Bone remodeling serum markers in children with systemic lupus erythematosus.

INDRODUCTION: SLE is an autoimmune multisystem disease. Glucocorticoid is an irreplaceable medication for SLE. Glucocorticoid and inflammatory mediators impact bone remodeling by OPG/RANKL/RANK signal system, which could lead to osteoporosis. Our aim is to detect the expression of RANKL/OPG in children with SLE, and to preliminarily explore the changes of bone remodeling serum markers in children with SLE. METHODS: Serum RANKL and OPG of 40 children with SLE and healthy children were detected by ELISA, while 25(OH)VitD3 was detected routinely. Clinical data of children with SLE were recorded, including gender, age, height, weight, BMI, SLEDAI, duration of the disease, cumulative dose of glucocorticoid, and correlation analysis was conducted with RANKL, OPG and 25(OH)VitD3. RESULTS: Serum RANKL concentrations in SLE group were significantly higher than health group (9.82 ± 7.20 vs. 6.80 ± 4.35 pg/ml and 0.081 ± 0.072 vs. 0.042 ± 0.034, P < 0.05) respectively, and the concentrations of OPG and 25(OH)VitD3 in serum were significantly lower than health group (156.34 ± 57.33 vs. 189.16 ± 68.70 pg/ml and 43.66 ± 31.27 vs. 59.04 ± 21.56 mmol/L, P < 0.05). Serum RANKL in children with SLE was positively correlated with the duration of SLE, cumulative dose of GC(r = 0.593, 0.727, P < 0.05). And it was negatively correlated with serum OPG and 25(OH)VitD3 (r = -0.601, -0.469, P < 0.05). In addition, serum OPG and 25(OH)VitD3 concentrations were inversely correlated with cumulative dose of GC (r = -0.66, -0.508, P < 0.05). CONCLUSION: Low levels of vitamin D3 and bone metabolic abnormalities still persist in children with SLE even if the disease is in remission, while serum RANKL level was elevated, OPG expression was reduced. In the case of disease remission, GC is involved in the occurrence and development of abnormal bone remodeling through RANKL/OPG.

Significance of Macrophage Subtypes in the Peripheral Blood of Children with Systemic Juvenile Idiopathic Arthritis.

INTRODUCTION: Symptomatic juvenile idiopathic arthritis (sJIA) is an autoinflammatory disease, and monocytes/macrophages play an important role. However, which macrophage subtype plays a major role in different stages of sJIA is still unclear. This study aimed to explore macrophage subtypes in different stages of sJIA. METHODS: Twenty-two children with sJIA who were followed up at Shanghai Children's Hospital from January 2018 to December 2020 were enrolled in this study. sJIA children were divided into an activity group (n = 12) and an inactivity group (n = 10). In the activity group, subjects with newly diagnosed sJIA and untreated were included; in the inactivity group, subjects with inactive sJIA meeting the 2011 ACR criteria for sJIA were recruited. Ten children with orthostatic proteinuria served as controls. Peripheral blood was collected. Flow cytometry was performed to detect macrophage subtypes: M1 (CD14+CD86+CD80+), M2a (CD14+CD206+CD301+), M2b (CD14+CD206+CD86+) and M2c (CD14+CD206+CD163+), and the contents of cytokines were also examined, including interleukins (IL) (IL-1ß, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10 and IL-17), interferon-α, interferon-γ, and tumor necrosis-α. RESULTS: M1 marker CD80 and M2 marker CD163, CD301 were highly expressed in children with active sJIA. The majority of macrophages were M1 and M2a in the activity group (P < 0.05). In the inactivity group, M2 tended to polarize into M2b and M2c (P < 0.05). IL-6 significantly increased in the activity group (P < 0.05), while IL-10, IL-4 and IL-17 markedly increased in the inactivity group (P < 0.05). CONCLUSIONS: In the active sJIA, M1 activation promotes inflammation, while M2a rapidly responds to inhibit inflammation; in the inactive sJIA, M2b and M2c play a major role in inhibiting inflammation.

