PubMed · 7579671
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1995. Expression systems.. https://doi.org/10.1016/0958-1669(95)80100-6
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STALARD (selective target amplification for low-abundance RNA detection) enables isoform-level quantification of low-abundance RNAs using conventional laboratory equipment. Here, we describe steps for RNA isolation, primer design, reverse transcription, selective target amplification, and downstream analysis. The protocol couples selective pre-amplification with a quantitative reverse-transcription PCR (RT-qPCR) readout and optional nanopore sequencing. Using 1 μg input RNA and 12 pre-amplification cycles, STALARD reduces Cq values by approximately 10-12 cycles, bringing the target into a reliably quantifiable range. For complete details on the use and execution of this protocol, please refer to Jeong et al.1.
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BACKGROUND: Recent studies of the molecular biology of cancer have demonstrated that p53 tumor suppressor gene aberration is associated with the development and progression of several different cancer types. METHODS: To analyze the expression of the p53 oncoprotein in parotid gland neoplasms, 72 parotid gland tumors (including 46 malignant and 26 benign cases) were studied immunocytochemically using the murine monoclonal DO-7 anti-p53 antibody. In parotid gland cancers, no and low expression (-/+) or moderate and high expression (++/+++) of the p53 oncoprotein were examined for correlation with patient survival and other clinicopathologic features, including clinical stage, tumor size, regional lymph node status, facial nerve paralysis, local infiltration, and distant failures. RESULTS: Positive staining was observed focally in 3 of 26 (11%) benign tumors and in 31 (67%) of 46 malignant tumors. Cancers showing moderate and high expression of p53 tended to be more advanced and larger than those with no expression or low expression, and presented at diagnosis more frequently, with signs of local aggressiveness. Tumors with moderate and high expression of p53 were associated more frequently with regional and distant metastases (P = 0.07 and P = 0.004, respectively). Multiple logistic regression analysis showed that regional and distant metastases were associated independently with p53 expression (P = 0.068 and P = 0.047, respectively). Moreover, patients whose cancers had moderate or high p53 expression had lower disease free and overall actuarial survival rates than those with no or low p53 expression (P = 0.021 and P = 0.033, respectively). Univariate and multivariate analysis confirmed the independent predictive prognostic value of p53 expression in patients with parotid gland cancer (P = 0.044 and P = 0.039, respectively). Furthermore, p53 expression did not correlate positively with patients' smoking habits in this series. CONCLUSION: The p53 tumor suppressor gene may be involved in salivary gland carcinogenesis, and its oncoprotein expression is an independent indicator of clinical aggressiveness in patients with carcinoma of the parotid gland.