The present investigation reveals the relationship between excess thermodynamic functions and the growth habits of the eutectic phases from the melt by continuous melt-growth technique. Excess thermodynamic functions computed for different compositions of the benzoic acid -cinnamic acid eutectic system have been found consistent with the criteria of spontaneity and Planck formulation, and their reliability has been ascertained by the application of Guggenheim lattice theory. The results on the kinetics of anisotropic growth of the eutectic phases from the melt, evidentially evince the dislocation mechanism. Evidences have been obtained for a parabolic variation of mechanical strength with growth velocity of the eutectic material grown anisotropically from the melt at different intervals, which offer supporting complement to the dislocation mechanism governing the dependence of growth velocity on supercooling ∆T in the solidus -liquidus interface in a form : V = k(∆T ) 2 . A moderate anisotropic growth region has been explored by unique results of strength properties and microscopic results as well, to growing a layer of lamellae in a unidirectional lamina. An anisotropic eutectic composite lamellae lamina developed by moderate growth velocity (7.3 x 10 -8 m 3 s -1 ), is of greater interest offering optimum hardness, approximately varying between three-and eight fold average increase in different modes of the mechanical strength in comparison to its isotropic growth carried out in an ice-bath (~273K), and manifold superior to its constituent phases irrespective of the growth mode. The directional lamina of uniform microstructural parameter lamellae, indicates that there is a perfect lamella-matrix equilibrium for which excess thermodynamic functions do vanish.

Cisplatin, that is, cis-diamminedichloroplatinum is a coordinate compound that is mainly preferred as prior treatment against several solid tumors and malignancies like ovaries, head and neck, testicular, and lung cancers because of its anticancer activity. Cisplatin binds at the N7 position of purine and forms adducts, leading to altered activity of DNA that triggers apoptosis. DNA damage is followed by several signaling pathways like induced oxidative stress, upregulated p53, mitogen-activated protein kinase (MAPK), and Jun N-terminal kinases (JNK) or Akt pathways along with induced apoptosis. Additionally, cisplatin treatment comes with few disadvantages such as toxic effects, that is, hepatotoxicity, cardiotoxicity, neurotoxicity, etc., and drug resistance. Furthermore, to overcome cisplatin resistance and toxicological effects, combination drug therapy has been considered. The aim of the review is to focus on the molecular mechanism of action of cisplatin and combination drug therapy to reduce the side effects in cancer therapy.