Cancer is a multifactorial disease, causing behavioral and metabolic alterations, leading to uncontrolled cell proliferation with collateral weakening of immune system. Crucial balance between cell proliferation and cell death determines the fate of a cell, which might progress towards survival or apoptosis. Apoptosis is a complex, programmed, and highly regulated process causing dramatic morphological and biochemical perturbations in the cellular machinery. Ganoderma lucidum is a basidiomycetes, polypore mushroom known for its pharmacological properties in cancer. The major bioconstituents in G. lucidum are terpenoids, polysaccharides, and proteins that target cancer-signaling factors like plasma membrane receptors proteins and adapter molecules. Of all constituents, the major terpenoid, i.e. Ganoderic acid is reported to interact with membrane receptors mainly, receptor tyrosine kinase (RTKs). Ganoderic acid interacts and modulates the signaling network in IR, IGFR-1, IGFR-2, VEGFR-1, VEFGR-2, and EGFR in cancer signaling pathways. It primarily targets NF-κB, RAS-MAPK, PI3K/Akt/mTOR, and cell cycle resulting in apoptosis. This review highlights the role of ganoderic acid in apoptosis and modulations of various signaling proteins in cancer.

Protein-Protein Interaction Sitesbase (PPInS), a high-performance database of protein-protein interacting interfaces, is presented. The atomic level information of the molecular interaction happening amongst various protein chains in protein-protein complexes (as reported in the Protein Data Bank [PDB]) together with their evolutionary information in Structural Classification of Proteins (SCOPe release 2.06), is made available in PPInS. Total 32468 PDB files representing X-ray crystallized multimeric protein-protein complexes with structural resolution better than 2.5 Å had been shortlisted to demarcate the protein-protein interaction interfaces (PPIIs). A total of 111857 PPIIs with ~32.24 million atomic contact pairs (ACPs) were generated and made available on a web server for on-site analysis and downloading purpose. All these PPIIs and protein-protein interacting patches (PPIPs) involved in them, were also analyzed in terms of a number of residues contributing in patch formation, their hydrophobic nature, amount of surface area they contributed in binding, and their homo and heterodimeric nature, to describe the diversity of information covered in PPInS. It was observed that 42.37% of total PPIPs were made up of 6–20 interacting residues, 53.08% PPIPs had interface area ≤1000 Å2 in PPII formation, 82.64% PPIPs were reported with hydrophobicity score of ≤10, and 73.26% PPIPs were homologous to each other with the sequence similarity score ranging from 75–100%. A subset “Non-Redundant Database (NRDB)” of the PPInS containing 2265 PPIIs, with over 1.8 million ACPs corresponding to the 1931 protein-protein complexes (PDBs), was also designed by removing structural redundancies at the level of SCOP superfamily (SCOP release 1.75). The web interface of the PPInS (http://www.cup.edu.in:99/ppins/home.php) offers an easy-to-navigate, intuitive and user-friendly environment, and can be accessed by providing PDB ID, SCOP superfamily ID, and protein sequence.

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Abstract. lung cancer, the most common cause of cancerrelated death in men and women, is responsible for 1.3 million deaths worldwide annually. Women are diagnosed to a greater extent than men with adenocarcinoma and small cell carcinoma, both of which are secretory-type tumors. never smokers diagnosed with lung cancer are also predominantly female, demonstrating the association of genetic factors with lung carcinogenesis. Several epidemiologic studies have associates certain CYP1A1 genotypes, alone or in combination, with an increased risk of estrogen-related cancer. The aim of this study was to investigate the impact of the cYP and GST polymorphisms along with estrogen and interleukin-6 (il-6) levels on the risk of lung cancer. eighty-six lung cancer patients and 60 controls were included in the study. a significantly higher frequency of polymorphisms in the genes was observed in lung cancer patients compared to controls. Mean estradiol concentration was reduced and il-6 levels were elevated in patients compared to controls. in conclusion, increased polymorphisms in metabolic genes may be the reason for the reduced estradiol and, thereby, the increased expression of il-6 in the serum of lung cancer patients.