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Background: The abnormal signaling from tyrosine kinase causes many types of cancers namely breast cancer, non-small cell lung cancer, and chronic myeloid leukemia. This research reports the in-silico, synthesis, and in-vitro study of novel pyrimidine derivatives as EGFR inhibitors. Objective: The objective of the research study is to discover more promising lead compounds using drug discovery process, in which the rational drug design is achieved by the molecular docking and virtual pharmacokinetic studies. Methods: The molecular docking studies were carried out using discovery studio 3.5-version software. The molecules with good docking and binding energy score were synthesized as well as their structures were confirmed by FT-IR, NMR, Mass and elemental analysis. Subsequently molecules were evaluated for their anticancer activity using MDA-MB-231, MCF-7 and A431 breast cancer cell lines by MTT and tyrosine kinase assay methodology. Results: Pyrimidine derivatives displayed anticancer activity. Particularly, compound R8 shows significant cytotoxicity against MDA-MB-231 with an IC50 18.5 ± 0.6 µM. Molecular docking studies proved that the compound R8 has good binding fitting by forming hydrogen bonds with amino acid residues at ATP binding sites of EGFR. Conclusion: Eight pyrimidine derivatives were designed, synthesized and evaluated against breast cancer cell lines. Compound R8 significantly inhibited the growth of MDA-MB-231 and MCF-7. Molecular docking studies reveled that compound R8 has good fitting by forming different Hydrogen bonding interactions with amino acids at ATP binding site of epidermal growth factor receptor target. Compound R8 was a promising lead molecule that showed better results as compared to other compounds in in-vitro studies.

Vascular complications in forms of venous and arterial thrombi are common scenario in antiphospholipid syndrome with raised titer of antibodies. Here we describe an 18 years old female who was admitted with right parotid swelling due to external carotid artery thrombi within gland parenchyma in antiphospholipid syndrome, with past history of right lower leg arterial occlusion and digital gangrene.

Superior vena cava (SVC) syndrome occurs because of SVC obstruction by mediastinal mass, with features of venous stasis and Pancoast syndrome manifested by tumour of the lung apex with features of invasion to adjacent bones, soft tissues and the nervous system. Small cell carcinoma lung is commonly found to cause SVC syndrome, Pancoast is a rare association. Only a few cases have been reported so far. In this report, we focus on a 45-year-old male patient who presented with both Pancoast and SVC syndrome because of small cell carcinoma of the lung.

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