miRNAs in the prognosis of triple-negative breast cancer: A review.

Triple-Negative Breast Cancer (TNBC) is a highly aggressive and invasive type of breast cancer (BC) with high mortality rate wherein effective target medicaments are lacking. It is a very heterogeneous group with several subtypes that account for 10-20% of cancer among women globally, being negative for three most important receptors (estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2)), with an early and high recurrence resulting in poor survival rate. Therefore, a more thorough knowledge on carcinogenesis of TNBC is required for the development of personalized treatment options. miRNAs can either promote or suppress tumorigenesis and have been linked to a number of features of cancer progression, including proliferation, metastasis, apoptosis, and epithelial-mesenchymal transition (EMT). Recent miRNA research shows that there is great potential for the development of novel biomarkers as they have emerged as drivers of tumorigenesis and provide opportunities to target various components involved in TNBC, thus helping to solve this difficult-to-treat disease. In this review, we summarize the most relevant miRNAs that play an essential role in TNBC biology. Their role with regard to molecular mechanisms underlying TNBC progression has been discussed, and their potential use as therapeutic or prognostic markers to unravel the intricacy of TNBC based on the pieces of evidence obtained from various works of literature has been briefly addressed.

Onco-Pathogen Mediated Cancer Progression and Associated Signaling Pathways in Cancer Development.

Infection with viruses, bacteria, and parasites are thought to be the underlying cause of about 8-17% of the world's cancer burden, i.e., approximately one in every five malignancies globally is caused by an infectious pathogen. Oncogenesis is thought to be aided by eleven major pathogens. It is crucial to identify microorganisms that potentially act as human carcinogens and to understand how exposure to such pathogens occur as well as the following carcinogenic pathways they induce. Gaining knowledge in this field will give important suggestions for effective pathogen-driven cancer care, control, and, ultimately, prevention. This review will mainly focus on the major onco-pathogens and the types of cancer caused by them. It will also discuss the major pathways which, when altered, lead to the progression of these cancers.

Advances in the Lung Cancer Immunotherapy Approaches.

Despite the progress in the comprehension of LC progression, risk, immunologic control, and treatment choices, it is still the primary cause of cancer-related death. LC cells possess a very low and heterogeneous antigenicity, which allows them to passively evade the anticancer defense of the immune system by educating cytotoxic lymphocytes (CTLs), tumor-infiltrating lymphocytes (TILs), regulatory T cells (Treg), immune checkpoint inhibitors (ICIs), and myeloid-derived suppressor cells (MDSCs). Though ICIs are an important candidate in first-line therapy, consolidation therapy, adjuvant therapy, and other combination therapies involving traditional therapies, the need for new predictive immunotherapy biomarkers remains. Furthermore, ICI-induced resistance after an initial response makes it vital to seek and exploit new targets to benefit greatly from immunotherapy. As ICIs, tumor mutation burden (TMB), and microsatellite instability (MSI) are not ideal LC predictive markers, a multi-parameter analysis of the immune system considering tumor, stroma, and beyond can be the future-oriented predictive marker. The optimal patient selection with a proper adjuvant agent in immunotherapy approaches needs to be still revised. Here, we summarize advances in LC immunotherapy approaches with their clinical and preclinical trials considering cancer models and vaccines and the potential of employing immunology to predict immunotherapy effectiveness in cancer patients and address the viewpoints on future directions. We conclude that the field of lung cancer therapeutics can benefit from the use of combination strategies but with comprehension of their limitations and improvements.