Knowing and describing the pathophysiological mechanisms of cancer is a complex task.
In recent years, the development of new technologies has made it possible to learn about various aspects of the physiology of cancer.
In the clinical setting, this has resulted in the introduction of tumor biomarkers (molecules that are expressed at abnormal levels in certain types of cancer and can be detected to diagnose or analyze the evolution of a disease) and the identification of potential therapeutic targets.
The process by which normal cells transform into cancers is called carcinogenesis, and this progressive transformation of normal cells to highly malignant derivatives originates from alterations in the genetic material (mutations).
These mutations give a cell the ability to divide at a higher rate and generate offspring that retain this mutation (clones). Subsequently, the daughter cells accumulate subsequent and diverse mutations that allow the generation of different clones with greater capacity for survival and growth.
Normally, the cells of the immune system are able to kill these tumor cells, in a process called tumor immunosurveillance. However, some of these clones may acquire new capabilities that allow them to evade these control mechanisms and a neoplasm develops.
The role of genetic alterations in carcinogenesis was revealed by discovering in the human genome, genes homologous to retroviral genes previously related to the development of tumors. In normal human cells these genes are called proto-oncogenes and are related to the growth and proliferation of normal cells.
When they are mutated, they are called oncogenes and their mutation is of a dominant type, that is, it is only necessary that one of the alleles undergoes a mutation for the protein it encodes to gain functionality.
Another type of genes closely related to the physiology of this disease are tumor suppressor genes, which control proliferation, cell repair and apoptosis (cell death). In cancer, tumor suppressor genes undergo loss-of-function mutations of the proteins they encode and, therefore, a failure in the internal control and repair mechanisms of the cell, allowing their uncontrolled proliferation and growth, in addition to the accumulation of new mutations.
Cells have complex and redundant mechanisms for the repair of DNA damage or alterations, in which DNA repair genes are involved. When these mutate, cells become more sensitive to agents that damage DNA and to the acquisition and accumulation of new mutations that promote carcinogenesis. Some individuals carry heterozygous mutations in these genes, which is associated with a greater susceptibility to developing different types of cancer.
Mutations of the genes responsible for carcinogenesis can be inherited or acquired de novo, generally the product of exposure to environmental substances (carcinogens) or biological agents (oncogenic viruses).
After an exhaustive analysis of everything previously published, 6 characteristics that are shared by tumor cells were described:
Independence of growth signals.
Insensitivity to stimuli that inhibit growth.
Invasiveness and metastasis.
Unlimited potential for replication.
The latest discoveries have opened up a range of possibilities to improve cancer management.
The introduction of new specific biomarkers has been allowed to improve, for example, tumor diagnosis or response to therapy. On the other hand, the identification of potential therapeutic targets has motivated the explosive increase in pharmacological research in the last decade. Likewise, much more research is needed to finally get the best results for the patient.
*Please note that we are not in a position to give you medical advice. Every case is different and every woman needs specific care. You can refer to your physician if you are seeking medical consultation.
Conocer y describir los mecanismos fisiopatológicos del cáncer es una tarea compleja.
Durante los últimos años, el desarrollo de nuevas tecnologías ha permitido conocer diversos aspectos de la fisiología celular.