Abdul Aziz

Purpose: Early discontinuation of antidepressants continues to be a major challenge in treating mood and anxiety disorders, despite strong evidence supporting ongoing pharmacotherapy to prevent relapse and enhance long-term outcomes. This narrative review aimed to identify potential patient-level, medication-level, prescriber-level, and system-level factors of early discontinuation and to highlight strategies to improve long-term adherence. Methods: First, guideline recommendations from Canada, the United States, the United Kingdom, Europe, and international bodies were reviewed to contextualize recommended treatment durations. Then, a literature search was performed, including studies published from 2000 to 2025. We used PubMed, Google Scholar, PsycINFO, and Web of Science databases. Findings from observational studies, clinical guidelines, and qualitative research were synthesized to identify key factors contributing to early discontinuation and to outline strategies to improve adherence. Results: Early antidepressant discontinuation was often associated with low socioeconomic status, immigrant background, older age, prior substance use, comorbid psychiatric conditions, and misconceptions about treatment, although findings varied depending on the operational definition and study settings. Medication‑related contributors included adverse effect burden, initiation on tricyclic antidepressants, and cost‑related non-adherence. Prescriber‑level and system‑level contributors included limited follow‑up, high workload, variability in prescribing practices, and communication barriers. Several strategies to improve adherence can be adopted, including patient-centered communication, culturally competent care, selecting well‑tolerated first‑line agents, structured follow‑up, pharmacist‑led support, and digital/telehealth‑based interventions. Conclusions: Early antidepressant discontinuation is common and influenced by intersecting social, clinical, and structural factors, including equity-related determinants. Multifaceted, coordinated approaches, including effective communication, appropriate medication selection, and strengthened follow‑up processes, are needed to improve adherence.

Background: Cancer is a significant global health challenge, affecting millions of people every year. Overall survival rates have improved over time, but some patients exhibit treatment resistance, prompting ongoing research to find suitable and effective sensitizers. Resveratrol, a natural polyphenolic compound, has demonstrated significant effects in inhibiting the growth and spread of cancer. However, the molecular mechanisms and applications of resveratrol remain unclear. Objective: In this updated narrative review, we aimed at discussing the role and related molecular mechanisms of resveratrol in various cancers and providing an overview of its therapeutic potential for the treatment and prevention of these cancers. Methodology: We conducted an extensive literature search across four major databases, including PubMed, Google Scholar, Web of Science, and ScienceDirect, to identify all relevant articles. Result: Resveratrol is a naturally occurring polyphenolic compound, specifically a stilbene, found in significant quantities in grapes, berries, peanuts, and various other plants. Resveratrol significantly contributes to the reduction of various human cancers, including those of the breast, cervix, thyroid, prostate, brain, skin, colon, bone, and ovarian cancers. Resveratrol has been shown to influence cell cycle arrest, activate apoptosis, and suppress metastasis, all of which are achieved through various signaling pathways. Additionally, several in vivo studies have shown promising results suggesting it may reduce tumor development and extend lifespan in animal cancer models, among other benefits. Conclusion: This review indicates that resveratrol could serve as a prototype for developing more efficacious and less toxic therapeutic agents for the treatment of various cancers.

Cancer is a significant global health challenge, affecting millions of people every year. Overall survival rates have improved over time, but some patients exhibit treatment resistance, prompting ongoing research to find suitable and effective sensitizers. Resveratrol, a natural polyphenolic compound, has demonstrated significant effects in inhibiting the growth and spread of cancer. However, the molecular mechanisms and applications of resveratrol remain unclear. In this updated narrative review, we aimed at discussing the role and related molecular mechanisms of resveratrol in various cancers and providing an overview of its therapeutic potential for the treatment and prevention of these cancers. We conducted an extensive literature search across four major databases, including PubMed, Google Scholar, Web of Science, and ScienceDirect, to identify all relevant articles. Resveratrol is a naturally occurring polyphenolic compound, specifically a stilbene, found in significant quantities in grapes, berries, peanuts, and various other plants. Resveratrol significantly contributes to the reduction of various human cancers, including those of the breast, cervix, thyroid, prostate, brain, skin, colon, bone, and ovarian cancers. Resveratrol has been shown to influence cell cycle arrest, activate apoptosis, and suppress metastasis, all of which are achieved through various signaling pathways. Additionally, several in vivo studies have shown promising results suggesting it may reduce tumor development and extend lifespan in animal cancer models, among other benefits. This review indicates that resveratrol could serve as a prototype for developing more efficacious and less toxic therapeutic agents for the treatment of various cancers.

