Early season weed mapping in rice crops using multi-spectral UAV data

In this article, we propose an automatic procedure for classification of UAV imagery to map weed presence in rice paddies at early stages of the growing cycle. The objective was to produce a weed map (common weeds and cover crop remnants) to support variable rate technologies for site-specific weed management. A multi-spectral ortho-mosaic, derived from images acquired by a Parrot Sequoia sensor mounted on a quadcopter, was classified through an unsupervised clustering algorithm; cluster labelling into â weed/no weed classes was achieved using geo-referenced observations. We tested the best set of input features among spectral bands, spectral indices and textural metrics. Weed mapping performance was assessed by calculating overall accuracy (OA) and, for the weed class, omission (OE) and commission errors (CE). Classification results were assessed under an alarmist approach in order to minimise the chance of overestimating weed coverage. Under this condition, we found that best results are provided by a set of spectral indices (OA= 96.5%, weed CE = 2.0%). The output weed map was aggregated to a grid layer of 5 x 5 m to simulate variable rate management units; a weed threshold was applied to identify the portion of the field to be subject to treatment with herbicides. Ancillary information on weed and crop conditions were derived over the grid cells to support precision agronomic management of rice crops at the early stage of growth

DNA damage repair and survival outcomes in advanced gastric cancer patients treated with first-line chemotherapy

The DNA damage response (DDR) network is exploited by cancer cells to withstand chemotherapy. Gastric cancer (GC) carries deregulation of the DDR and harbors genetic defects that fuel its activation. The ATM-Chk2 and ATR-Chk1-Wee1 axes are deputed to initiate DNA repair. Overactivation of these pathways in cancer cells may represent an adaptive response for compensating genetic defects deregulating G1 -S transition (e.g., TP53) and ATM/ATR-initiated DNA repair (e.g., ARID1A). We hypothesized that DDR-linked biomarkers may predict clinical outcomes in GC patients treated with chemotherapy. Immunohistochemical assessment of DDR kinases (pATM, pChk2, pChk1 and pWee1) and DNA damage markers (\u3b3-H2AX and pRPA32) was performed in biological samples from 110 advanced GC patients treated with first-line chemotherapy, either in phase II trials or in routine clinical practice. In 90 patients, this characterization was integrated with targeted ultra-deep sequencing for evaluating the mutational status of TP53 and ARID1A. We recorded a positive association between the investigated biomarkers. The combination of two biomarkers (\u3b3-H2AXhigh /pATMhigh ) was an adverse factor for both progression-free survival (multivariate Cox: HR 2.23, 95%CI: 1.47-3.40) and overall survival (multivariate Cox: HR: 2.07, 95%CI: 1.20-3.58). The relationship between the \u3b3-H2AXhigh /pATMhigh model and progression-free survival was consistent across the different TP53 backgrounds and was maintained in the ARID1A wild-type setting. Conversely, this association was no longer observed in an ARID1A-mutated subgroup. The \u3b3-H2AXhigh /pATMhigh model negatively impacted survival outcomes in GC patients treated with chemotherapy. The mutational status of ARID1A, but apparently not TP53 mutations, affects its predictive significanc

DNA damage repair and survival outcomes in advanced gastric cancer patients treated with first-line chemotherapy

