MEMP Magazine July 2018


Cancer in Egypt: A special report written by Aalaa Abdou, a Clinical Oncology Specialist in Ministry of Health of Egypt. Page 38.

  1. Ibrahim AS, Khaled HM, Mikhail NN, Baraka H, Kamel H (2014) Cancer incidence in egypt: results of the national population-based cancer registry program. J Cancer Epidemiol2014: 437971.
  2. WHO Cancer country profiles 2014
  3. Ministry of health and population, Specialised Medical Centre web site
  4. Hajdu, Steven I. (alone or with co-authors) “A Note From History: Landmarks in History of Cancer, Part 1~6.” Cancer, v. 117/5, 117/12, v.118/4, v. 118/8, 118/20 & 119/23 (2011-2013).
  5. Zheng YL, Amr S, Saleh D, Dash C, Ezzat S, Mikhail NN, et al. Urinary bladder cancer risk factors in Egypt: a multi-center case-control study. Cancer Epidemiol Biomarkers Prev. 2012;21:537–46.
  6. El-Akel W, El-Sayed MH, El Kassas M, et al. National treatment programme of hepatitis C in Egypt: hepatitis C virus model of care. J Viral Hepat. 2017;24(4):262–267.

Atavistic Chemotherapy: Breaking away from expensive and ineffective cancer drugs, written by Dr Frank Arguello, MD Director of Atavistic Chemotherapy Clinical Trial. Page 44.

  1. Ward, E., “Childhood and Adolescent Cancer Statistics,” CA Cancer J Clin., 64/2 (2014), 83–103
  2. “WHO EMRO | Cancer | Health Topics,”, 2018 <> [accessed 8 June 2018]
  3. Fojo, T.,, “Unintended Consequences of Expensive Cancer Therapeutics—The Pursuit of Marginal Indications and a Me-Too Mentality That Stifles Innovation and Creativity,” JAMA Otolaryngology–Head & Neck Surgery. 140/12 (2014), 1225
  4. Morgan, G.,, “The contribution of cytotoxic chemotherapy to 5-year survival in adult malignancies,” Clin Oncol. 16/5 (2004), 49-60
  5. Workman, P.,, “How Much Longer Will We Put Up With $100,000 Cancer Drugs?” Cell. 168/4 (2017), 579-583
  6. Prigerson, HG.,, “Chemotherapy Use, Performance Status, and Quality of Life at the End of Life,” JAMA Oncol. 1/6 (2015), 778-84
  7. Mann, D., “Majority of Advanced Cancer Patients Believe Chemotherapy Can Cure Them,” WebMD <> [accessed 8 June 2018]
  8. Twombly, R., “Cancer surpasses heart disease as leading cause of death for all but the very elderly,” J Natl Cancer Inst. 97/330 (2005)
  9. Bailar, J.C., 3rd, Gornik, H.L. “Cancer undefeated,” N Eng J Med. 336/22 (1997), 1569-74
  10. Karagiannis G.,, “Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism,” Sci Transl Med. 9/399 (2017)
  11. Sun Y.,, “Treatment-induced damage to the tumor microenvironment promotes prostate cancer therapy resistance through WNT16B,” Nat Med. 18/9 (2012), 1359-1368
  12. “Top 10 Oncology Pharmaceutical Companies 2017” <> [accessed 8 June 2018]
  13. “Global Cancer Drugs Market Size & Share Will Grow USD 161.30 Billion by 2021: Zion Market Research” <> [accessed 8 June 2018]
  14. Arguello, F., “Atavistic Metamorphosis: a New and Logical Explanation for the Origin and Biological Nature of Cancer,” Charleston: CreateSpace Publisher 1 (2011)
  15. Nazaryan, A, “Getting Cancer Wrong: You Cannot Cure What You Do Not Understand,” 2014 <> [accessed 8 June 2018]
  16. Snow HL. A treatise, practical and theoretic, on cancers and the cancer-process. London: Churchill; 1893

Compounding tablets in the Middle East: Benefits of small-scale tablet manufacturing systems written by Dr Michael Gamlen. Page 50.

