Background:
Prostate cancer is the most common visceral neoplasia in men and frequently present chemotherapy resistance.
In this context, lemongrass (Cymbopogon citratus (D.C.) Stapf) has been studied, since it presents many important biological activities,
such as anticancer. Objective: We investigated the antitumor effect of lemongrass and in chemotherapy activity using prostate cancer
cells line (DU-145).
Methods:
DU-145 cells were exposed to different concentrations of aqueous extract of lemongrass (30; 100; 300; 500 and 1000 μg/mL),
isolated and in combination with docetaxel, during 24 and 72 hours. After, cell viability and proliferation, oxidative metabolism, colony
formation and cell cycle analyses were performed. Also, we exposed African green monkey kidney cell line (VERO) to the same
lemongrass concentrations to investigate a possible toxicity of this extract.
Results:
Our findings suggested that lemongrass presented an antitumor effect and improved docetaxel chemotherapy activity by
decreasing cell viability and proliferation as well as colony formation. Moreover, we found an oxidative stress increased and cell cycle
arresting in G0/G1 phase. In addition, this extract presented selectivity action for cancer cells, since it did not cause cytotoxicity in
normal cells, ensuring non-toxic therapeutic concentrations.
Conclusion:
Lemongrass is a promising medicinal plant that could be used during chemotherapeutic treatment, in order to potentiate the
antitumor response and decrease the resistance of prostate cancer.
6061 Background: Platinum-based chemotherapy in association to cetuximab is the standart first-line treatment for metastatic HNSCC. There is no established biomarker for cetuximab efficacy in HNSCC. We have previously shown that PTEN loss of expression is a bad prognostic factor for patients treated with platinum-based chemotherapy and cetuximab. The aim of the present study was evaluate the prognostic impact of PTEN loss of expression in patients treated with or without cetuximab and to evaluate its predictive value to cetuximab benefit. Methods: One hundred and nineteen patients with metastatic or locally recurrent HNSCC were included. Clinical data on treatment and outcomes was retroespectively colected from medical charts. Tissue micro-array was constructed to evaluate PTEN protein expression through immunohistochemistry. Citoplasmatic staining was evaluated using H-score. Tumors with H-score < 10 were considered to present PTEN loss of expression. Results: From the 119 patients 72 were treated with chemotherapy plus cetuximab while 47 were treated with chemotherapy alone. Median overall survival (mOS) was 9.2 months and median progression free survival (PFS) was 4.6 months. Patients treated with cetuximab compared to those who were not treated with cetuximab had a mOS of 11.4 vs 7.0 months (p = 0.770) and a median PFS of 6.2 vs 3.0 months (p = 0.249). Patients with PTEN loss of expression had a worse OS and PFS with mOS of 5.8 vs 10.5 months (p = 0.002) months and mPFS of 3.2 vs 5.2 (p = 0.015). On multivariate analysis including PTEN loss of expression and ECOG performance status both remained independently associated to survival with HR 2.25 (CI95% 1.28-3.97, p = 0.005) for PTEN loss of expression and a HR 1.63 (CI95% 1.07-2.50, p = 0.023) for ECOG. Negative prognostic impact of PTEN loss of expression was seen only in the cetuximab treated patients (mOS 7.3 vs 13.0 months; p = 0.002) but not in the chemotherapy only group (mOS 3.2 vs 7.5 months; p = 0.051). Interaction test for treatment group and PTEN loss of expression showed a p = 0.418. Conclusions: The present study confirms PTEN as a prognostic factor for metastatic HNSCC and suggests PTEN expression should be studied in larger cohorts to evaluate its predictive value to cetuximab response.
683 Background: Anti-EGFR plus chemotherapy (CT) promotes high response rates (RR) and median overall survival (OS) surpasses 30 months in RASwt/BRAFwt mCRC. After disease progression (PD), resistance mechanisms have been described. The aim of our study was to evaluate efficacy of anti-EGFR re-challenge (TRECC). Methods: We retrospectively analyzed a cohort of patients (pts) with mCRC. All pts had received anti-EGFR plus CT and were discontinued for different reasons. During the treatment, there was re-challenge with an anti-EGFR + CT. We aimed to evaluate progression-free survival (PFS) and OS after re-challenge and prognostic factors associated with PFS. Results: Sixty eight pts met the study criteria. Median follow-up after re-challenge was 39.3m. Discontinuation after first exposure was 25% due to PD; 75% for other reasons. Median anti-EGFR free interval was 10.5m. At re-challenge, main CT regime was: FOLFIRI 58.8%, Cetuximab and Panitumumab were used in 59 and 9 pts respectively. mPFS after re-challenge was 6.6m; mOS was 24.4m. Objective response rate (CR + PR) at re-challenge was 42.6%. In an univariate analysis, adverse prognostic factors related to PFS were: absence of objective response at 1st EGFR exposure (HR 2.12, CI:1.20-3.74 p = 0.009); PD as reason for 1st discontinuation (HR 3.44, CI:1.88-6.29 p < 0.0001); re-challenge at fourth or later lines (HR 2,51, CI:1.49-4.23 p = 0.001); panitumumab use (HR 2.26 CI:1.18-5.54 p = 0.017). In a multivariate model, only PD as reason for 1st discontinuation remained statistically significant (HR = 2.63, CI:1.14-6.03 p = 0.022). mPFS was 3.3m and 8.4m and mOS was 7,5m and 33,4m in patients with PD as reason for 1st discontinuation and other reasons respectively. Conclusions: Re-challenge therapy is commonly used due to paucity of effective lines of treament for mCRC. In our analysis, pts that stopped 1st anti-EGFR therapy due to PD have shorter survival, suggesting these pts do not benefit from TRECC. However, interruption due to treatment holiday after PR/CR resulted in longer PFS. In conclusion, for a selected group of pts, TRECC could be considered a strategy of treatment. Due to the limited number of pts, our data should be evaluated in a prospective cohort of patients.
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