The DNA damage response (DDR) network is exploited by cancer cells to withstand chemotherapy. Gastric cancer (GC) carries deregulation of the DDR and harbors genetic defects that fuel its activation. The ATM-Chk2 and ATR-Chk1-Wee1 axes are deputed to initiate DNA repair. Overactivation of these pathways in cancer cells may represent an adaptive response for compensating genetic defects deregulating G1-S transition (e.g., TP53) and ATM/ATR-initiated DNA repair (e.g., ARID1A). We hypothesized that DDR-linked biomarkers may predict clinical outcomes in GC patients treated with chemotherapy. Immunohistochemical assessment of DDR kinases (pATM, pChk2, pChk1 and pWee1) and DNA damage markers (\uce\ub3-H2AX and pRPA32) was performed in biological samples from 110 advanced GC patients treated with first-line chemotherapy, either in phase II trials or in routine clinical practice. In 90 patients, this characterization was integrated with targeted ultra-deep sequencing for evaluating the mutational status of TP53 and ARID1A. We recorded a positive association between the investigated biomarkers. The combination of two biomarkers (\uce\ub3-H2AXhigh/pATMhigh) was an adverse factor for both progression-free survival (multivariate Cox: HR 2.23, 95%CI: 1.47\ue2\u80\u933.40) and overall survival (multivariate Cox: HR: 2.07, 95%CI: 1.20\ue2\u80\u933.58). The relationship between the \uce\ub3-H2AXhigh/pATMhigh model and progression-free survival was consistent across the different TP53 backgrounds and was maintained in the ARID1A wild-type setting. Conversely, this association was no longer observed in an ARID1A-mutated subgroup. The \uce\ub3-H2AXhigh/pATMhigh model negatively impacted survival outcomes in GC patients treated with chemotherapy. The mutational status of ARID1A, but apparently not TP53 mutations, affects its predictive significance

Expression of the Hippo transducer TAZ in association with WNT pathway mutations impacts survival outcomes in advanced gastric cancer patients treated with first-line chemotherapy

Background: An extensive crosstalk co-regulates the Hippo and Wnt pathway. Preclinical studies revealed that the Hippo transducers YAP/TAZ mediate a number of oncogenic functions in gastric cancer (GC). Moreover, comprehensive characterization of GC demonstrated that the Wnt pathway is targeted by oncogenic mutations. On this ground, we hypothesized that YAP/TAZ- and Wnt-related biomarkers may predict clinical outcomes in GC patients treated with chemotherapy. Methods: In the present study, we included 86 patients with advanced GC treated with first-line chemotherapy in prospective phase II trials or in routine clinical practice. Tissue samples were immunostained to evaluate the expression of YAP/TAZ. Mutational status of key Wnt pathway genes (CTNNB1, APC and FBXW7) was assessed by targeted DNA next-generation sequencing (NGS). Survival curves were estimated and compared by the Kaplan-Meier product-limit method and the log-rank test, respectively. Variables potentially affecting progression-free survival (PFS) were verified in univariate Cox proportional hazard models. The final multivariate Cox models were obtained with variables testing significant at the univariate analysis, and by adjusting for all plausible predictors of the outcome of interest (PFS). Results: We observed a significant association between TAZ expression and Wnt mutations (Chi-squared p = 0.008). Combined TAZ expression and Wnt mutations (TAZpos/WNTmut) was more frequently observed in patients with the shortest progression-free survival (negative outliers) (Fisher p = 0.021). Uni-and multivariate Cox regression analyses revealed that patients whose tumors harbored the TAZpos/WNTmutsignature had an increased risk of disease progression (univariate Cox: HR 2.27, 95% CI 1.27-4.05, p = 0.006; multivariate Cox: HR 2.73, 95% CI 1.41-5.29, p = 0.003). Finally, the TAZpos/WNTmutsignature negatively impacted overall survival. Conclusions: Collectively, our findings indicate that the oncogenic YAP/TAZ-Wnt crosstalk may be active in GC, conferring chemoresistant traits that translate into adverse survival outcomes

Expression of the Hippo transducer TAZ in association with WNT pathway mutations impacts survival outcomes in advanced gastric cancer patients treated with first-line chemotherapy