Functional Regulation of Macrophage Phenotypes by MicroRNAs in Inflammatory Arthritis.

Inflammatory arthritis including rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) exhibit the shared feature of changes in activation and polarization of circulating monocytes and tissue macrophages. Numerous microRNAs (miRs) have been found to have key functions in regulating inflammation and macrophage polarization. Although there is increasing interest in the roles of miRs in both RA and JIA, less is known regarding how miRs relate to functional properties of immune cells, including monocytes and macrophages. Interestingly, miRs can function both to promote inflammatory phenotypes and pro-inflammatory polarization, as well as through negative-feedback loops to limit inflammation. Here, we review the functional roles of several miRs in macrophages in inflammatory arthritis, with a particular focus on vivo effects of miR alteration in experimental arthritis. We also consider how current efforts to target miRs clinically could modify functional monocyte and macrophage polarization in vivo, and serve as novel therapies for diseases such as RA and JIA.

The NK1 receptor antagonist NKP608 inhibits proliferation of human colorectal cancer cells via Wnt signaling pathway.

BACKGROUND: Neurokinin1 (NK1) receptor has played a vital role in the development of tumor. However, NKP608 as a NK1 receptor antagonist whether has the effect of the resistance of colorectal cancer is still unclear. Thereby, in this study, we investigated the role of NKP608 on human colorectal cancer and explored the underlying mechanism. METHODS: The cell proliferation of colorectal cancer cells was detected by cell counting kit-8 (CCK8) assay, cell migration and invasion were assessed by transwell assay, the apoptotic ratio of cells was assessed by Annexin V-fluorescein isothiocyanate/propidium iodide stained and flow cytometry. The involvement of molecular mechanisms was examined by western blot. RESULTS: In this study, we found that NKP608 inhibited the proliferation, migration/invasion of HCT116 cells. In addition, NKP608 reduced expressions of Wnt-3a, ß-catenin, Cyclin D1, and (vascular endothelial growth factor) VEGF while induced expression of E-Cadherin. Furthermore, flow cytometry analyzed that NKP608 induced apoptosis of HCT116 cells, consistently, western blotting detecting of apoptosis-related proteins revealed that NKP608 downregulated Bcl-2 while upregulated Bax and Active-Caspase-3. CONCLUSIONS: Taken together, our results demonstrated that NKP608 inhibited colorectal cancer cell proliferation, migration and invasion via suppressing the Wnt/ß-catenin signaling pathway. Therefore, NKP608 might represent a promising therapeutic agent in the treatment of colorectal cancer.

Breast-conservation Therapy After Neoadjuvant Chemotherapy Does Not Compromise 10-Year Breast Cancer-specific Mortality.

OBJECTIVES: Neoadjuvant chemotherapy can increase the rate of breast-conserving surgery by downstaging disease in patients with breast cancer. The aim of this study was to determine whether patients who received neoadjuvant chemotherapy have equal survival after breast-conservation therapy compared with mastectomy. MATERIAL AND METHODS: Using the New Jersey State Cancer Registry (NJSCR) patients with a primary breast cancer diagnosed between 1998 and 2003 who underwent neoadjuvant chemotherapy were selected (n=1,468). Of those, only patients who received lumpectomy plus radiation (n=276) or mastectomy without radiation (n=442) were included in the analysis. The main outcome measured included 10-year breast cancer-specific mortality, with 90% of patients with known vital status through the end of 2011. RESULTS: Baseline characteristics did not differ significantly between the breast-conservation and mastectomy without radiation groups except with respect to summary stage and lymph node involvement. After propensity score matching these differences were no longer statistically significant; however, both estrogen and progesterone status achieved statistical significance. The Kaplan-Meier survival curve showed that the breast-conservation group had significantly higher breast cancer-specific survival than the mastectomy group (P=0.0046). After adjusting for the propensity score in the regression model, the breast-conservation group continued to show significantly better survival than the mastectomy group (hazard ratios, 0.46; 95% confidence interval, 0.27-0.78). CONCLUSIONS: This study is consistent with previous research showing that breast-conserving surgery after neoadjuvant chemotherapy does not reduce breast cancer-specific survival. In fact, patients undergoing breast-conservation after neoadjuvant therapy appeared to have better survival than patients undergoing mastectomy without radiation.

