• Examining the receptors involved in the growth of cancer cells in cancer
  • Zahra Mollaei,1,*
    1. Msc of Molecular Genetic Department of Genetics, Zanjan Branch, Islamic Azad University, Zanjan, Iran.


  • Introduction: Many distinguishing traits are present in cancer cells. These are caused by cellular signal transduction dysregulation brought on by the genetic and epigenetic modifications that fuel cancer. This has an impact on not only the cancer cells themselves but also a larger signaling network that includes blood vessels, the immune system, the ECM, and other cells. In fact, systemic effects are ultimate what causes individuals to die from cancer, and metastatic cancer can be thought of as a systemic disease that affects signaling throughout the affected person. Examining the receptors involved in the development of cancer cells was the goal of this review study.
  • Methods: This review study has written about Examining the receptors involved in the growth of cancer cells in cancer from scientific databases such as Science Direct, Springer, Google Scholar, and PubMed.
  • Results: The study's findings were evident Cancer treatments have greatly benefited from pharmacological and antibody-based inhibitors that target signaling proteins downstream from these or proteins altered in malignancies. For instance, nonreceptor tyrosine kinase (NTK) Abl and receptor tyrosine kinase (RTK) ErbB2 inhibitors significantly lower patient mortality in chronic myelogenous leukemia and breast cancer, respectively. However, the incidence of recurrence is high due to the emergence of drug resistance. Other inhibitors, such as those that target B-Raf, EGFR, and the kinase ALK, generate substantial decreases in tumor volume and lengthen survival in patients with melanoma and nonsmall-cell lung carcinomas Due to the redundant pathways that regulate cell proliferation and survival, crosstalk between pathways, and feedback inhibitory mechanisms that result in pathway reactivation, the complexity of the cancer signaling network poses a significant obstacle for efforts to produce such anticancer treatments. There is the reason for optimism that methods based on targeting them will be effective because pathways like Ras-ERK and Akt-PI3K signaling regulate a wide range of characteristics of cancer cells, and because parts of these pathways, or upstream receptors, are frequently mutated in a number of cancers. However, there are a number of considerations that limit the effectiveness of medicines that target these pathways. Rewiring of signaling pathways, for instance, is connected to adaptive responses to driver mutation inhibition, and this is frequently caused by either a loss of feedback inhibition or an increase of stress pathways. In addition, elements from the tumor microenvironment may promote other pathways that continue to support cell survival even when the targeted pathways are inhibited. Alternately, rare tumor cells may be selected if they have drug-resistant forms of the targeted protein or mutations in other pathways that avoid dependence on the targeted route. Additionally, epigenetic or stochastic changes in the state of tumor cells may trigger intrinsic resistance pathways.
  • Conclusion: The degree of intratumoral genetic variability makes things more difficult. This is much more prevalent than previously thought, according to recent findings derived from the sequencing of individual patient tumors' single cells and various tumor areas. Only 45% of mutations were discovered over the entire tumor in one study of kidney cancers. Single biopsies might not be enough to individually tailor a patient's treatment because of this heterogeneity, which also strongly influences intratumoral variance in susceptibility to medications that target signaling proteins altered in cancer.
  • Keywords: cancer cells, receptors, mutations, signaling pathway