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Li Su

Publications and source records attributed to Li Su.

At least 19 recordsLinked to original sources
PubMed2026

ARHGAP22 as a Potential Prognostic Biomarker in Clear Cell Renal Cell Carcinoma: Insights into Tumor Immunity and Co-Expression Networks.

Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer and is characterized by substantial clinical heterogeneity, highlighting the need for reliable prognostic biomarkers. This study evaluated the expression pattern, prognostic relevance, and immune-related associations of ARHGAP22 in ccRCC using transcriptomic and clinical data from The Cancer Genome Atlas Kidney Renal Clear Cell Carcinoma (TCGA-KIRC) cohort, together with external validation data and protein-expression information from the Human Protein Atlas (HPA). ARHGAP22 expression was compared between tumor and adjacent normal tissues, and its associations with overall survival, clinicopathological characteristics, tumor microenvironment scores, and estimated immune-cell fractions were assessed. Co-expression and functional-enrichment analyses were also performed to characterize potential biological associations. ARHGAP22 was significantly upregulated in ccRCC tissues at the transcriptomic level, with corresponding differences observed in immunohistochemical images. High ARHGAP22 expression was associated with shorter overall survival, advanced clinicopathological features, and higher ImmuneScore, StromalScore, and ESTIMATEScore values. CIBERSORT-based analysis showed that the high-expression group had higher estimated fractions of M2 macrophages and regulatory T cells and lower estimated fractions of naïve B cells, resting mast cells, and activated dendritic cells after false discovery rate correction. Functional-enrichment analyses linked ARHGAP22-associated genes to immune-related processes, cell migration, and chemokine- and cytokine-mediated signaling pathways. These findings suggest that ARHGAP22 may represent a potential prognostic and immune-related biomarker in ccRCC, although further independent clinical and experimental validation is required.

Humans↗
PubMed2026

Germline determinants of risk and molecular subtype in young-onset lung cancer.

Young-onset lung cancer is enriched for never-smoking and oncogene-driven tumors, yet its inherited genetic basis remains poorly defined. We performed germline whole-genome sequencing in 251 young-onset lung cancer cases (median age 37), which we jointly analyzed with never-smoking cases (n=196; median age 68) and cancer-free controls (n=1,883). We identified enrichments of rare deleterious coding variants across 55 cancer-related gene sets, including EGFR/ERBB2 signaling and genes implicated by prior lung cancer GWAS. Exome-wide analyses of rare coding variants affirmed TP53 as a penetrant lung cancer predisposition gene (odds ratio [OR]=36.1, p=1.02x10-7) and discovered two novel exome-wide significant tumor subtype-dependent associations: IREB2 in cases with fusion-driven tumors (p=1.39x10-6) and SMAD6 in fusion-negative tumors (p=2.05x10-6). Structural variants contributed distinct risk, with enrichment in constrained, lung-expressed genes (OR=5.79, p=5.8x10-5) and very large germline deletions being markedly enriched in cases with fusion-driven tumors. Polygenic risk scores for lung cancer were inversely correlated with rare variant burden, consistent with additive risk from rare and common variants. Collectively, these findings delineate a complex germline architecture underlying susceptibility and molecular subtype in young-onset lung cancer.

Journal Article↗
PubMed2025

scBSP: a fast and accurate tool for identifying spatially variable features from high-resolution spatial omics data.

MOTIVATION: Emerging spatial omics technologies empower comprehensive exploration of biological systems from multi-omics perspectives in their native tissue location in 2D and 3D space. However, the limited sequencing depth, increasing spatial resolution, and growing spatial spots in spatial omics technologies present significant computational challenges in identifying biologically meaningful molecules with variable spatial distributions across various omics modalities. RESULTS: We introduce scBSP, an open-source, versatile, and user-friendly package for identifying spatially variable features in large-scale spatial omics data. scBSP demonstrates significantly enhanced computational efficiency, processing high-resolution spatial omics data within seconds, and exhibits robust cross-platform performance by consistently identifying spatially variable features with high reproducibility across various sequencing platforms. AVAILABILITY AND IMPLEMENTATION: scBSP is available for download from R CRAN at https://cran.r-project.org/web/packages/scBSP/index.html and PyPI at https://pypi.org/project/scbsp/.

