Author

Deo, Dayanand D., Rao, Ashwin P., Bose, Saideep S., Ouhtit, Allal, Baliga, Surendra B., Rao, Shilpa A., Trock, Bruce J., Thouta, Rajesh, Raj, Madhwa H.G., and Rao, Prakash N.

Subjects
Obesity -- Complications and side effects -- Research -- Risk factors, Prostate cancer -- Risk factors -- Research -- Complications and side effects, Leptin -- Physiological aspects -- Research, Biotechnology industry, High technology industry
Abstract

Obesity has been linked with an increased risk of prostate cancer. The formation of toxic free oxygen radicals has been implicated in obesity mediated disease processes. Leptin is one of the major cytokines produced by adipocytes and controls body weight homeostasis through food intake and energy expenditure. The rationale of the study was to determine the impact of leptin on the metastatic potential of androgen-sensitive (LNCaP) cells as well as androgen-insensitive (PC-3 and DU-145) cells. At a concentration of 200_nm, LNCaP cells showed a significant increase (20% above control; P < .0001) in cellular proliferation without any effect on androgen-insensitive cells. Furthermore, exposure to leptin caused a significant (P < .01 to P < .0001) dosedependent decrease in migration and invasion of PC3 and Du-145 prostate carcinoma cell lines. At the molecular level, exposure of androgen-independent prostate cancer cells to leptin stimulates the phosphorylation of MAPK at early time point as well as the transcription factor STAT3, suggesting the activation of the intracellular signaling cascade upon leptin binding to its cognate receptor. Taken together, these results suggest that leptin mediates the invasive potential of prostate carcinoma cells, and that this effect is dependent on their androgen sensitivity. Copyright © 2008 Dayanand D. Deo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited., 1. INTRODUCTION Prostate cancer is the second leading cause of cancer related death among American men [1]. Obesity has assumed epidemic proportions in the United States and has been linked [...]

Published
2008

70. Molecular Evidence of Helicobacter Pylori Infection in Prostate Tumors

Author

Al-Marhoon, Mohammed S., primary, Ouhtit, Allal, additional, Al-Abri, Aisha O., additional, Venkiteswaran, Krishna P., additional, Al-Busaidi, Qassim, additional, Mathew, Josephkunju, additional, Al-Haddabi, Ibrahim, additional, Shareef, Omar, additional, Aquil, Shahid, additional, Rahman, Khalid, additional, Al-Hashmi, Intisar, additional, Gupta, Ishita, additional, and Ganguly, Shyam S., additional

Published
2015
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75. Biochemical characterization of riboflavin carrier protein (RCP) in prostate cancer

Author

Johnson, Tanya, Ouhtit, Allal, Gaur, Rajiv, Fernando, Augusta, Schwarzenberger, Paul, Su, Joseph, Ismail, Mohamed F, El-Sayyad, Hassan I, Karande, Anjali, Elmageed, Zakaria Abd, Rao, Prakash, and Raj, Madhwa

Subjects
Biochemistry
Abstract

Riboflavin carrier protein (RCP) is a growth- and development-specific protein. Here, we characterized the expression of this protein in prostate cancer by polyclonal and monoclonal antibodies against chicken RCP. RCP was localized to both androgen-dependent and independent prostate cancer cell lines. Compared to controls, RCP was over-expressed in all 45 prostate adenocarcinomas, irrespective of the Gleason's score or the stage of the disease. The identified RCP had a molecular weight of 38 kDa, similar to RCP purified from chicken. Presence of this protein was also confirmed by siRNA inhibition analysis. Antibodies to chicken RCP inhibited incorporation of tritiated thymidine into DNA and prevented riboflavin uptake in PC3 prostate cancer cells, suggesting a critical function of this protein in prostate cancer cell growth. These data suggest that RCP can be used as a tumor biomarker in prostate cancer.

Published
2009

76. Towards a Better Understanding of the Molecular Mechanisms Involved in Sunlight-Induced Melanoma

Author

Williams, Mandy and Ouhtit, Allal

Subjects
Article Subject, neoplasms
Abstract

Although much less prevalent than its nonmelanoma skin cancer counterparts, cutaneous malignant melanoma (CMM) is the most lethal human skin cancer. Epidemiological and biological studies have established a strong link between lifetime exposure to ultraviolet (UV) light, particularly sunburn in childhood, and the development of melanoma. However, the specific molecular targets of this environmental carcinogen are not known. Data obtained from genetic and molecular studies over the last few years have identified the INK4a/ARF locus as the “gatekeeper” melanoma suppressor, encoding two tumour suppressor proteins in human, p16INK4a and p14ARF. Recent developments in molecular biotechnology and research using laboratory animals have made a significant gene breakthrough identifying the components of the p16p16INK4a/Rb pathway as the principal and rate-limiting targets of UV radiation actions in melanoma formation. This review summarizes the current knowledge of the molecular mechanisms involved in melanoma development and its relationship to sunlight UV radiation.

Published
2005
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84. BRIP1overexpression is correlated with clinical features and survival outcome of luminal breast cancer subtypes

Author

Gupta, Ishita, Ouhtit, Allal, Al-Ajmi, Adil, Rizvi, Syed Gauhar A, Al-Riyami, Hamad, Al-Riyami, Marwa, and Tamimi, Yahya

Abstract

In Oman, breast cancer is most common, representing approximately more than 25% of all cancers in women. Relatively younger populations of patients (25–40 years) present surprisingly with an aggressive phenotype and advanced tumor stages. In this study, we investigated differential gene expressions in Luminal A, Luminal B, triple-negative and Her2+ breast cancer subtypes and compared data to benign tumor samples. We identified a potential candidate gene BRIP1, showing differential expression in the four breast cancer subtypes examined, suggesting that BRIP1has the profile of a useful diagnostic marker, suitable for targeted therapeutic intervention. RT-qPCR and Western blotting analysis showed higher BRIP1expression in luminal samples as compared to triple-negative subtype patient’s samples. We further screened BRIP1for eventual mutations/SNPs/deletions by sequencing the entire coding region. Four previously identified polymorphisms were detected, one within the 5′-UTR region (c.141-64G > A) and three in the BRCA-binding domain (c.2755T > C, c.2647G > A and c.3411T > C). Kaplan–Meier analysis revealed that patients with overexpression of BRIP1displayed a poor survival rate (P< 0.05). BRIP1has a dual function of an oncogene and a tumor suppressor gene in addition to its role as a potential biomarker to predict survival and prognosis. Data obtained in this study suggest that BRIP1can plausibly have an oncogenic role in sporadic cancers.

Published
2018
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97. Simultaneous Inhibition of Cell-Cycle, Proliferation, Survival, Metastatic Pathways and Induction of Apoptosis in Breast Cancer Cells by a Phytochemical Super-Cocktail: Genes That Underpin Its Mode of Action

Author

Ouhtit, Allal, primary, Gaur, Rajiv Lochan, additional, Abdraboh, Mohamed, additional, Ireland, Shubha K., additional, Rao, Prakash N, additional, Raj, Shailaja G, additional, Al-Riyami, Hamad, additional, Shanmuganathan, Somya, additional, Gupta, Ishita, additional, Murthy, Subramanyam N, additional, Hollenbach, Andrew, additional, and Raj, Madhwa HG, additional

Published
2013
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