The NK1 receptor antagonist NKP608 inhibits proliferation of human colorectal cancer cells via Wnt signaling pathway

BACKGROUND: Neurokinin1 (NK1) receptor has played a vital role in the development of tumor. However, NKP608 as a NK1 receptor antagonist whether has the effect of the resistance of colorectal cancer is still unclear. Thereby, in this study, we investigated the role of NKP608 on human colorectal cancer and explored the underlying mechanism. METHODS: The cell proliferation of colorectal cancer cells was detected by cell counting kit-8 (CCK8) assay, cell migration and invasion were assessed by transwell assay, the apoptotic ratio of cells was assessed by Annexin V-fluorescein isothiocyanate/propidium iodide stained and flow cytometry. The involvement of molecular mechanisms was examined by western blot. RESULTS: In this study, we found that NKP608 inhibited the proliferation, migration/invasion of HCT116 cells. In addition, NKP608 reduced expressions of Wnt-3a, ß-catenin, Cyclin D1, and (vascular endothelial growth factor) VEGF while induced expression of E-Cadherin. Furthermore, flow cytometry analyzed that NKP608 induced apoptosis of HCT116 cells, consistently, western blotting detecting of apoptosis-related proteins revealed that NKP608 downregulated Bcl-2 while upregulated Bax and Active-Caspase-3. CONCLUSIONS: Taken together, our results demonstrated that NKP608 inhibited colorectal cancer cell proliferation, migration and invasion via suppressing the Wnt/ß-catenin signaling pathway. Therefore, NKP608 might represent a promising therapeutic agent in the treatment of colorectal cancer.

Disparities in Female Breast Cancer Stage at Diagnosis in New Jersey: A Spatial-Temporal Analysis.

BACKGROUND: Despite improvements in early detection of breast cancer, disparities persist in stage at diagnosis, which is an important prognostic factor. METHODS: We used the space-time scan statistic in SaTScan to identify geographic areas and time periods with significantly elevated proportions of female breast cancer diagnosed at the in situ or distant stage in New Jersey. The analyses were conducted with census tracts as the geographic unit of analysis, elliptical spatial windows, 3-year temporal windows, and Poisson models. Statistical significance was determined by 999 Monte Carlo simulations (P < .05); significant clusters were mapped in ArcMap. Breast cancer cases within the clusters were compared with breast cancer cases outside the clusters on demographic, socioeconomic, and clinical factors using the Pearson chi-square test (P < .05). In addition, populations within the clusters were compared with the population outside the clusters on demographic and socioeconomic factors. RESULTS: After exclusions, 126 756 cases of primary female breast cancer diagnosed in 1997 to 2011 from the New Jersey State Cancer Registry were included in the analysis. One distant stage breast cancer cluster was identified in northeastern New Jersey from 1997 through 2011 (n = 26 244, relative risk [RR] = 1.42, P < .001). Two in situ breast cancer clusters were found in northeastern New Jersey from 2004 through 2011 (n = 12 496, RR = 1.35, P < .001) and in central New Jersey from 2006 through 2011 (n = 29 319, RR = 1.24, P < .001). The distant stage cluster contained relatively high percentages of minority and lower socioeconomic status (SES) breast cancer cases and populations, whereas the in situ clusters had relatively low percentages of minority and lower SES breast cancer cases and populations. CONCLUSION: Although there have been improvements since an earlier study of distant stage breast cancer diagnosed in 1995 to 1997, disparities in stage at diagnosis continue. These findings can be used by our local cancer control partners to target specific populations for interventions such as breast cancer education and mammography screening, as well as by state legislative and public health authorities for resource allocation.

