がんの科学と治療

Herein, we present a mathematical model of tumour-immune interactions in presence of chemotherapy treatment. The model is governed by a system of delay differential equations with optimal control variables. A discrete time-delay is considered to justify the time-needed for the effector cells to develop a suitable response to the tumour cells. The control variables are included to justify the best treatment strategy with minimum side effects by reducing the production of new tumour cells and keeping the number of normal cells above the average of its carrying capacity. The numerical simulations show that the optimal treatment strategy reduces the load of tumour cells increases the effector cells after few days of therapy.

Background: Mediastinal masses include a wide variety of tumors; could be congenital or acquired, cystic or solid, primary or secondary. They may arise from anterior, middle or posterior mediastinum. Neurogenic tumors are commonest childhood lesions; whereas lymphomas and thymic lesions are commonest in adults. Methods: Retrospective analysis of all mediastinal masses presented to our unit from September 1st 2007 to July 1st 2015, all diagnostic modalities and and/or treatment by different surgical approaches are reviewed. Results: Eighty-five patients with mediastinal masses in different age groups and both genders were studied There were 46 males and 39 females. Fifty-nine patients had anterior mediastinal masses, 13 patients had mediastinal lymphadenopathy and 14 patients had posterior mediastinal masses. Lymphoma was the commonest pathology (32.94%) followed by thymic diseases (24.7%), germ cell tumors (11.76%) and neurogenic tumors (10.59%). From 17 patients in pediatric age group lymphoma was the commonest pathology (35.3%) followed by neurogenic tumors (29.4%). Conclusions: Mediastinal masses should be managed by a multidisciplinary team. Mediastinal Hydatid cyst in our locality is not uncommon disease. In mediastinal masses the role of surgery could be only diagnostic as in lymphoma cases thence we should be least invasive.

A successful treatment of cancers in the clinic has been difficult to achieve because of the emergence of drug resistant tumor cells. While various approaches have been tried to overcome multi-drug resistance, it has remained a major road block in achieving complete success in the clinic. Extensive research has identified various mechanisms, including overexpression of P-glycoprotein 170, modifications in activating or detoxification enzymes (phase I and II enzymes), and mutation and/or decreases in target enzymes in cancer cells. However, nitric oxide and/or nitric oxide-related species have not been considered an important player in cancer treatment and or drug resistance. Here, we examine the significance of nitric oxide in the treatment and resistance mechanisms of various anticancer drugs. Furthermore, we describe the significance of recently reported effects of nitric oxide on topoisomerases and the development of resistance to topoisomerase-poisons in tumor cells.