The Age-Adjusted Charlson Comorbidity Index Predicts Prognosis in Elderly Cancer Patients.

Purpose: The age-adjusted Charlson comorbidity index (ACCI) is a useful measure of comorbidity to standardize the evaluation of elderly patients and has been reported to predict mortality in various cancers. To our best knowledge, no studies have examined the relationship between the ACCI and survival of elderly patients with cancer. Therefore, the primary objective of this study was to investigate the relationship between the ACCI and survival of elderly patients with cancer. Patients and Methods: A total of 64 elderly patients (>80 years) with cancer between 2011 and 2021 were enrolled in this study. According to the ACCI, the age-adjusted comorbidity index was calculated by weighting individual comorbidities; patients with ACCI<11 were considered the low-ACCI group, whereas those with ACCI≥11 were considered the high-ACCI group. The correlations between the ACCI score and survival outcomes were statistically analyzed. Results: There was a significant difference in overall survival (OS) and progression-free survival (PFS) between the high-ACCI group and the low-ACCI group (P<0.001). The median OS time of the high-ACCI group and the low-ACCI group were 13.9 (10.5-22.0) months and 51.9 (34.1-84.0) months, respectively. The 2-, 3-, and 5-year survival rates of the high-ACCI group were 28.1%, 18.8%, and 4.2%, respectively, whereas the 2-, 3-, and 5-year survival rates of the low-ACCI group were 77.3%, 66.4%, and 39.1%, respectively. Multivariate analysis showed that ACCI was independently associated with OS (HR=1.402, 95% CI: 1.226-1.604, P < 0.05) and PFS (HR=1.353, 95% CI: 1.085-1.688, P = 0.0073). Conclusion: The ACCI score is a significant independent predictor of prognosis in elderly patients with cancer.

[Long Non-coding RNA Act as Regulators of Autophagy in Disease Treatment].

Long non-coding RNA (lncRNA) refer to transcripts longer than 200 nucleotides that have a low coding potential. Autophagy,a unique life phenomenon of eukaryotic cells,removes excess or damaged organelles during cell growth and development and plays a key role in maintaining homeostasis. As a key regulator of cellular metabolism,lncRNA are involved in disease treatment by regulating autophagy. This article summarizes the role of lncRNA in the treatment of cancer,cardiovascular and cerebrovascular diseases,neurodegenerative diseases,and bacterial infections and analyzes the molecular mechanisms of lncRNA in regulating autophagy,along with prospects of its applications in other areas.

[Detection and significance of APC gene promoter hypermethylation in serum of breast cancer patients].

BACKGROUND & OBJECTIVE: Detection of circulating tumor markers is one of current hot spots in tumor research. Free tumor DNA may exist in the peripheral blood of malignant tumor patients. Identical DNA mutations existing in both peripheral serum and primary tumor are found in many kinds of malignant tumors. This study used adenomatous polyposis coli (APC) gene promoter hypermethylation as a tumor marker to investigate the correlations of free tumor DNA to primary tumor and clinicopathologic features of breast cancer. METHODS: The methylation status of APC gene in tumor tissue, paracancer normal tissue, and paired peripheral serum from 84 patients with breast cancer and 10 patients with benign breast diseases were detected by methylation-specific polymerase chain reaction (MSP). RESULTS: The detection rate of APC gene promoter hypermethylation was 45.2% in tumor tissues and 31.0% in paired peripheral sera. APC gene hypermethylation in peripheral serum was significantly correlated to that in tumor tissue (r=0.977, P=0.002). The sensitivity of detecting APC gene hypermethylation in peripheral serum was 68.4%; the specificity was 97.8%. The aberrant methylation of APC gene in tumor tissue and peripheral serum had no correlation to patients' age, tumor stage, tumor size, histological type, and receptor status (P>0.05). No aberrant methylation of APC gene was found in the serum samples from healthy control and the patients without gene methylation in tumor tissue. CONCLUSION: The aberrant tumor gene methylation in peripheral serum of breast cancer patients is significantly correlated to that in primary tumor.

[Detection of free tumor-related DNA in the serum of breast cancer patients].