Background and Aims: Breast cancer (BC) is the most often diagnosed malignancy in women. The genetic factor is estimated to be responsible for the higher BC risk. BC development is thought to be closely linked to the ESR1 gene, which controls cell division and proliferation. Nevertheless, no research has been performed to investigate the relationship between this gene and Bangladeshi women's BC risk. Therefore, this case‐control study attempted to determine the association between ESR1 polymorphisms and breast cancer susceptibility. Methods: This study genotyped two ESR1 genetic variants (rs2234693 and rs9340799) in a total of 399 participants (201 cases and 198 controls) by applying the PCR‐RFLP method. SPSS software (v25.0) was used for statistical analysis, and SHEsis web program and Haploview (v4.2) were used for linkage disequilibrium and haplotype analyses, respectively. Results: A statistically significant association of rs2234693 variant with grade 3 tumor (OR = 0.17, p = 0.0004) and rs9340799 variant with overweight (OR = 0.46, p = 0.034), infiltrating breast cancer (OR = 0.25, p < 0.0001), and positive lymph node status (OR = 2.34, p = 0.005) were observed. The rs2234693 variant was also significantly associated with breast cancer in various models, including codominant 1 (OR = 0.60, p = 0.045), codominant 2 (OR = 0.50, p = 0.021), dominant (OR = 0.56, p = 0.020), and allelic model (OR = 0.73, p = 0.028). In the case of rs9340799 variant, no significant link was observed for breast cancer. Haplotype analysis revealed a significant correlation of TA and CA haplotypes with breast cancer susceptibility (OR = 1.37, p = 0.028 and OR = 0.41, p = 0.0002, respectively). Besides, both rs2234693 and rs9340799 are found to be in strong linkage disequilibrium (D' = 1.00, r ² = 0.697). Conclusions: In this study, a significant correlation of ESR1 rs2234693 and rs9340799 genetic variants with breast cancer susceptibility has been observed. The findings of this study need to be investigated further with larger sample sizes to confirm the association. A detailed investigation of understanding the functional role of polymorphisms is also required.

Background: Overexpression of rs3761936 of DCLRE1B gene has been observed in both breast cancer and cervical cancer patients. To justify the association of this polymorphism with these cancers, we performed this case-control study. Method: A total of 245 cancer patients and 108 healthy controls participated in the research. An efficient T-ARMS PCR method was used for genotyping. Results: The cancer patients showed higher mutant allele frequency compared to the controls. Mutant allele carrier breast cancer patients showed significantly increased risk in four genetic models, including additive model 1 (TC vs. TT: OR=2.31, 95% CI = 1.33–3.99, p-value = 0.0028), additive model 2 (CC vs. TT: OR=3.93, 95% CI = 1.36–11.38, p-value = 0.0116), dominant model (TC + CC vs. TT: OR=2.52, 95% CI = 1.50–4.25, p-value = 0.0005), and over-dominant model (TC vs. TT + CC: OR=1.93, 95% CI = 1.13–3.28, p-value = 0.0152). The allele frequency analysis showed that mutant allele C carriers among breast cancer patients had a significantly higher risk than the wild type T allele carriers (C vs. T: OR=2.15, 95% CI = 1.41–3.26, p-value = 0.0003). Likewise, the cervical cancer patients showed significant risk in three genetic models, including additive model 1 (TC vs. TT: OR=1.80, 95% CI = 1.01–3.20, p-value = 0.0444), additive model 2 (CC vs. TT: OR=3.17, 95% CI = 1.05–9.55, p-value = 0.0403), and dominant model (TC + CC vs. TT: OR=1.98, 95% CI = 1.15–3.41, p-value = 0.0138). The mutant allele C carriers had a significantly higher risk than the wild-type T allele carriers (C vs. T: OR=1.84, 95% CI = 1.19–2.85, p-value = 0.0065). Conclusion: DCLRE1B rs3761936 is strongly associated with breast cancer and cervical cancer risk in Bangladeshi women.

Background and Aims: Matrix metalloproteinase 2 (MMP2) and MMP9 are associated with the degradation of type IV collagen, leading to invasion and metastasis. Polymorphisms in these genes could influence their biological activities and contribute to cancer development and progression. This study evaluated the relationship between MMP2 (rs2285053) and MMP9 (rs3787268) gene polymorphisms and the susceptibility to breast cancer in Bangladeshi breast cancer patients.Methods: This case‐control study included 105 females diagnosed with breast cancer and 108 healthy controls. Following DNA extraction from the blood samples, genotyping was carried out by tetra‐primer amplification refractory mutation system‐polymerase chain (ARMS‐PCR) reaction and gel electrophoresis.Results: In the case of rs2285053 polymorphism, CT genotype (OR = 2.12, 95% CI = 1.03–4.36), dominant model (OR = 2.21, 95% CI = 1.08–4.52), overdominant model (OR = 2.10, 95% CI = 1.02–4.31), and alleles (OR = 2.13, CI = 1.08–4.18) were significantly associated with an increased breast cancer risk. For rs3787268 polymorphism, additive model 1 (OR = 0.20, 95% CI = 0.05–0.78), additive model 2 (OR = 0.23, 95% CI = 0.06–0.86), and dominant model (OR = 0.22, CI = 0.06–0.81) significantly decreased breast cancer risk in this population.Conclusion: Our results conclude that MMP2 (rs2285053) is associated with an increased risk of breast cancer, while MMP9 (rs3787268) polymorphisms may be correlated with a reduced risk of breast cancer in Bangladeshi females. Future studies are warranted to validate our findings in other populations.