A single-center analysis of Henoch-Schonlein purpura nephritis with nephrotic proteinuria in children.

BACKGROUND: In children with Henoch-Schonlein purpura nephritis (HSPN), the degree of proteinuria has been proven to be not only a sign of kidney damage, but also an accelerator of kidney disease progression. Nephrotic proteinuria at disease onset has been proposed as a predictor of a poor renal outcome. This study aims to assess the clinical and pathological features of HSPN with nephrotic proteinuria in a single center. METHODS: One hundred thirty-seven patients with HSPN who visited Shanghai Children's Hospital from January 2009 to December 2013 were retrospectively reviewed. The patients were divided into 2 groups based on the 24-h urinary protein levels: nephrotic proteinuria group (NP group: 24-h urinary protein ≥50 mg/kg) and non-nephrotic proteinuria group (NNP group: 24-h urinary protein <50 mg/kg). In addition, data regarding their sex, age, clinical features, renal pathology, and prognosis were collected. RESULTS: (1) There were 34 boys and 20 girls in the NP group with a mean age of 8.39 ± 2.85 years. The peak age of incidence was 6 to 11 years (72.22%). (2) There were 8 cases (14.81%) with joint symptoms and 9 cases (16.67%) with gastrointestinal symptoms in the NP group. According to the analysis of the laboratory test results, the serum albumin and IgG levels of the NP group were significantly lower than that of the NNP group (35.04 ± 8.45 in the NP group vs. 41.55 ± 4.46 in the NNP group, P < 0.0001; 7.68 ± 3.12 in the NP group vs. 9.53 ± 2.74 in the NNP group, P < 0.001, respectively); their blood urea nitrogen and cystatin C levels increased significantly (P < 0.05). (3) The majority of the pathological changes in the NP group were above the International Study of Kidney Disease in Children (ISKDC) grade III (62.97%). The NP group patients with tubulointerstitial injurie with grade 2 and above (50%) were prioritized. Immune complex deposition in the NP group was dominated by IgA. (4) The prognosis of the NP group was in complete remission (A), and their cases did not develop into end-stage renal disease; their prognosis was also associated with clinical classification (P < 0.01) but was not related to pathologic grading and tubulointerstitial injury (P > 0.05). CONCLUSION: The serum albumin and IgG levels of the NP group were significantly lower; however, their blood urea nitrogen and cystatin C levels were higher. The ISKDC grades were mainly above grade III. The prognosis of the NP group was associated with clinical classification and improved after a timely and early treatment.

Single dose of rituximab in children with steroid-dependent minimal change nephrotic syndrome.

Rituximab (RTX) can be used in children with nephrotic syndrome, particularly in those with steroid-dependent nephrotic syndrome (SDNS). However, at present there is no unified standard of how to use RTX, with regard to the amount of doses and frequency, in children with nephrotic syndrome. The study aimed to investigate the therapeutic efficacy of a single dose of RTX in children with steroid-dependent minimal change nephrotic syndrome (SD-MCNS). The patients with biopsy-proven minimal change disease (MCD) and clinical features of SDNS received a single dose of RTX (375 mg/m2). The toxicity and side effects of RTX were also observed. The study included 19 patients (10 males and 9 females). Follow-up of the patients was 1-50 months (28.1±16.6 months). B-cell depletion was achieved with RTX infusion (CD20<0.5%) and lasted 1-6 months (mean, 2.92±1.57 months). During follow-up, 10 patients remained in complete remission and did not relapse without administration of oral steroids or immunosuppressants for 4-50 months (mean, 30.1±12.6 months), despite recovery of the B-cell count. Nine patients relapsed in the process of reducing steroids, thus, treatment was maintained at a lower dosage (T=0, P<0.05) than prior to use of RTX. The number of relapses also decreased significantly (T=95, P<0.05). Five of the patients relapsed after stopping steroid for several months. At the end of follow-up, the efficacy of a single induction of RTX was 47.4% (9/19). There were no significant side effects associated with administration of RTX. In conclusion, RTX is a safe and effective alternative for children with SD-MCNS. RTX is an effective treatment for the rapid induction of remission and reduces relapse and steroid dependency. A single dose of RTX for children with SD-MCNS is recommended for rapid induction of remission, reduction of long-term steroid dosage, and decrease in the number of relapses, as it has few side effects.

