Background: Acute myeloid leukemia (AML) is clinically, cytogenetically, and molecularly heterogeneous. Advances in molecular research have greatly improved our understanding of the leukemogenesis in AML. Programmed cell death-4 (PDCD4) is a novel tumor suppressor that inhibits neoplastic transformation and tumor progression and invasion by suppressing activator protein (AP) -1 activation and protein translation. In the present study, we examined the PDCD4 expression levels in de novo AML and investigated correlation between altered expression of PDCD4 with patients’ clinical characteristics.Methods: Peripheral blood samples were collected from 56 patients with AML at the time of diagnosis and also, 10 healthy individuals. Quantification of PDCD4 mRNA expression by Real Time Quantitative PCR was performed. Mann-Whitney U test was used to compare PDCD4 expression differences among healthy and AML samples.Findings: PDCD4 mRNA expression was significantly diminished in patients with AML at diagnosis in comparison to the PB as normal samples (P<0.001). We observed a statistically lower expression in AML-M5 subtype in comparison to other AML subtypes (P=0.028). We have not found any significant correlation between PDCD4 expression level and clinical parameters of patients. Also, no significant correlation between the expression levels of PDCD4 and complete remission after induction therapy was observed.Conclusion: Our results shown that, like many epithelial cancers, the down-regulation of PDCD4 expression also occurs in AML.

Apoptosis or Programmed cell death is known as a conserved gene-directed mechanism for the specific elimination of unnecessary or unwanted cells from an organism and is involved in many immune system mechanisms and diseases. The main differences of this pathway with cell necrosis as two main pathways for elimination of unwanted cells are the absence of inflammation and the restricted effect on target cells. Apoptosis has an important role in biological processes such as normal development, tissue homeostasis, elimination of destroyed cells or virus infected cells and remove of self antigen-activated immune cells. Apoptosis is important for regulation of cell growth and proliferation, development and body health and many autoimmune diseases, cancers and viral infections are the result of impaired or inhibited Programmed cell death. Therefore the main objective of apoptosis research is to identify molecular components and regulatory mechanisms specially Bcl-2 and IAP family as the most important regulators of apoptosis and this information may lead to application of therapeutic agents that can modulate this process in the treatment of neurodegenerative disorders and proliferative diseases such as cancer.

Aim and Background: Programmed cell death (PCD) is involved in plant resistance responses to pathogens and environmental biotic and abiotic stresses and its function has been conserved in eukaryotes, plant and animal phylum’s.Material and Methods: In many human diseases such as the respiratory disorders and nervous related diseases such as the Alzheimer and Parkinson, it is observed that the PCD process is non functional and unregulated processed and does not work.Results: Different genes related to this biological mechanism in plants were identified by the researchers and the conserved genetical and biochemical pathways involved in activating the PCD almost fully determined.Discussion: Although, some of the morphological and biochemical changes that are generally occur in PCD in animals are also observe in plants, but there is a few knowledge available about how these process lead to cell death in plants.Conclusion: Regardless of the fact that the Programmed cell death appear to be a conserved process in animals and plant cells but from the genetical and biochemical point of view it take place completely different in plants.

Background: The Programmed cell death protein 1 (PD-1), which is a member of the CD28 receptor family, can negatively regulate antitumor immune responses by interacting with its ligands, PD-L1 or PD-L2. The PD-1– PD-L1 signaling pathway is a checkpoint mechanism that plays essential roles in downregulating immune responses in cancerous tissues. Thus, blocking this signaling pathway leads to enhanced antitumor immunity, potentially preventing tumor progression. Methods: We synthesized the extracellular domain of the PD-1 receptor (rPD-1) de novo by using a two-step polymerase chain reaction and the Phusion® DNA polymerase. The synthesized gene was cloned into the pET28 expression plasmid and transformed into competent Escherichia coli. Purification of rPD-1 was performed by metal-affinity chromatography, using a HisTrap column. Purified rPD-1 was characterized by western blotting and mass spectrometry using the SwissProt database and the Mascot program. Results: Designed and synthesized construct of rPD-1 was 500 bp in size. Analysis of the electrophoresis data of purified rPD-1 showed the presence of a protein with a molecular mass of 21 kDa. Mass spectrometry data using the SwissProt database and the Mascot program outputted the highest-scoring sequence to correspond to rPD-1. Conclusions: Synthesized de novo rPD-1 may have potential therapeutic applications in enhancing antitumor immune responses.