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1.
J Surg Oncol ; 117(8): 1806-1812, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29761503

RESUMO

BACKGROUND AND OBJECTIVES: Clinical experience suggests that cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC) play an important role in the management of ovarian cancer. In order to improve patient selection, the peritoneal surface disease severity score (PSDSS) was previously introduced for use in colorectal cancer patients. However, almost no data exist regarding the utility of the PSDSS index in ovarian cancer patients. METHODS: A retrospective study of the effectiveness of CRS and HIPEC was carried out in 59 patients with ovarian cancer. The PSDSS was based on three criteria: symptoms, extent of peritoneal dissemination, and primary tumor structure as assessed by histology and biomarker expression. RESULTS: The overall survival time for patients with ovarian cancer in PSDSS Stage I was 48 ± 25.3 months. For PSDSS Stage II, the survival time was 26.5 ± 4.7 months. For PSDSS Stage III, it was 15.5 ± 4 months, and for PSDSS Stage IV, it was 6 ± 4.3 months. A multivariate analysis showed that the PSDSS stage was the only independent survival predictor. CONCLUSIONS: These data demonstrate that a PSDSS based on two pathogenetic types may be useful for predicting survival outcomes in ovarian cancer patients treated with CRS/HIPEC.


Assuntos
Procedimentos Cirúrgicos de Citorredução , Hipertermia Induzida , Neoplasias Ovarianas/mortalidade , Neoplasias Ovarianas/terapia , Índice de Gravidade de Doença , Carcinoma/metabolismo , Carcinoma/mortalidade , Carcinoma/patologia , Carcinoma/terapia , Quimioterapia Adjuvante , Feminino , Humanos , Pessoa de Meia-Idade , Análise Multivariada , Terapia Neoadjuvante , Neoplasias Ovarianas/metabolismo , Neoplasias Ovarianas/patologia , Neoplasias Peritoneais/mortalidade , Neoplasias Peritoneais/secundário , Neoplasias Peritoneais/terapia , Prognóstico , Estudos Retrospectivos , Análise de Sobrevida , Proteína Supressora de Tumor p53/metabolismo
2.
Sci Rep ; 9(1): 11634, 2019 08 12.
Artigo em Inglês | MEDLINE | ID: mdl-31406165

RESUMO

Tumor-associated macrophages (TAMs) are prominent components of tumor stroma that promotes tumorigenesis. Many soluble factors participate in the deleterious cross-talk between TAMs and transformed cells; however mechanisms how tumors orchestrate their production remain relatively unexplored. c-Myb is a transcription factor recently described as a negative regulator of a specific immune signature involved in breast cancer (BC) metastasis. Here we studied whether c-Myb expression is associated with an increased presence of TAMs in human breast tumors. Tumors with high frequency of c-Myb-positive cells have lower density of CD68-positive macrophages. The negative association is reflected by inverse correlation between MYB and CD68/CD163 markers at the mRNA levels in evaluated cohorts of BC patients from public databases, which was found also within the molecular subtypes. In addition, we identified potential MYB-regulated TAMs recruiting factors that in combination with MYB and CD163 provided a valuable clinical multigene predictor for BC relapse. We propose that identified transcription program running in tumor cells with high MYB expression and preventing macrophage accumulation may open new venues towards TAMs targeting and BC therapy.


Assuntos
Neoplasias da Mama/genética , Regulação Neoplásica da Expressão Gênica/imunologia , Macrófagos/imunologia , Proteínas Proto-Oncogênicas c-myb/metabolismo , Microambiente Tumoral/imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Antígenos CD/metabolismo , Antígenos de Diferenciação Mielomonocítica/metabolismo , Mama/patologia , Neoplasias da Mama/imunologia , Neoplasias da Mama/mortalidade , Neoplasias da Mama/patologia , Proliferação de Células , Estudos de Coortes , Conjuntos de Dados como Assunto , Feminino , Perfilação da Expressão Gênica , Humanos , Estimativa de Kaplan-Meier , Macrófagos/metabolismo , Pessoa de Meia-Idade , Prognóstico , Receptores de Superfície Celular/metabolismo , Microambiente Tumoral/genética
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