Melanoma Outcomes in Transplant Recipients With Pretransplant Melanoma.

BACKGROUND: There are limited data on outcomes in transplant recipients with a history of pretransplant melanoma. OBJECTIVE: To determine whether pretransplant melanoma is associated with differences in survival or posttransplant melanoma risk. MATERIALS AND METHODS: We evaluated the outcomes of 185,039 US transplant recipients from the Transplant Cancer Match Study. We also evaluated the impact of transplantation on 141,441 patients with melanoma identified in cancer registries. RESULTS: There were 336 transplant recipients (0.18%) with pretransplant melanoma; they had increased risk of melanoma-specific mortality (hazard ratio [HR], 27; 95% confidence interval [CI], 11-64, p < .0001), overall mortality (HR, 1.3; 95% CI, 1.0-1.5, p = .02), and incident melanoma (HR, 5.4; 95% CI, 2.9-9.8, p < .0001) after transplant, compared with recipients without pretransplant melanoma. The 10-year absolute risk difference was 2.97% for melanoma-specific mortality, 3.68% for incident melanoma, and 14.32% for overall mortality. Among the 141,441 patients with melanoma in the general population, 68 (0.05%) subsequently received a transplant. Transplantation increased melanoma-specific mortality, but not significantly (HR, 1.7; 95% CI, 0.61-4.5, p = .32). CONCLUSION: Pretransplant melanoma is associated with increased melanoma-specific mortality, overall mortality, and incident melanoma after transplant. Nonetheless, the rarity of melanoma-related events supports the current practice for listing transplant candidates with a history of melanoma.

Response gene to complement 32 regulates the G2/M phase checkpoint during renal tubular epithelial cell repair.

BACKGROUND: The aim of this study was to evaluate the influence of RGC-32 (response gene to complement 32) on cell cycle progression in renal tubular epithelial cell injury. METHODS: NRK-52E cells with overexpressed or silenced RGC-32 were constructed via transient transfection with RGC-32 expression plasmid and RGC-32 siRNA plasmid, and the cell cycle distribution was determined. The expression levels of fibrosis factors, including smooth muscle action (α-SMA), fibronectin (FN) and E-cadherin, were assessed in cells with silenced RGC-32. RESULTS: The cells were injured via TNF-α treatment, and the injury was detectable by the enhanced expression of neutrophil gelatinase-associated lipocalin (NGAL). RGC-32 expression also increased significantly. The number of cells at G2/M phase increased dramatically in RGC-32 silenced cells, indicating that RGC-32 silencing induced G2/M arrest. In addition, after treatment with TNF-α, the NRK-52E cells with silenced RGC-32 showed significantly increased expression of α-SMA and FN, but decreased expression of E-cadherin. CONCLUSIONS: The results of this study suggest that RGC-32 probably has an important impact on the repair process of renal tubular epithelial cells in vitro by regulating the G2/M phase checkpoint, cell fibrosis and cell adhesion. However, the exact mechanism needs to be further elucidated.

Invasive Cervical Cancer Incidence Disparities in New Jersey--a Spatial Analysis in a High Incidence State.

