Rabbit Anti-Human CCND1 (Phospho-Thr286) polyclonal antibody

Background: Multiple myeloma (MM) primarily origins from terminally differentiated B cells. The Cyclin D1 (CCND1) gene polymorphism is located on the long arm of chromosome 11 in exon 4, and coding of the Cyclin D1 protein is reported in MM. This study aimed at investigating the relationship between CCND1 polymorphism and MM in northern part of Iran. Materials and Methods: This case-control study was performed on 87 patients with MM (case group) and 70 healthy individuals (control group). The population was selected from Touba Clinic, the largest referral center in Mazandaran province, Iran. Data analysis was done in SPSS software version 19. Results: The participants were aged 18-83 years (mean age: 53.8 +/- 16.7 years), including 72 (45.9%) males and 85 (54.1%) females. The adjusted odds ratio (aOR) for GG genotype was found to be significant (aOR = 4.28, confidence interval [CI] 95% = 1.21-15.13). In addition, the presence of G allele compared to allele A increased the odds ratio (OR) of MM (OR = 2.28, CI 95% = 1.45-3.57). The age and sex aOR by age and sex was 2.08, CI 95% = 1.10-3.93. Conclusion: The current study elucidated that, unlike most previous surveys on Cyclin D1 G870A gene polymorphism that associated AA genotype with various types of malignancies, the GG genotype is a risk factor for MM.

Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are an approved first-line therapy against unresectable or advanced non-small cell lung cancer (NSCLC) harboring EGFR gene activating mutations. However, the majority of tumors develop acquired resistance against EGFR-TKIs and some tumors exhibit natural resistance. A number of resistance mechanisms against the latest third-generation EGFR-TKIs have been reported, including tertiary EGFR C797S mutation and several gene alterations activating EGFR or other signaling pathways. The current study aimed to identify the frequency of natural EGFR-TKI resistance in pretreatment NSCLC and to predict the therapeutic effect of EGFR-TKIs. A total of 246 EGFR-TKI-naive NSCLC patients harboring known EGFR gene mutations were identified. The presence of EGFR C797S and T790M mutations were determined using the peptide nucleic acid-locked nucleic acid PCR clamp method. ERBB2, MET, EGFR, ALK, BRAF, FGFR1, MYC, RET, CCND1, CCND2, CDK4, CDK6, MDM2 and MDM4 gene amplification, which can lead to resistance against any generation EGFR-TKIs, was determined using the multiplex ligation-dependent probe amplification assay. No concurrent C797S mutation with known EGFR mutations were identified. T790M mutation was identified in 12 patients (4.9%). ERBB2 or MET gene amplification was found in some patients (0.0-0.4%). MDM2 gene amplification was associated with tumor recurrence and shorter progression-free survival (PFS) for first- or second-generation EGFR-TKIs. De novo EGFR C797S mutation was not identified. Other resistance mechanisms against EGFR-TKIs were indicated in some patients with EGFR-TKI-naive NSCLC. MDM2 gene amplification, which can lead to altered cell cycle, was associated with tumor recurrence and shorter PFS in EGFR-TKI therapy.