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TNBCs or Triple negative breast cancers are characterized by the deficiency of progesterone and estrogen receptors and also the absence down regulation of Human epithelial growth receptor type 2 (HER2). TNBCs have low prognosis rate because of heterogeneity.The heterogeneous nature of this cancer has constrained the effective progress in drug targeting among certain people.. In general HER2, PR and ER and the rate of proliferation are main predictive and prognostic factors in the detection of cancer of breast.Several pathways are involved in the progression of triple negative breast cancer from basal like cancer cells. The foremost being the loss by BRCA1-mediated pathway or mutation in the expression of several receptors.Certain groups have made some progress in unwinding TNBC's biological diversity and relating patterns of gene expression to molecular or genotypic subtypes.Earlier molecular categories of breast cancer use PAM50 via gene expression analysis to separate the breast cancer into the 4 intrinsic subtypes classified among many TNBCs in basal (BL) group and others divided between HER2 and luminal rich group. Currently, targeted therapy for TNBCs has not been approved. Nonetheless, a continuous progress has been made to detect the tumors at specific site for targeting and establish novel improved therapy.This review speaks about different approaches to TNBC treatment like cytotoxic therapy, targeted strategies, and chemotherapeutics by damage to DNA and targeting for repair of DNA and potent Nano carriers for targeting TNBC.

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At the air-water interface, the tear film lipid layer (TFLL), a combination of lipids and proteins plays an important role in surface tension of the tear and is necessary for the physiological hydration of the ocular surface and maintenance of ocular homeostasis. Alteration in lacrimal fluid rheology, differences in lipid constitution or down regulation of particular tear proteins are found in maximum types of ocular surface disease including dry eye disease (DED). Dry eye is a disorder of the tear film due to tear deficiency or excessive tear evaporation, which causes damage to the interpalpebral ocular surface and is associated with symptoms of discomfort. It results in changes on the ocular surface epithelia causing reduced tear quantity and surface sensitivity which leads to inflammation reactions. Managing this inflammation is very helpful in dry eye disease patients. In this article we revise the current understanding of tear film properties, ocular surface and review the effectiveness of topically applied tear supplements, thermo sensitive atelocollagen punctal plug, subtrasal ultrasonic transducers, novel liposome based gelling tear formation and insulin based ophthalmic delivery systems which help in restoring the healthy tear film.