Although invasive cervical cancer incidence has declined, disparities persist. We identified spatial clusters of census tracts with elevated invasive cervical cancer incidence rates using New Jersey State Cancer Registry cases 20 years or older diagnosed in 2005-2009. Each cluster's population was compared with the rest of New Jersey's population on demographic and socioeconomic characteristics. Odds ratios that assessed associations between statistically significant characteristics (from a univariate comparison of cases in the clusters versus cases in the rest of New Jersey) and being a case in a cluster versus being a case in the rest of New Jersey were calculated from logistic regression models. Significant incidence clusters were identified around Newark, Trenton, and Camden. Being Black (all areas), Hispanic (Newark, Camden), unmarried (Newark), and uninsured/Medicaid-insured (Trenton) were significantly associated with being a case in these areas. These study results can be used to target invasive cervical cancer prevention efforts more effectively.

Cancer Among Children With Perinatal Exposure to HIV and Antiretroviral Medications--New Jersey, 1995-2010.

BACKGROUND: Concerns remain regarding the cancer risk associated with perinatal antiretroviral (ARV) exposure among infants. No excessive cancer risk has been found in short-term studies. METHODS: Children born to HIV-infected women (HIV-exposed) in New Jersey from 1995 to 2008 were identified through the Enhanced HIV/AIDS Reporting System and cross-referenced with data from the New Jersey State Cancer Registry to identify new cases of cancer among children who were perinatally exposed to ARV. Matching of individuals in the Enhanced HIV/AIDS Reporting System to the New Jersey State Cancer Registry was conducted based on name, birth date, Social Security number, residential address, and sex using AutoMatch. Age- and sex-standardized incidence ratio (SIR) and exact 95% confidence intervals (CIs) were calculated using New Jersey (1979-2005) and US (1999-2009) cancer rates. RESULTS: Among 3087 children (29,099 person-years; median follow-up: 9.8 years), 4 were diagnosed with cancer. Cancer incidence among HIV-exposed children who were not exposed to ARV prophylaxis (22.5 per 100,000 person-years) did not differ significantly from the incidence among children who were exposed to any perinatal ARV prophylaxis (14.3 per 100,000 person-years). Furthermore, the number of cases observed among individuals exposed to ARV did not differ significantly from cases expected based on state (SIR = 1.21; 95% CI: 0.25 to 3.54) and national (SIR = 1.27; 95% CI: 0.26 to 3.70) reference rates. CONCLUSIONS: Our findings are reassuring that current use of ARV for perinatal HIV prophylaxis does not increase cancer risk. We found no evidence to alter the current federal guidelines of 2014 that recommend ARV prophylaxis of HIV-exposed infants.

[Features of clinical phenotype and genotype in Alport syndrome: a monocentric study].

OBJECTIVE: To analyze the clinical features and gene mutation of Chinese children with Alport syndrome(AS). METHOD: From May 2011 to May 2014, clinical and pathological information gathered from 25 patients was retrospectively analyzed. COL4A5, COL4A4 and COL4A3 genes were analyzed using next-generation sequencing in these patients, and gene mutations of related family members were identified by Sanger method. RESULT: Of these 25 cases, 19(76%) had X-linked Alport syndromes (XL-AS), 6 had autosomal recessive Alport syndromes (AR-AS). Twenty five patients had an onset of hematuria and proteinuria and in 8 cases the disease was induced by upper respiratory tract infections. Hearing loss was present in 2 of 25 (8%) cases and ocular lesions in 1 of 25 (4%). Renal pathology showed that 16 of them had minimal change disease (MCD), 8 mesangial proliferative glomerulonephritis (MsPNG), 1 focal segmental glomerulo-sclerosis (FSGS). Extensive lamination and split of glomerular basement membrane (GBM) dense layers were found in 2 (8%) of 25 patients. Twenty one of 25 patients (84%) showed abnormal renal α-chain distribution. COL4A5, COL4A4 and COL4A3 genes of 25 patients (23 families) were analyzed and 24 pathogenic mutations were identified: 18 in COL4A5, 1 in COL4A3 and 5 in COL4A4. It was observed that 13 patients inherited the mutation from the mother, 3 patients inherited from the father, 2 patients inherited 1 mutation from the mother and another mutation from the father, and 7 patients carried the novel mutations. CONCLUSION: XL is the main inherited type in AS. Most of patients showed MCD and MsPNG in renal biopsy. This research examined 24 mutations and 16 mutations were not reported previously.