Background and Aims: Schizophrenia (SCZ) is among the most persistent and devastating psychological problems. Different genetic polymorphisms are responsible for the predisposition of SCZ, and we screened NOTCH4 (rs2071287, rs204993) and CYP2E1 (rs2070673) polymorphisms in this study to find the connection with SCZ development.Methods: We investigated a total of 420 samples (210 patients and 210 controls) and used the PCR–RFLP technique to genotype all SNPs. For statistical analyses, SPSS (version 25.0) was applied.Results: In the case of NOTCH4 rs2071287, no evidence of a link was found in any genetic models, whereas NOTCH4 rs204993 and CYP2E1 rs2070673 showed a significant linkage in four genetic models with SCZ risk (for NOTCH4 rs204993, additive model 2: OR = 3.39, CI = 1.84–6.23, p = 0.0001; dominant: OR = 1.84, CI = 1.22–2.76, p = 0.0032; recessive: OR = 2.67, CI = 1.53–4.64, p = 0.0005; allelic: OR = 1.75, CI = 1.32–2.30, p = 0.0001 and for CYP2E1 rs2070673, additive model 2: OR = 0.39, CI = 0.22–0.69, p = 0.0013; recessive: OR = 0.45, CI = 0.29–0.68, p = 0.0002; overdominant: OR = 1.49, CI = 1.02–2.19, p = 0.0408; allelic: OR = 0.61, CI = 0.46–0.80, p = 0.0004).Conclusions: The findings of our study suggest that the polymorphisms NOTCH4 rs204993 and CYP2E1 rs2070673 in the Bangladeshi ethnicity are connected to the risk of SCZ.

Background and Aims: Breast cancer is one of the deadliest diseases affecting women in Bangladesh, and its prevalence is increasing year by year. Although several IL‐6 single nucleotide polymorphisms have been implicated in BC susceptibility and prognosis in various studies, no research has been done to investigate the relationship between breast cancer and IL‐6 in Bangladeshi women. This investigation aimed to explore the linkage between the rs1800797 variant of IL‐6 and the susceptibility to breast carcinoma among women in Bangladesh. Methods: The IL‐6 rs1800797 variant was genotyped in 218 subjects (110 cases and 108 controls) using the tetra‐primer ARMS‐PCR method. The statistical analysis was applied utilizing the SPSS software version 24.0. UALCAN database was used for IL‐6 mRNA analysis, and genotype‐based gene expression was retrieved from GTEx Portal. Results: This study found a significant link between IL‐6 rs1800797 variants and increased chance of breast cancer across different genetic inheritance models, including additive model 1 (AG vs. GG: OR = 2.16, p = 0.035); dominant model (AG + AA vs. GG: OR = 2.26, p < 0.05); overdominant model (AG vs. GG + AA: OR = 2.08, p < 0.05); and allelic model (A vs. G: OR = 2.15, p < 0.05). However, an insignificant association of breast cancer was found in both additive model 2 (AA vs. GG: OR = 2.91, p > 0.05) and the recessive model (AA vs. GG + AG: OR = 2.52, p > 0.05). Under the analysis of the probability of false positive reports, no significant values were found in different models when the OR was 1.5, and the prior probability was 0.25. Conclusions: A significant relationship was found between the IL‐6 rs1800797 genetic variant and the risk of breast cancer. However, the findings of the study should be further investigated with a larger sample size to validate the correlation.

Background and Aims: Pharmacists have been recognized as one of the most qualified healthcare professionals in the clinical implementation of pharmacogenomics, yet its widespread implementation in clinical pharmacy practice has remained limited. The review aims to systematically investigate knowledge, perceptions, and attitudes toward pharmacogenomics among pharmacists and pharmacy students to inform the future delivery of pharmacogenomics education programs.Methods: PubMed, MEDLINE, Embase, Scopus, and the International Pharmaceutical Abstracts were searched up to May 17, 2022. Studies were selected if they included data on pharmacists' or pharmacy students' knowledge, perception, or attitude about pharmacogenomics and were published in a peer‐reviewed, English‐language journal with full‐text availability. Any published study not deemed original research was excluded. All included studies were critically appraised using the Center for Evidence‐Based Management's critical appraisal tools. The data were descriptively analyzed and presented based on pharmacists' and pharmacy students' knowledge/awareness, perception/attitudes toward pharmacogenomic (PGx), confidence in using or interpreting PGx testing results, and their desire to get further PGx education or their most preferred method of further education.Results: A combined total of 12,430 pharmacists and pharmacy students from 26 countries are represented in the 52 included studies. Despite overwhelmingly positive attitudes and perceptions toward pharmacogenomics among pharmacists and pharmacy students, an overall lack of adequate knowledge and confidence was found. The review also found a strong desire for further pharmacogenomics education among pharmacists and pharmacy students.Conclusion: Pharmacists and pharmacy students have positive perceptions and attitudes toward pharmacogenomics, which is hindered by a lack of knowledge and confidence. However, inadequate control for confounders, limited representativeness of the studied population or region, and small sample sizes diminish the generalizability of the review results. Knowledge and confidence could be improved through enhanced delivery of pharmacogenomic courses within the pharmacy curriculum and continuing education programs.