Balanced translocation resulting in fusion of the Abelson gene (ABL₁) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2 is the pathognomonic molecular driver of CML. The resulting BCRABL 1 fusion gene is both the diagnostic as well as therapeutic target of CML. The first agent with tyrosine kinase inhibitor activity that was licenced in 2000 for treatment of CML patients, was Imatinib, gradually followed by multiple agents with higher efficacy.

Cancer has its own disease burden and patients usually suffer from symptom clusters when they are referred for palliative treatment. Identification of symptom cluster trajectories will help clinician to take into account measures that can optimize quality of life of palliative patients. Therefore the aim of this paper is to determine the overall prevalence of symptoms and symptoms clusters in different disease groups according to etiology at the time of first visit to Palliative care clinic by using HIS Palliative First Assessment note indicating Edmonton symptom scale.

Although NK cells are recognized as effector lymphocytes of the innate immune system, they also regulate the adaptive immune response by releasing inflammatory cytokines and developing immunological memory. Unlike other lymphocytes such as T or B cells, NK cells do not express rearrangeable, antigen-specific receptors. 

Damage-Associated Molecular Patterns (DAMPs) are known by their nature to cause inflammatory responses in numerous disease states from cancer, trauma to age related diseases (e.g. atherosclerosis, Alzheimer’s and Parkinson’s diseases), these molecules are released by cells undergoing cell death.

The transient receptor potential mucolipin 1 (TRPML1) is an endolysosomal channel belonging to the TRP family. Clinically, mutations of TRPML1 have been responsible for a severe lysosomal storage disorder called mucolipidosis type IV.