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  • 1.
    Banerji, Shantanu
    et al.
    Manitoba Institute of Cell Biology, Winnipeg, Manitoba, Canada .
    Los, Marek Jan
    Manitoba Institute of Cell Biology, Cancer Care Manitoba; Manitoba Institute of Child Health; Department of Biochemistry and Medical Genetics; Department of Human Anatomy and Cell Science, University Manitoba, Winnipeg, Canada.
    Important differences between topoisomerase-I and -II targeting agents2006In: Cancer Biology & Therapy, ISSN 1538-4047, E-ISSN 1555-8576, Vol. 5, no 8, p. 965-966Article in journal (Other academic)
    Abstract [en]

    Commentary to: Activation of ATM and Histone H2AX Phosphorylation Induced by Mitoxantrone But Not by Topotecan is Prevented by the Antioxidant N-acetyl-L-Cysteine Xuan Huang, Akira Kurose, Toshiki Tanaka, Frank Traganos, Wei Dai and Zbigniew Darzynkiewicz

     

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  • 2.
    El-Awady, Raafat A
    et al.
    College of Pharmacy, University of Sharjah, Sharjah, United Arab Emirates; Sharjah Institute of Medical Research, University of Sharjah, Sharjah, United Arab Emirates; Pharmacology, Clinical Biochemistry and Molecular Biology Units, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt; College of Medicine, University of Sharjah, Sharjah, United Arab Emirates.
    Hersi, Fatema
    Sharjah Institute of Medical Research, University of Sharjah, Sharjah, United Arab Emirates.
    Al-Tunaiji, Hala
    Sharjah Institute of Medical Research, University of Sharjah, Sharjah, United Arab Emirates.
    Saleh, Ekram M
    Pharmacology, Clinical Biochemistry and Molecular Biology Units, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt.
    Abdel-Wahab, Abdel-Hady A
    Pharmacology, Clinical Biochemistry and Molecular Biology Units, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt.
    Al Homssi, Amer
    College of Medicine, University of Sharjah, Sharjah, United Arab Emirates.
    Suhail, Mousa
    College of Medicine, University of Sharjah, Sharjah, United Arab Emirates.
    El-Serafi, Ahmed Taher
    College of Medicine, University of Sharjah, Sharjah, United Arab Emirates, College of Medicine, Suez Canal University, Ismaileya, Egypt.
    Al-Tel, Taleb
    College of Pharmacy, University of Sharjah, Sharjah, United Arab Emirates; Sharjah Institute of Medical Research, University of Sharjah, Sharjah, United Arab Emirates.
    Epigenetics and miRNA as predictive markers and targets for lung cancer chemotherapy2015In: Cancer Biology & Therapy, ISSN 1538-4047, E-ISSN 1555-8576, Vol. 16, no 7, p. 1056-1070Article in journal (Refereed)
    Abstract [en]

    Lung cancer cells show inherent and acquired resistance to chemotherapy. The lack of good predictive markers/novel targets and the incomplete understanding of the mechanisms of resistance limit the success of lung cancer response to chemotherapy. In the present study, we used an isogenic pair of lung adenocarcinoma cell lines; A549 (wild-type) and A549DOX11 (doxorubicin resistant) to study the role of epigenetics and miRNA in resistance/response of non-small cell lung cancer (NSCLC) cells to doxorubicin. Our results demonstrate differential expression of epigenetic markers whereby the level of HDACs 1, 2, 3 and4, DNA methyltransferase, acetylated H2B and acetylated H3 were lower in A549DOX11 compared to A549 cells. Fourteen miRNAs were dys-regulated in A549DOX11 cells compared to A549 cells, of these 14 miRNAs, 4 (has-mir-1973, 494, 4286 and 29b-3p) have shown 2.99 – 4.44 fold increase in their expression. This was associated with reduced apoptosis and higher resistance of A549DOX11cells to doxorubicin and etoposide. Sequential treatment with the epigenetic modifiers trichostatin A or 5-aza-2'-deoxycytidine followed by doxorubicin resulted in: (i) enhanced sensitivity of both cell lines to doxorubicin especially at low concentrations, (ii) enhanced doxorubicin-induced DNA damage in both cell lines, (iii) dysregulation of some miRNAs in A549 cells. In conclusion, A549DOX11 cells resistant to DNA damaging drugs have epigenetic profile and miRNA expression different from the sensitive cells. Moreover, epigenetic modifiers may reverse the resistance of certain NSCLC cells to DNA damaging agents by enhancing induction of DNA damage. This may open the door for using epigenetic profile/miRNA expression of some cancer cells as resistance markers/targets to improve response of resistant cells to doxorubicin and for the use of combination doxorubicin/epigenetic modifiers to reduce doxorubicin toxicity.