Cancer survival disparities by health insurance status.

Previous studies found that uninsured and Medicaid insured cancer patients have poorer outcomes than cancer patients with private insurance. We examined the association between health insurance status and survival of New Jersey patients 18-64 diagnosed with seven common cancers during 1999-2004. Hazard ratios (HRs) with 95% confidence intervals for 5-year cause-specific survival were calculated from Cox proportional hazards regression models; health insurance status was the primary predictor with adjustment for other significant factors in univariate chi-square or Kaplan-Meier survival log-rank tests. Two diagnosis periods by health insurance status were compared using Kaplan-Meier survival log-rank tests. For breast, colorectal, lung, non-Hodgkin lymphoma (NHL), and prostate cancer, uninsured and Medicaid insured patients had significantly higher risks of death than privately insured patients. For bladder cancer, uninsured patients had a significantly higher risk of death than privately insured patients. Survival improved between the two diagnosis periods for privately insured patients with breast, colorectal, or lung cancer and NHL, for Medicaid insured patients with NHL, and not at all for uninsured patients. Survival from cancer appears to be related to a complex set of demographic and clinical factors of which insurance status is a part. While ensuring that everyone has adequate health insurance is an important step, additional measures must be taken to address cancer survival disparities.

Cancer incidence in world trade center rescue and recovery workers, 2001-2008.

BACKGROUND: World Trade Center (WTC) rescue and recovery workers were exposed to a complex mix of pollutants and carcinogens. OBJECTIVE: The purpose of this investigation was to evaluate cancer incidence in responders during the first 7 years after 11 September 2001. METHODS: Cancers among 20,984 consented participants in the WTC Health Program were identified through linkage to state tumor registries in New York, New Jersey, Connecticut, and Pennsylvania. Standardized incidence ratios (SIRs) were calculated to compare cancers diagnosed in responders to predicted numbers for the general population. Multivariate regression models were used to estimate associations with degree of exposure. RESULTS: A total of 575 cancers were diagnosed in 552 individuals. Increases above registry-based expectations were noted for all cancer sites combined (SIR = 1.15; 95% CI: 1.06, 1.25), thyroid cancer (SIR = 2.39; 95% CI: 1.70, 3.27), prostate cancer (SIR = 1.21; 95% CI: 1.01, 1.44), combined hematopoietic and lymphoid cancers (SIR = 1.36; 95% CI: 1.07, 1.71), and soft tissue cancers (SIR = 2.26; 95% CI: 1.13, 4.05). When restricted to 302 cancers diagnosed ≥ 6 months after enrollment, the SIR for all cancers decreased to 1.06 (95% CI: 0.94, 1.18), but thyroid and prostate cancer diagnoses remained greater than expected. All cancers combined were increased in very highly exposed responders and among those exposed to significant amounts of dust, compared with responders who reported lower levels of exposure. CONCLUSION: Estimates should be interpreted with caution given the short follow-up and long latency period for most cancers, the intensive medical surveillance of this cohort, and the small numbers of cancers at specific sites. However, our findings highlight the need for continued follow-up and surveillance of WTC responders.

Thyroid cancer incidence in New Jersey: time trend, birth cohort and socioeconomic status analysis (1979-2006).

The study's purpose was to investigate thyroid cancer incidence time trends, birth cohort effects, and association with socioeconomic status (SES) in New Jersey (NJ), a high incidence state, using NJ State Cancer Registry data. Thyroid cancer incidence rates in each sex, nearly all age groups, two major histologies and all stages significantly increased between 1979 and 2006. For each sex, age-specific incidence rates began greatly increasing in the 1924 birth cohort and, generally, the highest thyroid cancer incidence rate for each five-year age group occurred in the latest birth cohort and diagnosis period. Thyroid cancer incidence rates were significantly higher in NJ Census tracts with higher SES and in counties with a higher percentage of insured residents. These results support further investigation into the relationship between rising thyroid cancer incidence and increasing population exposure to medical (including diagnostic) radiation, as well as widespread use of more sensitive diagnostic techniques.