Software↗
PubMed2003

Association between self-reported environmental tobacco smoke exposure and lung cancer: modification by GSTP1 polymorphism.

Environmental Tobacco Smoke (ETS) exposure has been associated with lung cancer risk. ETS is composed of emissions from cigarette smoke and contains a higher concentration of tobacco smoke carcinogens than mainstream smoke. Polymorphisms in genes that metabolize tobacco smoke carcinogens have been studied as effect modifiers of the association between active smoking and lung cancer risk. GSTP1 is a polymorphic gene that encodes for GST pi, a detoxification enzyme and has a high expression in the lung. We investigated the association between ETS and lung cancer risk and the modification of this association by the GSTP1 polymorphism. Using a case-control design, individuals were genotyped for GSTP1 using PCR-RFLP techniques. All analyses were carried out using multiple logistic regression. The association between ETS exposure and lung cancer risk was evaluated in different strata based on smoking habits to evaluate the consistency of results. The effect of the GSTP1 polymorphisms on lung cancer risk was evaluated by considering the joint effect of having both an ETS exposure and the GSTP1 GG genotype compared to the absence of ETS exposure and the GSTP1 AA genotype as a reference group as well as doing stratified analysis by genotype. ETS exposure was associated consistently with higher lung cancer risk in all the strata considered. The adjusted odds ratios (AOR) evaluating the association between ETS and lung cancer risk for the different strata were: nonsmokers (Cases/Controls 66/413; AOR = 1.38; 95% CI = 0.78-2.43), ex-smokers (Cases/Controls 560/527; AOR = 1.66; 95% CI = 1.22-2.25), current smokers (Cases/Controls 415/219; AOR = 1.56; 95% CI = 1.00-2.41). The AORs for ex-smokers and light smoking subgroups were: ex-smokers who quit for 19 years or more (Cases/Controls 144/244; AOR = 2.64; 95% CI = 1.55-4.50), ex-smokers who quit for 10-19 years (Cases/Controls 141/128; AOR = 1.16; 95% CI = 0.66-2.04), ex-smokers who quit for 10 years or less (Cases/Controls 247/122; AOR = 1.45; 95% CI = 0.83-2.55) and participants who had <15 packyears and nonsmokers combined (Cases/Controls 143/640; AOR = 1.52; 95% CI = 1.02-2.28). Among those with the GSTP1 GG genotype the ETS-lung cancer risk association was greater than those with the GSTP1 AA genotype: nonsmokers (GSTP1 GG AOR = 7.84; 95% CI = 0.80-76.68; GSTP1 AA AOR = 1.15; 95% CI = 0.46-2.90), ex-smokers (GSTP1 GG AOR = 2.32; 95% CI = 0.90-5.96; GSTP1 AA AOR = 2.15; 95% CI = 1.34-3.44), current smokers (GSTP1 GG AOR = 1.75; 95% CI = 0.42-7.32; GSTP1 AA AOR = 1.32; 95% CI = 0.67-2.58) and participants who had <15 packyears and nonsmokers (GSTP1 GG AOR = 1.93; 95% CI = 0.54-6.97; GSTP1 AA AOR = 1.58; 95% CI = 0.83-3.01). We found that ETS exposure is associated with higher lung cancer risk. Furthermore, the presence of the GSTP1 GG genotype appears to enhance the magnitude of the association between ETS exposure and lung cancer. Larger studies will be needed to confirm these preliminary findings.

Adenocarcinoma↗
PubMed2003

AF-6 controls integrin-mediated cell adhesion by regulating Rap1 activation through the specific recruitment of Rap1GTP and SPA-1.