Background: An extensive crosstalk co-regulates the Hippo and Wnt pathway. Preclinical studies revealed that the Hippo transducers YAP/TAZ mediate a number of oncogenic functions in gastric cancer (GC). Moreover, comprehensive characterization of GC demonstrated that the Wnt pathway is targeted by oncogenic mutations. On this ground, we hypothesized that YAP/TAZ- and Wnt-related biomarkers may predict clinical outcomes in GC patients treated with chemotherapy. Methods: In the present study, we included 86 patients with advanced GC treated with first-line chemotherapy in prospective phase II trials or in routine clinical practice. Tissue samples were immunostained to evaluate the expression of YAP/TAZ. Mutational status of key Wnt pathway genes (CTNNB1, APC and FBXW7) was assessed by targeted DNA next-generation sequencing (NGS). Survival curves were estimated and compared by the Kaplan-Meier product-limit method and the log-rank test, respectively. Variables potentially affecting progression-free survival (PFS) were verified in univariate Cox proportional hazard models. The final multivariate Cox models were obtained with variables testing significant at the univariate analysis, and by adjusting for all plausible predictors of the outcome of interest (PFS). Results: We observed a significant association between TAZ expression and Wnt mutations (Chi-squared p = 0.008). Combined TAZ expression and Wnt mutations (TAZ pos /WNT mut ) was more frequently observed in patients with the shortest progression-free survival (negative outliers) (Fisher p = 0.021). Uni-and multivariate Cox regression analyses revealed that patients whose tumors harbored the TAZ pos /WNT mut signature had an increased risk of disease progression (univariate Cox: HR 2.27, 95% CI 1.27-4.05, p = 0.006; multivariate Cox: HR 2.73, 95% CI 1.41-5.29, p = 0.003). Finally, the TAZ pos /WNT mut signature negatively impacted overall survival. Conclusions: Collectively, our findings indicate that the oncogenic YAP/TAZ-Wnt crosstalk may be active in GC, conferring chemoresistant traits that translate into adverse survival outcomes

Prevalence of anal human papillomavirus infection and cytologic abnormalities among HIV-infected and HIV-uninfected men who have sex with men

Introduction: Human papillomavirus (HPV) is responsible for 85% of anal cancers. Recently, anal cancer incidence has been increasing, particularly in men who have sex with men (MSM). Cytology may be a useful tool for the detection of anal precancerous lesions. We assessed the prevalence and determinants of anal HPV infection and cytologic abnormalities among HIV-infected and -uninfected MSM. Materials and Methods: MSM ≥18-year-old attending an STI clinic in Rome (Italy) were enrolled. Anal cytologic samples were collected in PreservCyt (Hologic) using a Dacron swab. The Linear Array HPV Genotyping Test (Roche Diagnostics) was used for the detection and genotyping of 37 mucosal HPV types. Liquid-based cytological slides were obtained using a ThinPrep2000 processor (Hologic). The morphology of the anal pap-test was classified following the Bethesda 2001 guidelines. Results: We enrolled 180 HIV-infected (median age 41 years, IQR 33–47) and 438 HIV-uninfected MSM (median age 32 years, IQR: 27–39). Most of the individuals were Caucasian (92.2% and 97.0%, respectively). HPV prevalence, both overall (93.3% vs 72.4%, p<.001) and by high-risk (HR) HPV types (80.5% vs 56.0%, p<.001), was significantly higher among HIV-infected than HIV-uninfected individuals. HPV-multiple infections were evidenced in 48.2% of the HIV-uninfected and 76.1% of the HIV-infected MSM (p<.001). HPV16 was the most prevalent genotype in both groups (23.3% in HIV-positive and 17.6% in HIV-negative MSM). HPV6 and 84 were the most frequent low-risk types in both cohorts. Anal cytologic abnormalities were found in a significantly higher proportion of HIV-infected MSM (46.1% vs 27.9%, p<.001). H-SILs (high-grade squamous intraepithelial lesions) were exclusively observed among the HIV-infected individuals, although at a low prevalence (1.2%). Conclusions: A high prevalence of anal HPV infection and cytologic abnormalities was evidenced in both populations. Nonetheless, HIV-infected MSM showed a significantly higher rate of HPV infection and abnormal cytology, confirming that HIV-1 infection poses a significant risk for anal HPV infection as well as for anal cellular abnormalities. Screening for anal cancer, which is currently the most frequent non-AIDS-defining cancer in HIV-positive MSM, should be considered for this population. Moreover, vaccination strategies for the prevention of HPV infection should be taken into account

Prevalence of anal human papillomavirus infection and cytologic abnormalities among HIV-infected and HIV-uninfected men who have sex with men

