OBJECTIVE: To evaluate the genetic tests is fundamental for the adequate treatment of non-small cell lung cancer (NSCLC) with tyrosine kinase inhibitors (TKI). Given that access to this evaluation is still limited for those who depend on the Brazilian Public Health System, it seems important to provide regulatory agencies with epidemiological and prognostic information to guide future health policies and guidelines in Brazil. This work aims to characterize EGFR and KRAS mutations in NSCLC and associating them with patients demographic and tumor clinical-pathologic features.
METHODS: From 2004 to 2017, 237 metastatic NSCLC patients treated at Erasto Gäertner Cancer Hospital were included in this study. Electronic medical records were retrospectively reviewed and the mutational status EGFR and KRAS were defined.
RESULTS: We detected EGFR mutation in 20 samples (15.7%), and KRAS mutation in 26 samples (21.5%). The majority of EGFR mutations was detected within the exon 19 (n=9, 45.0%), and for KRAS G12V (n=8, 30.8%) and G12C (n=8, 30.8%) were the hotspots. The median overall survival was 11 months. We did not detect any statistical differences in survival rates between mutated and wild-type tumors neither for EGFR (p=0.898) nor for KRAS (p=0.458). Only two patients had access to TKI and were considered outliers with the best survival rates.
CONCLUSION: We described important information about NSCLC biological behavior in a population treated in a reference public cancer center in South Brazil. Studies like this highlight the magnitude that TKI treatment could have in the overall survival of patients with NSCLC after being introduced into the SUS. Future studies that address the economic impact of this issue are also needed. Here we also make a comparison of our results with other regions of Brazil that have different genetic backgrounds to evaluate the impact of targeted therapies.
Keywords: Lung Neoplasms, Genes, erbB-1, Kirsten murine sarcoma virus, Public Health, Brazil.
In the last decade, important advances have been made in the treatment of metastatic prostate cancer, resulting in a better understanding of the biology underlying the disease, and in the approval of several therapeutic agents such as immunotherapy, new generation antiandrogens, cytotoxic chemotherapies, and radiopharmaceuticals. All these recent advances have been incorporated in clinical guidelines and a critical analysis of the data available should be important to help the decision-making process. In addition, the incorporation of well established therapies in early disease stages have demonstrated a robust overall survival gain for patients with castration-sensitive metastatic prostate cancer. However, no predictive biomarkers of response are available and the selection of the best therapeutic option is still challenging depending on clinical and pathological factors. Many questions related to the optimal sequencing of agents, or comparison of its efficacy remain unanswered.
Keywords: Prostate; Review/drug therapy; Receptors; Androgen; Androgen Antagonists; Advanced Treatment; Prostate-Specific Antigen
Metastatic castration-resistant prostate cancer (mCRPC) is an extremely severe disease that relentlessly evolves to death. Over the past few years, we have seen significant improvements in the different types of treatments available, which have positively impacted several clinical outcomes, including higher survival rates and better quality of life. Since Radium-223 approval by FDA in 2013, nuclear medicine has been incorporated to the therapeutic arsenal. Progress in this field have motivated a pursuit for new targeted therapies using radioactive isotopes. Recent reports addressing the first cases treated with this technique are impressive due to the high response rates obtained in refractory patients. Here we report the case of a patient with mCRPC who had been previously treated with several lines of anti-androgen therapy and cytotoxic chemotherapy, recently treated with PSMA labeled with the alpha-emitting radioisotope Actinium-225 (225Ac).
Keywords: Prostatic Neoplasms; Castration-Resistant; Nuclear Medicine; Alpha Particles
Giant-cell tumor is a relatively rare neoplasia, benign but locally aggressive, that causes significant bone destruction with predilection for epiphyseal and metaphyseal regions of long bones and the spine. Definitive treatment is surgical, with complete tumoral resection followed by autograft, homograft, arthrodesis, unconventional endoprostheses or methylmethacrylate. In most cases, surgery is accompanied by high morbidity and variable recurrence rates, depending on the site, size and type of surgical intervention.Denosumab, a RANKL inhibitor, acts by decreasing tumoral osteoclastic activity and is approved by the Food and Drug Administration for treatment of GCT when surgery is not possible or when it is associated with high morbidity. This report of cases is based on the review of medical records from the Ambulatory Service for Adolescents and Young Adults (AYA), aiming to show the experience of the Service with the use of denosumab for neoadjuvant purposes.
Keywords: Denosumab; RANK Ligand; Giant Cell Tumors.
Applications for 68Ga-PSMA PET-CT continue to expand beyond prostate cancer. The objective of this case report is to illustrate a rare phenomenon known as tumor-totumor metastasis in which precise histological diagnosis is an essential prerequisite for correct clinical management of patients. A 89-year-old man with prostate cancer underwent 68Ga-PSMA PET-CT study for rescreening after increasing prostate specific antigen (PSA), revealing abnormal uptake of the radioindicator in the prostate and bilateral lung nodules. A biopsy was performed on one of the left lung nodules and the results of the pathology examination revealed that the lesion consisted of metastatic prostatic adenocarcinoma within a primary lung adenocarcinoma.
Keywords: 68Ga-PSMA; Tumor-to-tumor metastasis; Prostate cancer; Lung cancer.