In the present study, we showed that SPA-1, a Rap1 GTPase-activating protein (GAP), was bound to a cytoskeleton-anchoring protein AF-6. SPA-1 and AF-6 were co-immunoprecipitated in the 293T cells transfected with both cDNAs as well as in normal thymocytes. In vitro binding studies using truncated fragments and their mutants suggested that SPA-1 was bound to the PDZ domain of AF-6 via probable internal PDZ ligand motif within the GAP-related domain. The motif was conserved among Rap1 GAPs, and it was shown that rapGAP I was bound to AF-6 comparably with SPA-1. RapV12 was also bound to AF-6 via the N-terminal domain, and SPA-1 and RapV12 were co-immunoprecipitated only in the presence of AF-6, indicating that they could be brought into close proximity via AF-6 in cells. Immunostaining analysis revealed that SPA-1 and RapV12 were co-localized with AF-6 at the cell attachment sites. In HeLa cells expressing SPA-1 in a tetracycline-regulatory manner, expression of AF-6 inhibited endogenous Rap1GTP and beta(1) integrin-mediated cell adhesion to fibronectin in SPA-1-induced conditions, whereas it affected neither of them in SPA-1-repressed conditions. These results suggested that AF-6 could control integrin-mediated cell adhesion by regulating Rap1 activation through the recruitment of both SPA-1 and Rap1GTP via distinct domains.

Animals↗
PubMed2003

P53 (codon 72) and P21 (codon 31) polymorphisms alter in vivo mRNA expression of p21.

p21 (Waf1/Cip1) is a downstream target of p53. We evaluated the association between p21 polymorphism (codon 31), p53 polymorphism (codon 72) and their corresponding in vivo mRNA expression. In this study, p21 and p53 genetic polymorphisms (using standard PCR-RFLP techniques) and p21 and p53 gene expressions (using a radiolabelled ribonuclease protection assay (RPA) technique) were evaluated in the peripheral leukocytes of 84 individuals (63 with lung cancer). Log-transformed values of mRNA expression by RPA, which approximated a normal distribution, were analyzed. p53 genotypes did not correlate with p53 mRNA log-expression (P>0.05 for all comparisons), but the Pro allele variants of p53 were associated with a significant decrease in mRNA log-expression of its downstream target, p21. The variant Arg allele of p21 was also associated with a significant decrease in p21 mRNA log-expression. When individuals with at least one variant allele of both p53 and p21 (double-variants) were compared with all other genotype groups, these double-variants had significantly lower log-expression of p21 (P<0.005 by both t-tests (crude) and linear regression analyses (adjusted)). This is translated into an approximate 48% reduction in the geometric mean of the mRNA expression of the double-variants, when compared with all other groups. Results were consistent in both patients with lung cancer (n=63) and in normal controls (n=21). In conclusion, the presence of a p53 Pro allele and/or p21 Arg allele is associated with lower downstream target gene expression of p21.

Aged↗
PubMed2003

Percutaneous sonographically guided microwave coagulation therapy for hepatocellular carcinoma: results in 234 patients.

OBJECTIVE: The objective of our study was to evaluate the long-term results of percutaneous microwave coagulation therapy for the treatment of hepatocellular carcinoma in a large patient population. SUBJECTS AND METHODS: Survival rates were determined in 234 patients with 339 nodules of hepatocellular carcinoma who had undergone percutaneous microwave coagulation therapy (208 men, 26 women; mean age, 54.8 years; mean tumor size, 4.1 +/- 1.9 cm; range, 1.2-8.0 cm; mean follow-up period, 27.9 months). Patients were those who had been rejected as candidates for surgery by the surgery department, who fit our study's criteria, and who agreed to participate. After baseline imaging studies were performed, the patients were followed up using the same combination of imaging (sonography, CT, or MR imaging) and posttreatment biopsy. RESULTS: After percutaneous microwave coagulation therapy, color Doppler flow signals disappeared in 92.0% (263/286) of the lesions. No enhancement was apparent in 89.2% (190/213) and 89.1% (41/46) of the lesions on contrast-enhanced CT and MR imaging, respectively. Posttreatment biopsies of 194 nodules showed no evidence of surviving tumor tissue in 180 nodules (92.8%). Resections of six lesions revealed complete tumor necrosis in five. The 1-, 2-, 3-, 4-, and 5-year cumulative survival rates were 92.70%, 81.60%, 72.85%, 66.37%, and 56.70%, respectively. The relationships between survival curves and the degree of hepatocellular carcinoma tumor differentiation and between survival curves and tumor size were statistically significant (p = 0.021). No severe complications were seen. CONCLUSION: Sonographically guided microwave coagulation proved to be safe and effective for the treatment of hepatocellular carcinoma. This therapy resulted in a high percentage of cases without evidence of residual tumor and satisfactory long-term results.

