MARCELO LUIZ BALANCIN
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- Mutational Profiling of Driver Tumor Suppressor and Oncogenic Genes in Brazilian Malignant Pleural Mesotheliomas(2020) CAMPANELLA, Nathalia C.; SILVA, Eduardo Caetano; DIX, Gustavo; VAZQUEZ, Fabiana de Lima; PAULA, Flavia Escremim de; BERARDINELLI, Gustavo N.; BALANCIN, Marcelo; CHAMMAS, Roger; V, Rossana Mendoza Lopez; SILVEIRA, Henrique Cesar S.; CAPELOZZI, Vera Luiza; REIS, Rui ManuelBackground:Malignant pleural mesothelioma (MPM) is a highly lethal disease comprising a heterogeneous group of tumors with challenging to predict biological behavior. The diagnosis is complex, and the histologic classification includes 2 major subtypes of MPM: epithelioid (similar to 60% of cases) and sarcomatous (similar to 20%). Its identification depends upon pathological investigation supported by clinical and radiological evidence and more recently ancillary molecular testing. Treatment options are currently limited, with no known targeted therapies available.Objectives:To elucidate the mutation profile of driver tumor suppressor and oncogenic genes in a cohort of Brazilian patients.Methods:We sequenced 16 driver genes in a series of 43 Brazilian malignant mesothelioma (MM) patients from 3 distinct Brazilian centers. Genomic DNA was extracted from formalin-fixed paraffin-embedded tumor tissue blocks, and theTERTpromoter region was amplified by PCR followed by direct capillary sequencing. The Illumina TruSight Tumor 15 was used to evaluate 250 amplicons from 15 genes associated with solid tumors (AKT1, GNA11, NRAS, BRAF, GNAQ, PDGFRA, EGFR, KIT, PIK3CA, ERBB2, KRAS, RET, FOXL2, MET,andTP53). Library preparation with the TruSight Tumor 15 was performed before sequencing at the MiSeq platform. Data analysis was performed using Sophia DDM software.Results:Out of 43 MPM patients, 38 (88.4%) were epithelioid subtype and 5 (11.6%) were sarcomatoid histotype. Asbestos exposure was present in 15 (39.5%) patients with epithelioid MPM and 3 (60%) patients with sarcomatoid MPM. We founda TERTpromoter mutation in 11.6% of MM, and the c.-146C>T mutation was the most common event. The next-generation sequencing was successful in 33 cases. A total of 18 samples showed at least 1 pathogenic, with a median of 1.8 variants, ranging from 1 to 6. The most mutated genes wereTP53andERBB2with 7 variants each, followed byNRASBRAF,PI3KCA,EGFRandPDGFRAwith 2 variants each.KIT,AKT1, andFOXL2genes exhibited 1 variant each. Interestingly, 2 variants observed in thePDGFRAgene are classic imatinib-sensitive therapy.Conclusions:We concluded that Brazilian MPM harbor mutation in classic tumor suppressor and oncogenic genes, which might help in the guidance of personalized treatment of MPM.
conferenceObject A dynamic macrophagic environment in xanthogranulomatous mastitis: a broader clue to xanthomatous diseases pathophysiology and clinical evolution?(2020) CLEMENTE, L. Campos; MARQUES-PIUBELLI, M.; BALANCIN, M.; REIS, L.; CAPELOZZI, V. L.- The path to a better biomarker: application of a risk management framework for the implementation of PD-L1 and TILs as immuno-oncology biomarkers in breast cancer clinical trials and daily practice(2020) I, Paula Gonzalez-Ericsson; STOVGAARD, Elisabeth S.; SUA, Luz F.; REISENBICHLER, Emily; KOS, Zuzana; CARTER, Jodi M.; MICHIELS, Stefan; QUESNE, John Le; NIELSEN, Torsten O.; LAENKHOLM, Anne-Vibeke; FOX, Stephen B.; ADAM, Julien; BARTLETT, John M. S.; RIMM, David L.; QUINN, Cecily; PEETERS, Dieter; V, Maria Dieci; VINCENT-SALOMON, Anne; CREE, Ian; I, Akira Hida; BALKO, Justin M.; HAYNES, Harry R.; FRAHM, Isabel; ACOSTA-HAAB, Gabriela; BALANCIN, Marcelo; BELLOLIO, Enrique; YANG, Wentao; KIRTANI, Pawan; SUGIE, Tomoharu; EHINGER, Anna; CASTANEDA, Carlos A.; KOK, Marleen; MCARTHUR, Heather; SIZIOPIKOU, Kalliopi; BADVE, Sunil; FINEBERG, Susan; GOWN, Allen; VIALE, Giuseppe; SCHNITT, Stuart J.; PRUNERI, Giancarlo; PENAULT-LLORCA, Frederique; HEWITT, Stephen; THOMPSON, E. Aubrey; ALLISON, Kimberly H.; SYMMANS, William F.; BELLIZZI, Andrew M.; BROGI, Edi; MOORE, David A.; LARSIMONT, Denis; DILLON, Deborah A.; LAZAR, Alexander; LIEN, Huangchun; GOETZ, Matthew P.; BROECKX, Glenn; BAIRI, Khalid El; HARBECK, Nadia; CIMINO-MATHEWS, Ashley; SOTIRIOU, Christos; ADAMS, Sylvia; LIU, Shi-Wei; LOIBL, Sibylle; CHEN, I-Chun; LAKHANI, Sunil R.; JUCO, Jonathan W.; DENKERT, Carsten; BLACKLEY, Elizabeth F.; DEMARIA, Sandra; LEON-FERRE, Roberto; GLUZ, Oleg; ZARDAVAS, Dimitrios; EMANCIPATOR, Kenneth; ELY, Scott; LOI, Sherene; SALGADO, Roberto; SANDERS, MelindaImmune checkpoint inhibitor therapies targeting PD-1/PD-L1 are now the standard of care in oncology across several hematologic and solid tumor types, including triple negative breast cancer (TNBC). Patients with metastatic or locally advanced TNBC with PD-L1 expression on immune cells occupying >= 1% of tumor area demonstrated survival benefit with the addition of atezolizumab to nab-paclitaxel. However, concerns regarding variability between immunohistochemical PD-L1 assay performance and inter-reader reproducibility have been raised. High tumor-infiltrating lymphocytes (TILs) have also been associated with response to PD-1/PD-L1 inhibitors in patients with breast cancer (BC). TILs can be easily assessed on hematoxylin and eosin-stained slides and have shown reliable inter-reader reproducibility. As an established prognostic factor in early stage TNBC, TILs are soon anticipated to be reported in daily practice in many pathology laboratories worldwide. Because TILs and PD-L1 are parts of an immunological spectrum in BC, we propose the systematic implementation of combined PD-L1 and TIL analyses as a more comprehensive immuno-oncological biomarker for patient selection for PD-1/PD-L1 inhibition-based therapy in patients with BC. Although practical and regulatory considerations differ by jurisdiction, the pathology community has the responsibility to patients to implement assays that lead to optimal patient selection. We propose herewith a risk-management framework that may help mitigate the risks of suboptimal patient selection for immuno-therapeutic approaches in clinical trials and daily practice based on combined TILs/PD-L1 assessment in BC. (c) 2020 Pathological Society of Great Britain and Ireland.
