Genome-wide accumulations of non-random adaptive point mutations drive westward evolution of Helicobacter pylori.

Background: For last seven decades we remained convinced that the natural point mutations occur randomly in the genome of an organism. However, our whole genome sequence analyses show that for the gastric pathogen Helicobacter pylori, which causes peptic ulcer and gastric cancer, accumulations of point mutations in the genome are non-random and they contribute to its unidirectional evolution. Based on the oncoprotein CagA, the pathogen can be classified into Eastern (East Asian countries like China and Japan; high incidence of gastric cancer) and Western (Europe, Africa, South-West Asian countries like India; low incidence of gastric cancer) types.

Molecular Insights on Signaling Cascades in Breast Cancer: A Comprehensive Review.

The complex signaling network within the breast tumor microenvironment is crucial for its growth, metastasis, angiogenesis, therapy escape, stem cell maintenance, and immunomodulation. An array of secretory factors and their receptors activate downstream signaling cascades regulating breast cancer progression and metastasis. Among various signaling pathways, the EGFR, ER, Notch, and Hedgehog signaling pathways have recently been identified as crucial in terms of breast cancer proliferation, survival, differentiation, maintenance of CSCs, and therapy failure.

Osteopontin: A Key Multifaceted Regulator in Tumor Progression and Immunomodulation.

The tumor microenvironment (TME) is composed of various cellular components such as tumor cells, stromal cells including fibroblasts, adipocytes, mast cells, lymphatic vascular cells and infiltrating immune cells, macrophages, dendritic cells and lymphocytes. The intricate interplay between these cells influences tumor growth, metastasis and therapy failure. Significant advancements in breast cancer therapy have resulted in a substantial decrease in mortality.

Gastrointestinal microbiome in the context of Helicobacter pylori infection in stomach and gastroduodenal diseases.

Infectious origins of a set of severe gastroduodenal diseases viz. gastritis, duodenal ulcer, gastric ulcer, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma were appreciated only after the discovery of H. pylori in 1983.

Peptic Ulcer and Gastric Cancer: Is It All in the Complex Host-Microbiome Interplay That Is Encoded in the Genomes of "Us" and "Them"?

It is increasingly being recognized that severe gastroduodenal diseases such as peptic ulcer and gastric cancer are not just the outcomes of infection in the stomach. Rather, both diseases develop and progress due to the perfect storms created by a combination of multiple factors such as the expression of different virulence proteins, consequent human immune responses, and dysbiosis in gastrointestinal microbiomes. In this mini review, we have discussed how the genomes of and other gastrointestinal microbes as well as the genomes of different human populations encode complex and variable virulome-immunome interplay, which influences gastroduodenal health.