Administration, Cutaneous↗
PubMed2003

Polymorphisms in the DNA repair genes XRCC1 and ERCC2, smoking, and lung cancer risk.

XRCC1 (X-ray cross-complementing group 1) and ERCC2 (excision repair cross-complementing group 2) are two major DNA repair proteins. Polymorphisms of these two genes have been associated with altered DNA repair capacity and cancer risk. We have described statistically significant interactions between the ERCC2 polymorphisms (Asp312Asn and Lys751Gln) and smoking in lung cancer risk. In this case-control study of 1091 Caucasian lung cancer patients and 1240 controls, we explored the gene-environment interactions between the XRCC1 Arg399Gln polymorphism, alone or in combination with the two ERCC2 polymorphisms, and cumulative smoking exposure in the development of lung cancer. The results were analyzed using logistic regression models, adjusting for relevant covariates. Overall, the adjusted odds ratio (OR) of XRCC1 Arg399Gln polymorphism (Gln/Gln versus Arg/Arg) was 1.3 [95% confidence interval (CI), 1.0-1.8]. Stratified analyses revealed that the ORs decreased as pack-years increased. For nonsmokers, the adjusted OR was 2.4 (95% CI, 1.2-5.0), whereas for heavy smokers (>/=55 pack-years), the OR decreased to 0.5 (95% CI, 0.3-1.0). When the three polymorphisms were evaluated together, the adjusted ORs of the extreme genotype combinations of variant alleles (individuals with 5 or 6 variant alleles) versus wild genotype (individuals with 0 variant alleles) were 5.2 (95% CI, 1.7-16.6) for nonsmokers and 0.3 (95% CI, 0.1-0.8) for heavy smokers, respectively. Similar gene-smoking interaction associations were found when pack-years of smoking (or smoking duration and smoking intensity) was fitted as a continuous variable. In conclusion, cumulative cigarette smoking plays an important role in altering the direction and magnitude of the associations between the XRCC1 and ERCC2 polymorphisms and lung cancer risk.

Adult↗
PubMed2003

[Experimental pathological study of subacute intoxication by Dioscorea bulbifera L].

OBJECTIVE: To study the pathological change and the toxic mechanism of Dioscorea bulbifera L in mice. METHODS: Sixty ICR mice were randomly assigned to four groups poisoned respectively with 200% Dioscorea bulbifera L of 1/4 LD50, 1/10LD50, 1/30LD50 and a control group treated with distilled water by oral administration. All animals were pathologically examined with LM and some of them were examined with TEM when the mice died during the experiment or the survival mice were sacrificed after thirty days. RESULTS: The pathological changes showed fatty change and the increasing glycogen of liver cells; degeneration and necrosis of the epithelia of uriniferous tubules. The serum BUN and ALT of the experimental groups mice were higher than that of control group. Enzyme histochemical staining showed the decreasing activity of G-6-P and SDH in the liver cells in the experimental groups. CONCLUSION: The experiment suggests that the target organs were liver and kidney. The toxic mechanism of Dioscorea bublifera L was the damage of the mitochondrional and endoplasmic reticulum membrane directly. As a result, the activity of the SDH and G-6-P decreased, the metabolism was affected.

Animals↗
PubMed2002

Combinations of the variant genotypes of GSTP1, GSTM1, and p53 are associated with an increased lung cancer risk.