OBJECTIVE: To study the APC and E-cadherin gene promoter hypermethylation as tumor marker and to investigate the correlation of free tumor-related DNA in serum and tumor tissue with clinicopathological parameters. Their feasibility in early diagnosis, predicting therapeutic effect and monitoring recurrence was evaluated. METHODS: 84 cases with operated breast cancer were recruited from March 2002 to August 2002 at Beijing Cancer Hospital. Aberrant methylation of E-cadherin and APC genes was detected in tumor tissues, adjacent normal tissues and peripheral blood serum by methylation-specific PCR (MSP). 10 cases with benign breast diseases were selected as control group. RESULTS: The positive rate of promoter hypermethylation of E-cadherin and APC genes in tumor tissues was 52.4% and 45.2%, in the paired serum was 33.3% and 31.0%, respectively. Aberrant methylation of free DNA in serum presented the same alteration in tumor tissues. E-cadherin and APC hypermethylation in serum and tumor samples significantly correlated each other (E-cadherin P < 0.001; APC P = 0.002). The sensitivity of detection of free DNA methylation of E-cadherin and APC genes in serum was 63.6% and 63.2%, respectively. The specificity was 100% and 95.7%, respectively. There was no correlation for the aberrant methylation in cancer tissues and serum with the clinicopathological parameters of patients including age, tumor staging, tumor size, histological type and receptor. None of the aberrant methylation was found in adjacent normal tissues and control group serum. CONCLUSION: The same aberrant methylation in cancer tissues and serum, not correlating with tumor staging, can be detected in about one third of breast cancer patients. The aberrant methylation in serum can disappear after operation. The results imply that this approach may be feasible for early diagnosis, evaluation of therapeutic effects and monitoring recurrence of breast cancers.

Establishment of a flow cytometric assay for determination of human platelet glycoprotein VI based on a mouse polyclonal antibody.

Glycoprotein VI (GPVI) is the major signaling receptor for collagen on platelets. Recent studies suggest that the surface density of GPVI is related to the activation of platelets by collagen. To measure the level of GPVI on platelets, a mouse polyclonal antibody BJ010 was prepared using an amplified fragment of extracellular domain in GPVI. The specific reactivity of BJ010 was identified by anti-GPVI specific monoclonal antibody 11a12 using immunoprecipitation, sandwich enzyme-linked immunosorbent assay (ELISA) and flow cytometry. The antibody BJ010 recognized both native and denatured human GPVI so that it was used to set up a flow cytometric assay to detect the level of GPVI in normal subjects. The relative level of GPVI on platelets was detected in 101 healthydonors. The median geometric mean fluorescence intensity (GMFI) of platelet GPVI level was 57.7. The variation between minimum and maximum values of platelet GPVI and integrin alpha2beta1 were found to be 3.5- and 4.1-fold, respectively, in the normal subjects. There was a week correlation between the amount of GPVI and integrin alpha2beta1 on platelet surfaces. For the method, the intraassay and interassay coefficient of variation was 6.3% and 8.8%, respectively. The flow cytometric assay described here provides a simple, reliable, reproducible, and readily available means of quantitation of collagen receptor GPVI density on the platelet surface in a larger number of blood samples.

[Detection of p53 gene mutation in the plasma of gastric cancer patients].

OBJECTIVE: To investigated p53 gene mutation in plasma of gastric cancer patients. METHODS: DNA extracted from plasma and matched tumor and tumor-adjacent normal tissues of 96 gastric cancer patients, and DNA from 20 healthy people were studied. Exons 5, 6, 7, and 8 of p53 were amplified by PCR. The mutation status was analyzed by denaturing high-performance liquid chromatography (DHPLC), followed by direct sequencing of cases with aberrant chromatographic patterns. RESULTS: Heterozygous mutations of p53 gene were detected in 19.9% (19/96) of primary tumor tissues and 5.2% (5/96) of corresponding plasma. All p53 gene mutations detected in plasma DNA consisted with mutations in the matched primary tumor samples. Neither the tumor-adjacent gastric mucosa tissues nor control plasma from healthy volunteers showed p53 gene mutation. No correlation was found between p53 mutation status and clinicopathological features of gastric cancer patients. CONCLUSION: p53 gene mutation in plasma can be detected in tissues and plasma of gastric cancer patients, which could be applied in screening and surveillance of this disease.