  • 3.
    Jain, Samatha M.
    et al.
    Chettinad Acad Res & Educ, India.
    Ravichandran, Shruthi Nagainallur
    Chettinad Acad Res & Educ, India.
    Kumar, Makalakshmi Murali
    Chettinad Acad Res & Educ, India.
    Banerjee, Antara
    Chettinad Acad Res & Educ, India.
    Sun-Zhang, Alexander
    Karolinska Inst, Sweden.
    Zhang, Hong
    Orebro Univ, Sweden.
    Pathak, Rupak
    Univ Arkansas Med Sci, AR USA; Univ Arkansas Med Sci, AR 72205 USA.
    Sun, Xiao-Feng
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Pathak, Surajit
    Chettinad Acad Res & Educ, India; Chettinad Acad Res & Educ, India.
    Understanding the molecular mechanism responsible for developing therapeutic radiation-induced radioresistance of rectal cancer and improving the clinical outcomes of radiotherapy - A review2024In: Cancer Biology & Therapy, ISSN 1538-4047, E-ISSN 1555-8576, Vol. 25, no 1, article id 2317999Article, review/survey (Refereed)
    Abstract [en]

    Rectal cancer accounts for the second highest cancer-related mortality, which is predominant in Western civilizations. The treatment for rectal cancers includes surgery, radiotherapy, chemotherapy, and immunotherapy. Radiotherapy, specifically external beam radiation therapy, is the most common way to treat rectal cancer because radiation not only limits cancer progression but also significantly reduces the risk of local recurrence. However, therapeutic radiation-induced radioresistance to rectal cancer cells and toxicity to normal tissues are major drawbacks. Therefore, understanding the mechanistic basis of developing radioresistance during and after radiation therapy would provide crucial insight to improve clinical outcomes of radiation therapy for rectal cancer patients. Studies by various groups have shown that radiotherapy-mediated changes in the tumor microenvironment play a crucial role in developing radioresistance. Therapeutic radiation-induced hypoxia and functional alterations in the stromal cells, specifically tumor-associated macrophage (TAM) and cancer-associated fibroblasts (CAF), play a crucial role in developing radioresistance. In addition, signaling pathways, such as - the PI3K/AKT pathway, Wnt/beta-catenin signaling, and the hippo pathway, modulate the radiation responsiveness of cancer cells. Different radiosensitizers, such as small molecules, microRNA, nanomaterials, and natural and chemical sensitizers, are being used to increase the effectiveness of radiotherapy. This review highlights the mechanism responsible for developing radioresistance of rectal cancer following radiotherapy and potential strategies to enhance the effectiveness of radiotherapy for better management of rectal cancer. [GRAPHICAL ABSTRACT]

  • 4.
    Maddika, Subbareddy
    et al.
    Manitoba Institute of Cell Biology, Cancer Care Manitoba; Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Canada .
    Mendoza, F. J.
    University of Manitoba; Winnipeg, Canada.
    Hauff, K.
    University of Manitoba; Winnipeg, Canada.
    Zamzow, C. R.
    University of Manitoba; Winnipeg, Canada.
    Paranjothy, T.
    University of Manitoba; Winnipeg, Canada.
    Los, Marek Jan
    Manitoba Institute of Cell Biology, Cancer Care Manitoba; Manitoba Institute of Child Health; Department of Biochemistry and Medical Genetics; Department of Human Anatomy and Cell Science, University Manitoba, Winnipeg, Canada, .
    Cancer-selective therapy of the future: Apoptin and its mechanism of action2006In: Cancer Biology & Therapy, ISSN 1538-4047, E-ISSN 1555-8576, Vol. 5, no 1, p. 10-19Article, review/survey (Refereed)
    Abstract [en]