GSTP1 and GSTM1 are genes involved in Phase II metabolism, whereas p53 is a tumor suppressor gene. Individually, functional polymorphisms of these genes have been studied as risk factors for lung cancer. Small sample sizes have hindered the detection of possible increases in risk associated with having two or more "at risk" polymorphisms of these three genes. In a large Caucasian population, we examined the association of combined variant genotypes [or double-variants (DVs)] of these three genes and lung cancer risk, compared with their corresponding "double-wild-type" genotypes. Because these DVs may promote lung carcinogenesis at an earlier age, a subgroup of individuals aged 55 years or younger was examined separately. Using a case-control design, individuals were genotyped for GSTM1, GSTP1, and p53 codon 72 using PCR-RFLP techniques. All of the analyses used multiple logistic regression. Indicator variables were created to evaluate the risk for individuals with the following DVs: GSTP1 GG + GSTM1-null and GSTP1 GG + p53 Arg/Pro or Pro/Pro. A total of 1694 cases and controls were evaluated. In the whole population, those with the double variants have a higher risk of lung cancer when compared with those with the double-wild-type genotypes, supporting our original hypothesis. Individuals with the GSTP1 and GSTM1, DV (P1-M1 DV) had a marginally significant higher risk of lung cancer compared with their double-wild-type counterparts [adjusted odds ratio (AOR), 1.60; 95% confidence interval (CI), 0.95-2.70]. A significantly higher risk was found for the GSTP1, p53 DV (P1-p53 DV; AOR, 1.99; 95% CI, 1.12-3.53). Among individuals aged 55 or younger, these risks were even higher: for the P1-M1 DV the AOR was 4.03 (95% CI, 1.47-11.1); for the P1-p53 DV the AOR was 5.10 (95% CI, 1.42-18.30). Specific DVs of GSTM1, GSTP1, and p53 codon 72 are associated with a higher lung cancer risk. This susceptibility is highest among younger individuals.

Adult↗
PubMed2002

[Influencing factors of local immunocyte infiltration in hepatocellular carcinoma tissues pre- and post-percutaneous microwave coagulation therapy].

OBJECTIVE: To investigate the influencing factors of the local immunity in tissues of hepatocellular carcinoma (HCC) before and after percutaneous microwave coagulation therapy (PMCT). METHODS: Seventy-eight patients with HCC diagnosed by needle biopsy of liver underwent PMCT. Before the treatment and three and 17 days after the treatment specimens of carcinoma tissues were obtained by ultrasound-guided liver biopsy. The extents of infiltration of CD3(+) cell, natural killer cells (CD56(+)), and macrophages (CD68(+)), and the expression rate of proliferating cell nuclear antigen (PCNA) were evaluated by immunohistochemistry. The relation between the extents of immunocyte infiltration and the clinical parameters was analyzed with multiple regression. RESULTS: Before PMCT infiltration of the three kinds of immunocytes was found in the carcinoma tissues to different degrees with a great variation among individuals. A remarkable increase in the extent of infiltration of the three kinds of immunocytes was found three days after the treatment and continued or remained till the 17th post-PMCT day (P < 0.01). The post-PMCT extent of immunocyte infiltration was positively correlated with the pre-PMCT extent (CD3(+): r = 0.256, P = 0.005; CD56(+): r = 0.257, P = 0.002; CD68(+): r = 0.275, P = 0.001). A negative correlation was found between the extent of immunocyte infiltration and serum alpha-fetal protein (AFP) and between the extent of immunocyte infiltration and tumor size (for serum AFP, CD3(+): r = -0.075, P = 0.049; CD56(+): r = -0.062, P = 0.041; CD68(+): r = -0.007, P = 0.035; for tumor size, CD3(+): r = -0.074, P = 0.051; CD56(+): r = -0.100, P = 0.012; CD68(+): r = -0.109, P = 0.038). No correlation was found between the extent of immunocyte infiltration and age of patient, Child-Pugh class of tumor, grade of tumor differentiation, and number of tumor. The extent of immunocyte infiltration was lesser in the carcinoma tissues with higher expression rate of PCNA. The extent of immunocyte infiltration was greater in the carcinoma tissues where PCNA expression was negative and carcinoma cells had necrotized but with their structure recognizable. No immunocyte infiltration was found in the necrotic and structureless tumor tissues. CONCLUSION: The local immunocyte infiltration in patients with HCC was influenced by serum AFP and the grade of tumor cell necrosis pre- and post-PMCT. Destruction of tumor tissue in situs by PMCT is the premise of increase of immunocyte infiltration. Before PMCT improving the immune status of the patients helps enhance the local immune response.

Adult↗
PubMed2002

Metal ions and flexibility in a viral RNA pseudoknot at atomic resolution.