Introduction: Human papillomavirus (HPV) is responsible for 85% of anal cancers. Recently, anal cancer incidence has been increasing, particularly in men who have sex with men (MSM). Cytology may be a useful tool for the detection of anal precancerous lesions. We assessed the prevalence and determinants of anal HPV infection and cytologic abnormalities among HIV-infected and -uninfected MSM. Materials and Methods: MSM ≥18-year-old attending an STI clinic in Rome (Italy) were enrolled. Anal cytologic samples were collected in PreservCyt (Hologic) using a Dacron swab. The Linear Array HPV Genotyping Test (Roche Diagnostics) was used for the detection and genotyping of 37 mucosal HPV types. Liquid-based cytological slides were obtained using a ThinPrep2000 processor (Hologic). The morphology of the anal pap-test was classified following the Bethesda 2001 guidelines. Results: We enrolled 180 HIV-infected (median age 41 years, IQR 33–47) and 438 HIV-uninfected MSM (median age 32 years, IQR: 27–39). Most of the individuals were Caucasian (92.2% and 97.0%, respectively). HPV prevalence, both overall (93.3% vs 72.4%, p<.001) and by high-risk (HR) HPV types (80.5% vs 56.0%, p<.001), was significantly higher among HIV-infected than HIV-uninfected individuals. HPV-multiple infections were evidenced in 48.2% of the HIV-uninfected and 76.1% of the HIV-infected MSM (p<.001). HPV16 was the most prevalent genotype in both groups (23.3% in HIV-positive and 17.6% in HIV-negative MSM). HPV6 and 84 were the most frequent low-risk types in both cohorts. Anal cytologic abnormalities were found in a significantly higher proportion of HIV-infected MSM (46.1% vs 27.9%, p<.001). H-SILs (high-grade squamous intraepithelial lesions) were exclusively observed among the HIV-infected individuals, although at a low prevalence (1.2%). Conclusions: A high prevalence of anal HPV infection and cytologic abnormalities was evidenced in both populations. Nonetheless, HIV-infected MSM showed a significantly higher rate of HPV infection and abnormal cytology, confirming that HIV-1 infection poses a significant risk for anal HPV infection as well as for anal cellular abnormalities. Screening for anal cancer, which is currently the most frequent non-AIDS-defining cancer in HIV-positive MSM, should be considered for this population. Moreover, vaccination strategies for the prevention of HPV infection should be taken into account

Circulating cell free DNA and citrullinated histone H3 as useful biomarkers of NETosis in endometrial cancer

Abstract Background Cancer mortality is mainly caused by organ failure and thrombotic events. It has been demonstrated that NETosis, a chromatin release mechanism implemented by neutrophils, may contribute to these lethal systemic effects. Our aim was to investigate NETosis biomarkers in endometrial cancer (EC). Methods The experiments were conducted on 21 healthy subjects (HS) with no gynecological conditions, and on 63 EC patients. To assess the presence of NETosis features, IHC and IF was performed using antibodies against citrullinated histone H3 (citH3), neutrophil elastase (NE) and histone 2B. Serum levels of cell free DNA (cfDNA), cell free mitochondrial DNA (cfmtDNA) and citH3 were measured by qPCR using one microliter of deactivated serum, and by ELISA assay respectively. Fragmentation pattern of serum cfDNA was analyzed using the Agilent 2100 Bioanalyzer and High Sensitivity DNA Chips. Receiver operating characteristic (ROC) analysis was used to identify a cut off for cfDNA and cfmtDNA values able to discriminate between ECs and HSs. Correlation analysis and multiple correspondence analysis (MCA) between cfDNA, mtcfDNA, citH3 and blood parameters were used to identify the potential association among serum parameters in EC grades. Results We demonstrated the presence of NETosis features in tissues from all EC grades. Serum cfDNA and cfmtDNA levels discriminate ECs from HSs and a direct correlation between citH3 and cfDNA content and an inverse correlation between cfmtDNA and citH3 in EC sera was observed, not detectable in HSs. MCA indicates cfDNA, cfmtDNA and citH3 as features associated to G1 and G2 grades. A correlation between increased levels of cfDNA, citH3 and inflammation features was found. Finally, serum nucleosomal cfDNA fragmentation pattern varies in EC sera and correlates with increased levels of cfDNA, citH3, lymphocytes and fibrinogen. Conclusion Our data highlight the occurrence of NETosis in EC and indicate serum cfDNA and citH3 as noninvasive biomarkers of tumor-induced systemic effects in endometrial cancer