Molecular Mechanisms of Distinct Diseases
By Adnan Batman, İrem Yalim Camci, Elif Kadioglu, Kezban Uçar Çifçi, Berçem Yeman Kıyak, Servet Tunoglu, Ezgi Nurdan Yenilmez Tunoglu and Yusuf Tutar
Molecular medicine describes molecular structures and mechanisms and this chapter focuses on molecular and genetics errors of diseases. Diseases can be classified into deficiency diseases, hereditary diseases, infectious diseases and physiological diseases and to get a glimpse of the mechanisms the chapter covers the most common disease of each class.
Part of the book: Methods in Molecular Medicine
Recent Advancements in Apoptosis-Based Therapeutic Approaches for Cancer Targeting
By Mehmet Evren Okur, Panoraia I. Siafaka, Merve Tutar and Yusuf Tutar
Apoptosis, known as programmed cell death, has been considered a potent target for the pharmacy industry. The scientific community has actively participated to research which evaluate active molecules for possible inhibition or induction of apoptosis. Nanocarriers especially for cancer targeting are widely found through literature; they mainly based on inorganic, lipid or polymer nanoparticles which incorporate anticancer drugs. Another important and innovative category of anticancer agents is that of microRNAs. In this chapter, a discussion about the most recent applications of apoptosis-based agents mainly focusing on cancer target is done.
Part of the book: Regulation and Dysfunction of Apoptosis
Role of p53 in Human Cancers
By Kubra Acikalin Coskun, Merve Tutar, Mervenur Al, Asiye Gok Yurttas, Elif Cansu Abay, Nazlican Yurekli, Bercem Yeman Kiyak, Kezban Ucar Cifci and Yusuf Tutar
TP53 codes tumor protein 53-p53 that controls the cell cycle through binding DNA directly and induces reversible cell-cycle arrest. The protein activates DNA repair genes if mutated DNA will be repaired or activates apoptotosis if the damaged DNA cannot be fixed. Therefore, p53, so-called the “guardian of the genome,” promote cell survival by allowing for DNA repair. However, the tumor-suppressor function of p53 is either lost or gained through mutations in half of the human cancers. In this work, functional perturbation of the p53 mechanism is elaborated at the breast, bladder, liver, brain, lung cancers, and osteosarcoma. Mutation of wild-type p53 not only diminishes tumor suppressor activity but transforms it into an oncogenic structure. Further, malfunction of the TP53 leads accumulation of additional oncogenic mutations in the cell genome. Thus, disruption of TP53 dependent survival pathways promotes cancer progression. This oncogenic TP53 promotes cell survival, prevents cell death through apoptosis, and contributes to the proliferation and metastasis of tumor cells. The purpose of this chapter is to discuss the contribution of mutant p53 to distinct cancer types.
Part of the book: p53
Drugs and Drug Candidates for the Treatment of Lymphoma
By Kubra Acikalin Coskun, Merve Tutar, Elif Cansu Abay, Nazlican Yurekli, Mervenur Al and Yusuf Tutar
Cancer is the biggest health problem worldwide due to its high mortality rate. Lymphoma is defined as a group of malignant diseases that is caused by clonal proliferation of lymphocytes and is classified under two major groups: Hodgkin lymphoma and non-Hodgkin lymphoma. Genetic predisposition and some environmental factors constitute risk factors. Symptoms of the disease include unexplained fever, swelling of lymph glands, swollen abdomen, tiredness, loss of appetite, frequent infections, and weight loss. Positron emission tomography (PET) and computed tomography (CT) scans, along with MRI, are widely used for the diagnosis of lymphoma. Advanced blood and lymph node biopsy tests are used to evaluate treatment effect on blood cells and to confirm the diagnosis of lymphoma, respectively. Current treatment options include chemotherapy, radiotherapy, and bone marrow/stem cell transplantation. Development of new treatment options for cancer medications includes small molecules and monoclonal antibodies for immunotherapy. In addition, the discovery of new phytochemical agents used in complementary and alternative medicine adds perspective to the treatment of lymphoma.
Part of the book: Lymphoma
Structure- and Design-Based Difficulties in Recombinant Protein Purification in Bacterial Expression
By Kubra Acikalin Coskun, Nazlıcan Yurekli, Elif Cansu Abay, Merve Tutar, Mervenur Al and Yusuf Tutar
Protein purification is not a simple task. Yet, overexpression at bacterial systems with recombinant modifications brings further difficulties. Adding a tag, an affinity label, and expressing particular domains of the whole protein, especially hydrophobic sections, make purification a challenging process. Protein folding pattern may perturb N- or C-terminal tag and this terminal preference may lead to poor purification yield. Codon optimization, solvent content and type, ionic conditions, resin types, and self-cleavage of recombinant proteins bring further difficulties to protein expression and purification steps. The chapter overviews problems of protein purification through a small peptide overexpression in bacteria (Recombinant anti-SARS Coronavirus 2 (SARS-Cov-2) Spike protein Receptor Binding Domain (RBD) antibody (Clone Sb#14). The chapter also covers troubleshooting at distinct steps and highlights essential points to solve crucial issues of protein purification.
Part of the book: Protein Detection
Molecular Mechanisms of Breast Cancer Metastasis View all chapters
By Nazlıcan Yurekli, Elif Cansu Abay, Merve Tutar, Ecem Cabri, Kubra Acikalin Coskun, Alev Kural and Yusuf Tutar
Breast cancer (BC) is one of the most frequently occurring diseases with high morbidity and mortality rates in the world today. BC cells live under stress with altered pathway signaling, chromosome and microsatellite instability, aneuploidy, hypoxia, low pH, and low nutrient conditions. In order to survive and reproduce in these stressful environments, BC cells rapidly undergo adaptive mutations, rearrange their chromosomes, and repress tumor suppressor genes while inducing oncogene activities that cause the natural selection of cancer cells and result in heterogeneous cancer cells in the tumor environment. Unfortunately, these genetic alterations result in aggressive BC cells that can not only proliferate aggressively but also migrate and invade the other tissues in the body to form secondary tumors. In this review, molecular mechanisms of metastasis of BC subtypes are discussed.
Part of the book: Cancer Metastasis