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1.
Biomol Biomed ; 23(5): 727-739, 2023 Sep 04.
Artículo en Inglés | MEDLINE | ID: mdl-37004241

RESUMEN

B-cell non-Hodgkin lymphoma (B-NHL) is a lymphoid malignancy derived from B-cells that remains difficult to treat. Moreover, relapses and refractory cases are common. Abnormalities in epigenetic mechanisms, such as imbalanced histone acetylation affecting certain genes, contribute to relapses and refractory cases. Chidamide (tucidinostat) is a novel histone deacetylase inhibitor that can reverse this epigenetic imbalance and has been approved for the treatment of T-cell malignancies. However, the use of chidamide for B-NHL remains limited, and the lack of relevant literature exacerbates this limitation. We conducted this review to summarize the anticancer activity of chidamide against B-NHL and its clinical applications to overcome drug resistance. This systematic review was conducted according to the PRISMA 2020 guidelines, using some keyword combinations from MEDLINE and EBSCO. The inclusion and exclusion criteria were also defined. Of the 131 records retrieved from databases, 16 were included in the review. Nine articles revealed that chidamide limited tumor progression by modifying the tumor microenvironment, stopping the cell cycle, inducing apoptosis and autophagy, and enhancing complement-dependent and antibody-dependent cell-mediated cytotoxicities.According to seven other studies, administering chidamide in combination with another existing therapeutic regimen may benefit not only patients with relapsed/refractory B-NHL, but also those with newly diagnosed B-NHL. Chidamide plays many important roles in limiting B-NHL progression through epigenetic modifications. Thus, combining chidamide with other anticancer drugs may be more beneficial for patients with newly diagnosed and relapsed/refractory B-NHL.


Asunto(s)
Antineoplásicos , Linfoma de Células B , Humanos , Recurrencia Local de Neoplasia/inducido químicamente , Linfoma de Células B/inducido químicamente , Antineoplásicos/farmacología , Aminopiridinas/efectos adversos , Microambiente Tumoral
2.
Ann Med Surg (Lond) ; 67: 102532, 2021 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-34257962

RESUMEN

BACKGROUND: Breast cancer is one of the most common cancers in women. About 30%-85% of breast cancers will metastasize to the bone during the course of the illness. Many studies have shown that molecular marker/subtypes can be useful in determining incidence of different and inconsistent bone metastases. This study aimed to determine the correlation of the risk of bone metastases in breast cancer based on the expression of molecular markers. METHODS: The research was conducted retrospectively by searching patients' medical record data. The target population of this study was all patients diagnosed with breast cancer who came to our tertiary hospital in the Nuclear Medicine and Molecular Imaging Department from January 2012 to December 2016. RESULTS: One hundred and thirty patients (n = 130) were enrolled during the study period with characteristics of sex, age, and immunohistochemical/molecular subtype examination that underwent bone scintigraphy. Mean of age was 50.2 (23-79) years. There were no significant correlations between ER, PR, and HER-2 expressions with bone metastases in breast cancer patients. Ki-67 was showed to be correlated with bone metastases in breast cancer patients in our bivariate analysis. Molecular subtype/markers had no statistically significant correlation with bone metastases in patients with breast cancer. CONCLUSION: Ki-67 with high proliferation index was the most powerful molecular marker to determine the risk of bone metastases. The prevalence of bone metastases in the group with Ki-67 expression with high proliferation (≥20) was 1.8 times greater than the prevalence of bone metastases in the weakest HER-2 group.

3.
World J Nucl Med ; 18(3): 283-286, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31516372

RESUMEN

One of the treatment options for benign thyroid nodules is radioactive iodine (RAI). However, this treatment is more effective for hot/warm solid thyroid nodules. Cold thyroid solid nodules are characterized by the lack of iodine uptake compared to normal thyroid tissue. Oral retinoic acid (RA) is a synthetic derivative of Vitamin A. The effect of RA on the uptake of RAI is still controversial. The aim of this study was to evaluate the effect of RA in the ability of a cold solid thyroid nodule to take up RAI. Individuals with a cold solid thyroid nodule based on ultrasonography and thyroid scintigraphy were included. Participants with liver dysfunction, smokers, and pregnant patients were excluded from the study. Each participant underwent thyroid uptake scintigraphy twice (pre- and post-RA consumption) using 35-37 MBq NaI-131. Participants consumed RA at a dose of 1 mg/kg body weight (BW) followed with 1.5 mg/kg BW. This study was approved by Dr. Hasan Sadikin General Hospital Ethic Committee. A total of 12 cold thyroid solid nodules were evaluated. The mean percentage of the nodule uptake value pre- and post-intervention was 1.11% and 0.62%, respectively (P = 0.004), while normal thyroid tissue uptake values pre- and post-intervention were 27.57% and 13.40%, respectively (P = 0.002). The percentage alteration of nodules and normal thyroid tissue uptake value were 42.4% and 51.5% lower, respectively (P = 0.354). This study showed that RA reduces the ability of cold solid thyroid nodule, as well as normal thyroid tissue, to take up RAI.

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