Hormonal influences on cancer progression and prognosis.
Cell differentiation, proliferation, apoptosis, and cell motility are induced and regulated by a host of growth factors, vitamins, and hormones. The mode of function of these modifiers of biological response, the signaling pathways that they activate, and the interacting pathways that can influence the biological outcome have been the focus of attention. Especially recognized and discussed in this review is the deregulation of their function, leading to abnormalities in cell proliferation, alteration of intercellular adhesive cohesion, remodeling of the extracellular matrix, and invasive behavior and metastatic deposition that are so characteristic of tumor development and progression, which strongly underscores the concept of molecular progression of cancer constructed on the basis of the relationship between genetic changes and the biological events associated with cancer progression. The molecular changes associated with hormone- and vitamin-driven responses and the deregulation of the expression and function of their target genes seem to correlate with specific biological events linked with cancer invasion and progression, and these findings could lead to the establishment of new markers of progression and to the development of new strategies for patient management. The scope of this work has been restricted by design and is dictated by the field of interest of the author's laboratory, but it is hoped that this field would be regarded adequately to reflect the wide genre of scientific interest in this field of human disease.
Sherbet
G V
GV
School of Electrical, Electronic, and Computer Engineering, University of Newcastle upon Tyne, Newcastle upon Tyne NE7 6RU, United Kingdom.
D000818:Animals; D001943:Breast Neoplasms / Q000473:pathology / Q000503:physiopathology; D002453:Cell Cycle; D002455:Cell Division; D004967:Estrogens; D005260:Female; D015870:Gene Expression; D006728:Hormones / Q000502:physiology*; D006801:Humans; D008297:Male; D054778:NM23 Nucleoside Diphosphate Kinases; D009361:Neoplasm Invasiveness; D009369:Neoplasms / Q000473:pathology / Q000503:physiopathology; D009701:Nucleoside-Diphosphate Kinase / Q000502:physiology; D011333:Pro-Opiomelanocortin; D011372:Progestins; D011379:Prognosis; D011471:Prostatic Neoplasms; D011944:Receptors, Androgen; D011960:Receptors, Estrogen / Q000502:physiology; D011980:Receptors, Progesterone / Q000502:physiology; D000071163:Trefoil Factor-1; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000502:physiology; D000521:alpha-MSH
D004967:Estrogens; D006728:Hormones; D054778:NM23 Nucleoside Diphosphate Kinases; D011372:Progestins; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C051838:TFF1 protein, human; D000071163:Trefoil Factor-1; D025521:Tumor Suppressor Proteins; D000521:alpha-MSH; D011333:Pro-Opiomelanocortin; D009701:Nucleoside-Diphosphate Kinase