Knowledge of the Molecular Signaling Pathways Improves the Chances of Treatment of Gastrointestinal Stromal Tumors. Gastrointestinal Stromal Tumors are the most common mesenchymal tumors of the gastrointestinal tract. A better molecular understanding of this entity, as Christopher L. Cordless in Modern Pathology in 20141 demonstrated, GISTs mainly a result from two-level changes in two Oncogenes
Having knowledge of the oncogenic pathways of this condition, allows the possibility of creating models that stratify the risk of recurrence of GIST after surgery. This risk is determined by analyzing three factors in very low risk patients, low risk, medium and high risk, according to the model of NIH.
Emphasis on tumors where rupture of the tumor capsule occurs, always have indication for adjuvant treatment. Imatinib is a tyrosine inhibitor developed in the early 1990’s as a treatment chronic myelogenous leukemia due to its capacity of inhibiting the fusion oncoprotein BCR-ABL. Owing to structural similarities with KIT,
This demonstrated that imatinib has a strong activity against KIT – mutant GIST cell lines. Until then, treatment options for patients with the diagnosis of GIST was poor. However, surgery was the state of art for localized GIST. With conventional chemotherapy the response rate was less than 5% with a median survival for advanced
In cases where a patient was treated with imatinib and developed liver metastases, one of the recommendations may be increasing the dose according to the patient’s tolerance and their comorbidities, since with this approach we may accomplish a good partial response and with a stable disease . The results showed a significant increase in progression free survival, but no improvement in overall survival.
The work Demitri GD, et al.9 showed an improvement in progression free time of sunitinib. For third-line treatments a new molecule appeared regorafenib.