Differentiated thyroid cancer ( DTC ) is usually not very common ( incidence is about 1 % of all cancers and women are more often affected than men ). However, higher incidences has been reported in many parts of South East Asia particularly in iodine deficient areas. Unlike other solid tumors, DTC is potentially curable with documented survival rate of > 90 %. Even if the disease is not totally cured, through repeated high dose radio iodine therapy the progress of the disease can be controlled with significant improvement in quality of life for many years. This is possible if a proper and state of the art therapeutic approach is made. Since the incidence is relatively low, individual experience of treating physicians or centers is mostly inadequate leading to improper management with subsequent increase in morbidity and mortality. The purpose of this review is to evolve a rational management protocol for the treatment of thyroid cancer. Centers which do not have all facilities like high dose radio iodine therapy etc. may still follow the protocol by referring the patient for a particular step to another centre. What is needed is the awareness of the treating physician about the appropriate management of DTC. In recent years, there have been some important developments in the management of differentiated thyroid cancer like use of recombinant human thyrotropin (rhTSH), use of retinoic acid for redifferentiation etc. Some of these developments having practical relevance have been briefly mentioned.
Introduction To evaluate if early tamoxifen toxicity can be detected by comparing pre-and post-treatment optic nerve head parameters and visual function using Heidelberg Retinal Tomograph III (HRT III) and Pattern Visual Evoked Potential (Pattern VEP). Method This is a prospective study involving 76 eyes of 38 breast cancer patients treated with tamoxifen in Hospital Universiti Sains Malaysia, Kelantan, Malaysia. These patients were examined by a single doctor and the investigations were done by a single technician. The visual acuity, optic nerve function, visual field, optic nerve head parameters on HRT III and Pattern VEP were assessed. The examination was performed before and three months after treatment initiation. Results There was no tamoxifen ocular toxicity found three months post-treatment with tamoxifen. There was no change in visual acuity and optic nerve function post-treatment initiation. There were no statistically significant changes found in optic nerve head parameters on HRT III and P 100 peak latency and amplitude on Pattern VEP. Conclusion Ocular toxicity is a recognized complication of tamoxifen treatment. Tamoxifen optic neuropathy is a potentially irreversible, visually disabling complication. Tamoxifen ocular toxicity was not found three months after tamoxifen treatment initiation among estrogen receptor (ER)-positive breast cancer patients. No early changes in optic nerve head parameters and P 100 peak latency and amplitude changes were found after three months of treatment. A longer duration of monitoring with HRT III and Pattern VEP may be needed to adequately observe for early, subclinical changes in optic nerve head parameters and visual function among tamoxifen users.
Triple negative breast cancer (TNBC) is typically associated with poor and interindividual variability in treatment response. Cytochrome P450 family 1 subfamily B1 (CYP1B1) is a metabolizing enzyme, involved in the biotransformation of xenobiotics and anticancer drugs. We hypothesized that, single-nucleotide polymorphisms (SNPs), CYP1B1 142 C>G, 4326 C>G and 4360 A>G, and CYP1B1 mRNA expression might be potential biomarkers for prediction of treatment response in TNBC patients. CYP1B1 SNPs genotyping (76 TNBC patients) was performed using allele-specific polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism methods and mRNA expression of CYP1B1 (41 formalin-fixed paraffin embeddedblocks) was quantified using quantitative reverse transcription PCR. Homozygous variant genotype (GG) and variant allele (G) of CYP1B1 4326C>G polymorphism showed significantly higher risk for development of resistance to chemotherapy with adjusted odds ratio (OR): 6.802 and 3.010, respectively. Whereas, CYP1B1 142 CG heterozygous genotype showed significant association with goodtreatment response with adjusted OR: 0.199. CYP1B1 142C-4326G haplotype was associated with higher risk for chemoresistance with OR: 2.579. Expression analysis revealed that the relative expression of CYP1B1 was downregulated (0.592) in cancerous tissue compared with normal adjacent tissues. When analysed for association with chemotherapy response, CYP1B1 expression was found to be significantly upregulated (3.256) in cancerous tissues of patients who did not respond as opposed to those of patients who showed response to chemotherapy. Our findings suggest that SNPs together with mRNA expression of CYP1B1 may be useful biomarkers to predict chemotherapy response in TNBC patients.