  1. S Department of Health and Human Services. Food and Drug Administration. Human Drug Compounding. [FDA website.] Available at Accessed 11.06.18
  1. Professional Compounding Centers of America. Compounding resources for patients. [PCCA website]. Available at Accessed 11.06.18
  1. American Pharmacists Association. Compounding resources for your practice. [APhA website]. Available at Accessed 11.06.18
  1. ALLEN L. The Art, Science, and Technology of Pharmaceutical Compounding. 5th ed. American Pharmacists Association. 2016
  1. S. Pharmacopeia Convention. Compounding. [USP website]. Available at Accessed 11.06.18.
  1. Pellagatti T. Warfarin personalized dosage: Re-compounding for a more suitable therapy and better compliance. Int J Pharm Compd 2017 May-Jun;21(3): 247-250.
  1. United Nations. World Population Prospects. [United Nations website]. Available at Accessed 11.06.18
  1. The World Factbook. The World Factbook. [CIA website]. Available at Accessed 11.06.18
  1. GM Insights: Compounding Pharmacies Market 2018 – 2024 Report: May 2018. Available at Accessed 11.06.18

Non-alcoholic fatty liver disease: Does genetics have a role? Written by Dr Ravi Kanth. Page 62.

  1. Sharma M, Mitnala S, Vishnubhotla RK, Mukherjee R, Reddy DN, Rao PN. The Riddle of Nonalcoholic Fatty Liver Disease: Progression From Nonalcoholic Fatty Liver to Nonalcoholic Steatohepatitis. J Clin Exp Hepatol 2015; 5: 147-158.
  2. Sanyal AJ, Yoon SK, Lencioni R. The etiology of hepatocellular carcinoma and consequences for Oncologist 2010; 15 Suppl 4: 14-22.
  3. Younossi Z, Anstee QM, Marietti M et al. Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention. Nat Rev Gastroenterol Hepatol. 2018;15(1):11-20.
  4. Loomba R, Schork N2, Chen CH et al. Heritability of Hepatic Fibrosis and Steatosis Based on a Prospective Twin Study. Gastroenterology. 2015;149(7):1784-93.
  5. Romeo S, Kozlitina J, Xing C et al. Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease. Nat Genet. 2008;40(12):1461-5.
  6. Kozlitina J, Smagris E, Stender S, et al. Exomewide association study identifies a TM6SF2 variant that confers susceptibility to nonalcoholic fatty liver disease. Nat Genet 2014;46: 352-356.
  7. Holmen OL, Zhang H, Fan Y, et al. Systematic evaluation of coding variation identifies a candidate causal variant in TM6SF2 influencing total cholesterol and myocardial infarction risk. Nat Genet 2014; 46: 345-351.
  8. Mahdessian H, Taxiarchis A, Popov S et al. TM6SF2 is a regulator of liver fat metabolism influencing triglyceride secretion and hepatic lipid droplet content. Proc Natl Acad Sci USA 2014; 111: 8913-8918.

Abbreviations used

NAFLD – Non alcoholic fatty liver disease; NASH – Non alcoholic steato hepatitis; HCC – hepatocellular carcinoma; USA – United states of America; IRS-1 –  Insulin Receptor Substrate 1; ENPP1 – Ectonucleotide Pyrophosphatase/Phosphodiesterase 1; GCKR – Glucokinase regulatory protein; PPARG –  peroxisome proliferator-activated receptor; TCF7L2 – Transcription Factor 7 Like 2; SLC2A1 – Solute Carrier Family 2 Member 1; SLC27A5 – Solute Carrier Family 27 Member 5; LIPN1 –  Lipin 1; MTTP – Microsomal Triglyceride Transfer Protein; PEMT –  Phosphatidylethanolamine N-Methyltransferase; ADIPOQ – Adiponectin; APOC3 – Apolipoprotein C3; APOE3 – Apolipoprotein E; NR1/2 (PXR) – Nuclear Receptor Subfamily 1 Group I Member 2; PPARA – Peroxisome Proliferator Activated Receptor  alpha; FADS1 – Fatty Acid Desaturase 1; HFE – Hemochromatosis; SOD2 –  Superoxide Dismutase 2; GCLC – Glutamate-Cysteine Ligase Catalytic Subunit; MRP2 (ABCC2) – Multidrug resistance-associated protein 2; MTHFR – methylenetetrahydrofolate reductase; TNF –  tumor necrosis factor; sTNFr-2 – Tumor necrosis factor receptor 2; FDFT1 – Farnesyl-Diphosphate Farnesyltransferase 1; IL6 – Interleukin 6; AGT – Angiotensinogen; ATGR1 – Angiotensin II Receptor Type 1; KLF6 –  Kruppel Like Factor 6; TGFb1 – Transforming Growth Factor Beta 1; COL13A1 – Collagen Type XIII Alpha 1 Chain; CDKN1A – Cyclin Dependent Kinase Inhibitor 1A; PNPLA3 –  Patatin Like Phospholipase Domain Containing 3; TM6SF2 – Transmembrane 6 Superfamily Member 2