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1.
World J Clin Cases ; 9(11): 2533-2541, 2021 Apr 16.
Artigo em Inglês | MEDLINE | ID: mdl-33889618

RESUMO

BACKGROUND: Primary ovarian mucinous carcinoma is a rare histologic subtype of epithelial ovarian carcinoma and exhibits considerable morphologic overlap with secondary tumour. It is hard to differentiate primary from metastatic ovarian mucinous carcinoma by morphological and immunohistochemical features. Because of the histologic similarity between primary ovarian mucinous carcinoma and metastatic gastrointestinal carcinoma, it has been hypothesized that ovarian mucinous carcinomas might respond better to non-gynecologic regimens. However, the standard treatment of advanced ovarian mucinous carcinoma has not reached a consensus. CASE SUMMARY: A 56-year-old postmenopausal woman presented with repeated pain attacks in the right lower quadrant abdomen, accompanied by diarrhoea, anorexia, and weight loss for about 3 mo. The patient initially misdiagnosed as having gastrointestinal carcinoma because of similar pathological features. Based on the physical examination, tumour markers, imaging tests, and genetic tests, the patient was clinically diagnosed with ovary mucinous adenocarcinoma. Whether gastrointestinal-type chemotherapy or gynecologic chemotherapy was a favourable choice for patients with advanced ovarian mucinous cancer had not been determined. The patient received a chemotherapy regimen based on the histologic characteristics rather than the tumour origin. The patient received nine cycles of FOLFOX and bevacizumab. This was followed by seven cycles of bevacizumab maintenance therapy for 9 mo. Satisfactory therapeutic efficacy was achieved. CONCLUSION: The genetic analysis might be used in the differential diagnosis of primary ovarian mucinous carcinoma and non-gynecologic mucinous carcinoma. Moreover, primary ovarian mucinous carcinoma patients could benefit from gastrointestinal-type chemotherapy.

2.
Mol Med Rep ; 12(5): 7335-43, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-26459009

RESUMO

Multidrug resistance (MDR) to doxorubicin (DOX) limits its effectiveness against tumor cells. Arsenic trioxide (As2O3) has been reported to reduce MDR in various types of cancer, but the mechanisms involving Ras and p-glycoprotein (P-gp) remain to be fully elucidated. The objectives of the present study were to evaluate As2O3 in reversing MDR to DOX, and to identify the association in antitumor activities between the effectiveness of DOX and Ras/phosphorylated (p­) extracellular signal­regulated kinase (ERK)1/2 signaling in SGC7901/ADM and SGC7901/S human gastric cancer cell lines. Cytotoxicity and sensitivity towards As2O3 were assessed using non­toxic and mildly­toxic concentrations (0.1 and 0.5 µM, respectively). The reversing effect of As2O3 on MDR was investigated prior to and following treatment with a cytokine activation of the recombinant human granulocyte colony stimulating factor ERK pathway. The SGC7901/ADM and SGC7901/S cells had the same sensitivity to As2O3. The SGC7901/ADM cells were resistant to DOX and As2O3 treatment reduced the level of resistance to DOX (P<0.01). The expression of P­glycoprotein (P-gp) in the SGC7901/ADM cells was higher than in the SGC7901/S cells (P<0.001). As2O3 treatment decreased the levels of P­gp in a time­ and dose­dependent manner (P<0.01). The expression of Ras was higher in the SGC7901/ADM cells than in the SGC7901/S cells, while the expression of p­ERK1/2 remained the same. As2O3 decreased the levels of Ras and p­ERK1/2 (P<0.01). Following pretreatment with rhG­CSF, the levels of Ras and p­ERK1/2 were further decreased (P<0.01). Drug­resistant gastric cancer cells had higher expression levels of P­gp and Ras, but not of p­ERK1/2. Non­ and mildly­toxic doses of As2O3 reduced MDR to DOX through Ras/p-ERK1/2 signaling.


Assuntos
Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo , Antineoplásicos/farmacologia , Arsenicais/farmacologia , Doxorrubicina/farmacologia , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Óxidos/farmacologia , Neoplasias Gástricas/tratamento farmacológico , Membro 1 da Subfamília B de Cassetes de Ligação de ATP/análise , Trióxido de Arsênio , Linhagem Celular Tumoral , Regulação para Baixo/efeitos dos fármacos , Resistência a Múltiplos Medicamentos/efeitos dos fármacos , Mucosa Gástrica/metabolismo , Humanos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Estômago/efeitos dos fármacos , Estômago/patologia , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Proteínas ras/metabolismo
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