Many pathogenic viruses use programmed -1 ribosomal frameshifting to regulate translation of their structural and enzymatic proteins from polycistronic mRNAs. Frameshifting is commonly stimulated by a pseudoknot located downstream from a slippery sequence, the latter positioned at the ribosomal A and P sites. We report here the structures of two crystal forms of the frameshifting RNA pseudoknot from beet western yellow virus at resolutions of 1.25 and 2.85 A. Because of the very high resolution of 1.25 A, ten mono- and divalent metal ions per asymmetric unit could be identified, giving insight into potential roles of metal ions in stabilizing the pseudoknot. A magnesium ion located at the junction of the two pseudoknot stems appears to play a crucial role in stabilizing the structure. Because the two crystal forms exhibit mostly unrelated packing interactions and local crystallographic disorder in the high-resolution form was resolvable, the two structures offer the most detailed view yet of the conformational preference and flexibility of an RNA pseudoknot.

Crystallization↗
PubMed2002

Gene-environment interaction for the ERCC2 polymorphisms and cumulative cigarette smoking exposure in lung cancer.

Excision repair cross-complementing group 2 (ERCC2), a major DNA repair protein, is involved in nucleotide excision repair and basal transcription. The ERCC2 polymorphisms have been associated with altered DNA repair capacity. We investigated two ERCC2 polymorphisms, Asp312Asn and Lys751Gln, in 1092 Caucasian lung cancer patients and 1240 spouse and friend controls. The results were analyzed using generalized additive models and logistic regression, adjusting for relevant covariates. The overall adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were 1.47 (95% CI, 1.1-2.0) for the Asp312Asn polymorphism (Asn/Asn versus Asp/Asp) and 1.06 (95% CI, 0.8-1.4) for the Lys751Gln polymorphism (Gln/Gln versus Lys/Lys). Gene-smoking interaction analyses revealed that the adjusted ORs for each of the two polymorphisms decreased significantly as pack-years increased. When comparing individuals with Asn/Asn + Gln/Gln versus individuals with Asp/Asp + Lys/Lys, the fitted ORs (95% CIs) were 2.56 (95% CI, 1.3-5.0) in nonsmokers and 0.69 (95% CI, 0.4-1.2) in heavy smokers (80 pack-years; P < 0.01 for the interaction term). Consistent and robust results were found when models incorporated different definitions of cumulative cigarette smoking. A stronger gene-smoking interaction was observed for the Asp312Asn polymorphism than for the Lys751Gln polymorphism. In conclusion, cumulative cigarette smoking modifies the associations between ERCC2 polymorphisms and lung cancer risk.

Adult↗
PubMed2002

Genetic polymorphisms in N-acetyltransferase-2 and microsomal epoxide hydrolase, cumulative cigarette smoking, and lung cancer.

N-acetyltrasferase-2 (NAT2) and microsomal epoxide hydrolase (mEH) are polymorphic genes that metabolize different tobacco carcinogens. Smaller studies found inconsistent relationships between NAT2 or mEH polymorphisms and lung cancer risk. To determine whether there is gene-environment interaction between NAT2 polymorphisms, alone or in combination with mEH polymorphisms, and cumulative smoking exposure in the development of lung cancer, we conducted a case control study of 1115 Caucasian lung cancer patients and 1250 spouse and friend controls. The results were analyzed using generalized additive models and logistic regression, adjusting for relevant covariates. There was no overall relationship between NAT2 genotype and lung cancer risk; the adjusted odds ratio (OR) of the rapid versus slow acetylator genotypes was 0.96 [95% confidence interval (CI), 0.79-1.16]. However, gene-environment interaction analyses revealed that the adjusted ORs increased significantly as pack-years increased. For nonsmokers, the fitted OR was 0.66 (95% CI, 0.44-0.99), whereas for heavy smokers (80 pack-years), the OR increased to 1.22 (95% CI, 0.89-1.67). When comparing the extreme genotype combinations of the NAT2 rapid acetylator, higher mEH activity genotype to the NAT2 slow acetylator, and very low mEH activity genotype, the corresponding ORs at 0 and 80 pack-years were 0.30 (95% CI, 0.14-0.62) and 2.19 (95% CI, 1.26-3.81), respectively. Results were similar with ORs derived from stratified models. In conclusion, NAT2 rapid acetylator genotypes are protective against lung cancer in nonsmokers but are risk factors in heavy smokers. The joint effects of NAT2 and mEH polymorphisms are consistent with an independent, additive effect of these two genes, modified by smoking history.

Adult↗
PubMed2002

[Ultrasonography in the diagnosis of hepatic malignant cystic tumors].