    Classical chemotherapy that specifically targets rapidly proliferating cells has been in existence for over eighty years and has proven to be fully successful in only a limited number of cancers. Thus, this review focuses on a novel, emerging approach for cancer therapy that uses alternative, and more unique features of cancer cells. This new approach facilitates the selective targeting of cancer, while sparing normal, non-transformed cells. Examples of molecules that kill cancer cells selectively are: apoptin, E4orf4, viral protein R (VpR), and Brevinin-2R. Below we focus on apoptin, a product of the third open reading frame (VP3) of the chicken anemia virus. Besides discussing apoptin's mechanism of action, we also provide concise insight into the biology of a chicken anemia virus infection. Since apoptin's cancer-selective toxicity depends on its nuclear localization, we broadly discuss mechanism(s) involved in its nuclear retention (both nuclear import and export). We also discuss recent findings on apoptin's molecular mechanism of action, with a focus on the role of Nur77 in apoptin's nucleo-cytoplasmic signaling. Finally, we compare the current findings on apoptin to the mechanism of cancer selective toxicity of E4orf4. In the 'summary' section, besides highlighting important issues related to cancer-selective therapy, we also discuss concurrent approaches towards therapy personalization, particularly those related to the in vivo, and real time cancer therapy efficacy monitoring, using "lab-on-the-chip" and other emerging technologies.

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  • 5.
    Meng, Wen-Jian
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology. Sichuan University, Peoples R China.
    Pathak, Surajit
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Ding, Zhen-Yu
    Sichuan University, Peoples R China.
    Zhang, Hong
    University of Örebro, Sweden.
    Adell, Gunnar
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Holmlund, Birgitta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Li, Yuan
    Sichuan University, Peoples R China.
    Zhou, Zong-Guang
    Sichuan University, Peoples R China; Sichuan University, Peoples R China.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology. Sichuan University, Peoples R China; Sichuan University, Peoples R China.
    Special AT-rich sequence binding protein 1 expression correlates with response to preoperative radiotherapy and clinical outcome in rectal cancer2015In: Cancer Biology & Therapy, ISSN 1538-4047, E-ISSN 1555-8576, Vol. 16, no 12, p. 1738-1745Article in journal (Refereed)
    Abstract [en]

    Our recent study showed the important role of special AT-rich sequence binding protein 1 (SATB1) in the progression of human rectal cancer. However, the value of SATB1 in response to radiotherapy (RT) for rectal cancer hasnt been reported so far. Here, SATB1 was determined using immunohistochemistry in normal mucosa, biopsy, primary cancer, and lymph node metastasis from 132 rectal cancer patients: 66 with and 66 without preoperative RT before surgery. The effect of SATB1 knockdown on radiosensitivity was assessed by proliferation-based assay and clonogenic assay. The results showed that SATB1 increased from normal mucosa to primary cancer, whereas it decreased from primary cancer to metastasis in non-RT patients. SATB1 decreased in primary cancers after RT. In RT patients, positive SATB1 was independently associated with decreased response to preoperative RT, early time to metastasis, and worse survival. SATB1 negatively correlated with ataxia telangiectasia mutated (ATM) and pRb2/p130, and positively with Ki-67 and Survivin in RT patients, and their potential interaction through different canonical pathways was identified in network ideogram. Taken together, our findings disclose for the first time that radiation decreases SATB1 expression and sensitizes cancer cells to confer clinical benefit of patients, suggesting that SATB1 is predictive of response to preoperative RT and clinical outcome in rectal cancer.

  • 6.
    Panigrahi, Soumya
    et al.
    Department of Physiology, University of Manitoba, Winnipeg, Canada; Manitoba Institute of Cell Biology, CancerCare Manitoba, University of Manitoba, Winnipeg, Manitoba, Canada, .
    Klonisch, Thomas
    Department of Human Anatomy and Cell Sciences, and Manitoba Institute of Child Health, Winnipeg, Canada.
    Los, Marek Jan
    BioApplications Enterprises, Winnipeg, MB, Canada.
    The art of killing: double stroke with apoptin and survivin as a novel approach in cancer therapy2008In: Cancer Biology & Therapy, ISSN 1538-4047, E-ISSN 1555-8576, Vol. 7, no 7, p. 1061-1062Article in journal (Other academic)
    Abstract [en]

    Commentary to:

    Survivin knockdown combined with apoptin overexpression inhibits cell growth significantly

     

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1 - 6 of 6
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