conferenceObject Adrenal Cystic Lesions of Lymphatic Origin: A Clinical and Pathological Study of 6 New Cases and Systematic Literature Review(2020) MARQUES-PIUBELLI, Mario; POMA-GONZALEZ, Eloiza; BALANCIN, Marcelo; GONCALVES, Victor; BOTELHO, Maria Luiza; FRAGOSO, Maria; ZERBINI, MariaconferenceObject Adrenal Cystic Lesions of Lymphatic Origin: A Clinical and Pathological Study of 6 New Cases and Systematic Literature Review(2020) MARQUES-PIUBELLI, Mario; POMA-GONZALEZ, Eloiza; BALANCIN, Marcelo; GONCALVES, Victor; BOTELHO, Maria Luiza; FRAGOSO, Maria; ZERBINI, Maria- In situ Evidence of Collagen V and Interleukin-6/Interleukin-17 Activation in Vascular Remodeling of Experimental Pulmonary Hypertension(2020) BATAH, Sabrina Setembre; ALDA, Maiara Almeida; FIGUEIRA, Rebeca Rodrigues Lopes Roslindo; CRUVINEL, Heloisa R.; SILVA, Luis Perdona Rodrigues da; MACHADO-RUGOLO, Juliana; VELOSA, Ana Paula; TEODORO, Walcy Rosolia; BALANCIN, Marcelo; SILVA, Pedro Leme; CAPELOZZI, Vera Luiza; FABRO, Alexandre TodorovicSeveral studies have reported the pathophysiologic and molecular mechanisms responsible for pulmonary arterial hypertension (PAH). However, the in situ evidence of collagen V (Col V) and interleukin-17 (IL-17)/interleukin-6 (IL-6) activation in PAH has not been fully elucidated. We analyzed the effects of collagen I (Col I), Col V, IL-6, and IL-17 on vascular remodeling and hemodynamics and its possible mechanisms of action in monocrotaline (MCT)-induced PAH. Twenty male Wistar rats were randomly divided into two groups. In the PAH group, animals received MCT 60 mg/kg intraperitoneally, whereas the control group (CTRL) received saline. On day 21, the pulmonary blood pressure (PAP) and right ventricular systolic pressure (RVSP) were determined. Lung histology (smooth muscle cell proliferation [alpha-smooth muscle actin; alpha-SMA] and periadventitial fibrosis), immunofluorescence (Col I, Col V, and alpha-SMA), immunohistochemistry (IL-6, IL-17, and transforming growth factor-beta [TGF-beta]), and transmission electron microscopy to detect fibronexus were evaluated. The RVSP (40 +/- 2 vs. 24 +/- 1 mm Hg, respectively; p < 0.0001), right ventricle hypertrophy index (65 +/- 9 and 25 +/- 5%, respectively; p < 0.0001), vascular periadventitial Col I and Col V, smooth muscle cell alpha-SMA+, fibronexus, IL-6, IL-17, and TGF-beta were higher in the MCT group than in the CTRL group. In conclusion, our findings indicate in situ evidence of Col V and IL-6/IL-17 activation in vascular remodeling and suggest that increase of Col V may yield potential therapeutic targets for treating patients with PAH.
conferenceObject Collagen V Expression Pattern as a Proposed Surrogate Marker for the Diagnosis of Malignant Mesothelioma(2020) BALANCIN, Marcelo; CLEMENTE, Leticia; REIS, Lucas; MARQUES-PIUBELLI, Mario; AB'SABER, Alexandre; CONTINI, Vitoria; VELOSA, Ana Paula Pereira; TEODORO, Walcy; SOUZA, Paola Da; CAPELOZZI, Vera LuizaconferenceObject Collagen V Expression Pattern as a Proposed Surrogate Marker for the Diagnosis of Malignant Mesothelioma(2020) BALANCIN, Marcelo; CLEMENTE, Leticia; REIS, Lucas; MARQUES-PIUBELLI, Mario; AB'SABER, Alexandre; CONTINI, Vitoria; VELOSA, Ana Paula Pereira; TEODORO, Walcy; SOUZA, Paola Da; CAPELOZZI, Vera Luiza