OBJECTIVE: To evaluate the clinical application of gray scale and color Doppler sonography in the diagnosis of hepatic malignant cystic tumors. METHODS: Characteristics of gray scale and color Doppler sonography were studied in 16 cases of malignant hepatic tumors confirmed by pathology. Tumor size, shape, number of lesion, thickness of cystic wall and echogenecity of the lesion were observed with gray scale sonography. Blood supply of the tumor and its velocity were observed with Color Doppler sonography. RESULTS: One single lesion was common in primary malignancy while multiple lesions signified metastasis. Sonographic findings revealed that the shape of the tumor was spheroid in 8 cases, irregular in 5 and leaf-shaped in 3, with the diameter varying from 1.9 cm to 13.6 cm. Sonography showed malignant cystic tumor with irregular thick wall in 15 cases, multiple septa in 7 cases and papillary projections in 6 on gray scale. Color Doppler flow signal was detected in the irregular thick wall, multiple septa or papillary projections in 14 cases, of which the arterial blood flow signals were demonstrated in 13. CONCLUSION: Color Doppler is able to clearly detect the blood flow signals in the irregular thick wall, multiple septa or papillary projections, providing an important sign for the diagnosis of hepatic malignant cystic tumors.

Adult↗
PubMed2002

Significance of changes in local immunity in patients with hepatocellular carcinoma after percutaneous microwave coagulation therapy.

OBJECTIVE: To assess the local immune response in patients with hepatocellular carcinoma after percutaneous microwave coagulation therapy (PMCT). METHODS: Seventy-eight patients with hepatocellular carcinoma underwent PMCT. Both cancerous and adjacent liver tissue were taken before, and 3, 17 and 30 days after PMCT using ultrasound-guided liver biopsy. Specimens were stained by immunohistochemical techniques for detecting CD3, CD45RO, CD56, CD68, and CD20 positive cells. RESULTS: A few CD3, CD45RO, CD56, CD68 and CD20 positive cells were observed in the cancer stroma and surrounding sinusoids in liver tissue pre-PMCT. The number of immunocytes, except for CD20 positive cells, was significantly increased both within the cancer and the adjacent liver tissue, with a larger increase in tumor tissue at day 3 post-PMCT compared with pre-PMCT. These immunocytes were enlarged in size. The number of CD3, CD45RO and CD56 positive cells peaked at day 17 and CD68 positive cells peaked at days 3 post-PMCT. At day 30 post-PMCT, this increase still existed. These infiltrating immunocytes distributed in the parenchyma of the tumor, and within the lumen of small blood vessels after PMCT. In addition, more infiltrated immune cells were seen in cancer cell spaces. CONCLUSIONS: A change in immunocyte infiltration takes place in number, configuration and location after patients with HCC are treated with percutaneous microwave coagulation, suggesting that local immune function is enhanced post-PMCT.

Adult↗
PubMed2002

Counterpoint: the myeloperoxidase -463G-->a polymorphism does not decrease lung cancer susceptibility in Caucasians.

The myeloperoxidase (MPO) G-to-A substitution polymorphism in the promoter region of the MPO gene has been associated with a 40-70% reduction in lung cancer risk in several studies, although a recent nested case-control study disputes these findings. MPO is involved in the activation of a number of procarcinogens, including benzo(a)pyrene. The variant A allele has been shown to reduce MPO mRNA expression, thus potentially decreasing carcinogen activation. To confirm results from smaller studies, we evaluated this MPO polymorphism in 988 incident Caucasian lung cancer cases and 1128 controls. Logistic regression evaluated the association between MPO genotype and lung cancer risk, adjusting for age, gender, smoking status, time since quitting smoking, and pack-years of smoking. In the controls, the A allele frequency was 21%, and genotype distribution was in the Hardy-Weinberg equilibrium. Compared with the wild-type G/G genotype, the adjusted odds ratios for the A/A and A/G genotypes were 1.15 (95% confidence interval 0.7-1.9, P > 0.2) and 1.03 (95% confidence interval 0.8-1.3, P > 0.20), respectively. A similar lack of association was seen in analyses stratified by smoking status, median age, a number of smoking variables, disease stage, tumor grade, and histological subtype. These findings are in contrast with earlier studies suggesting a protective effect of carrying the variant A allele.

Adult↗