Expression of response gene to complement-32 in renal tissue of children with immunoglobulin A nephropathy.

OBJECTIVE: This study aimed to investigate the expression and significance of response gene to complement-32 (RGC-32) in renal tissue of children with immunoglobulin A nephropathy (IgAN). MATERIAL AND METHODS: Forty-five patients diagnosed as having IgAN by renal biopsy were enrolled. The expression of RGC-32, α-smooth muscle actin (α-SMA) and transforming growth factor-ß(1) (TGF-ß(1)) was observed by immunohistostaining. The relationshis between the expression of RGC-32, α-SMA, TGF-ß1, degree of renal pathological lesions in IgAN and clinical index were assessed by Spearman correlation. RESULTS: Immunohistostaining analysis showed that RGC-32 protein was present in epithelial cells of renal tubules in normal and IgAN renal tissues. With more severe renal pathological lesions, the expression of RGC-32 in IgAN was increased. The expression of RGC-32 was positively correlated with that of α-SMA, TGF-ß(1) and the degree of renal pathological lesions in children with IgAN (p < 0.05), but had no relationship with serum creatinine, urinary N-acetyl-ß-d-glucosaminidase/creatinine, urinary microalbuminuria/creatinine, urinary microimmunoglobulin/creatinine or urinary α(1)-microglobulin/creatinine ratio (p > 0.05). CONCLUSION: Expression of RGC-32 can reflect the degree of renal pathological lesions in IgAN. RGC-32 may participate in the renal tubulointerstitial lesions in children with IgAN, especially in epithelial -mesenchymal transition induced by TGF-ß(1).

Cancer survival disparities by race/ethnicity and socioeconomic status in New Jersey.

We investigated racial/ethnic and socioeconomic disparities in cancer survival and assessed if racial disparities can be explained by socioeconomic status (SES) using New Jersey State Cancer Registry data. We included cancer cases diagnosed during 1986-1999 (n=471,939). Hazard ratios were calculated for all cancers combined and female breast, colorectal, lung, and prostate cancers by race/ethnicity and SES for cases diagnosed in 1993-1999. Survival rates were compared for diagnosis years 1986-1992 and 1993-1999. We observed worse survival in Black patients and a SES gradient in the risk of cancer death after adjusting for age and stage at diagnosis. Following adjustment by SES, the higher risks of cancer death for Blacks were attenuated for breast, colorectal, and prostate cancer and became non-significant for lung cancer. Racial/ethnic disparities in cancer survival can be partially explained by SES. Cancer survival rates improved significantly from 1986-1992 to 1993-1999 except for women in the poorest areas.

The impact of patient follow-up on population-based survival rates.

OBJECTIVE: This study was designed to measure the impact of variation in patient follow-up on survival statistics. METHODS: surveillance, epidemiology and end results (SEER) data were used to construct four additional datasets. These datasets simulated scenarios of complete, incomplete, and no follow-up of live patients; and complete and incomplete death ascertainment. Sixty-month observed survival proportions were calculated using the actual SEER data and the four additional datasets. RESULTS: The 60-month observed survival proportion increased from 54.44% under the original SEER dataset to 54.62% under complete ascertainment of deaths with no follow-up among live patients. Under complete death ascertainment, randomly imputing loss to follow-up among 20% of live cases resulted in a 1%-2% decrease in 60-month observed survival for 71 of the 102 SEER site categories. With follow-up limited to ascertainment of deaths, randomly missing 6% of deaths resulted in a 1% or greater increase in 60-month observed survival for 99 SEER site categories. CONCLUSIONS: This study provides evidence to support the importance of complete death ascertainment for producing accurate cancer survival statistics, and that ascertainment of deaths only should generally be sufficient for survival analysis.