Cancer Medicine by Alexandros G.Sfakianakis,Anapafseos 5 Agios Nikolaos,Crete 72100,Greece,tel :00302841026182 & 00306932607174
Κυριακή 13 Δεκεμβρίου 2015
Should ALPPS be Used for Liver Resection in Intermediate-Stage HCC?
Abstract
Background
Extended liver resections in patients with hepatocellular carcinoma (HCC) are problematic due to hepatitis, fibrosis, and cirrhosis. Associating liver partition with portal vein ligation for staged hepatectomy (ALPPS) has been promoted as a novel method to induce hypertrophy for patients with extensive colorectal liver metastases, but outcomes in HCC have not been well investigated.
Methods
All patients registered in the international ALPPS Registry (www.alpps.org) from 2010 to 2015 were studied. Hypertrophy of the future liver remnant, perioperative morbidity and mortality, age, overall survival, and other parameters were compared between patients with HCC and patients with colorectal liver metastases (CRLM).
Results
The study compared 35 patients with HCC and 225 patients with CRLM. The majority of patients undergoing ALPPS for HCC fall into the intermediate-stage category of the Barcelona clinic algorithm. In this study, hypertrophy was rapid and extensive for the HCC patients, albeit lower than for the CRLM patients (47 vs. 76 %; p < 0.002). Hypertrophy showed a linear negative correlation with the degrees of fibrosis. The 90-day mortality for ALPPS used to treat HCC was almost fivefold higher than for CRLM (31 vs. 7 %; p < 0.001). Multivariate analysis showed that patients older than 61 years had a significantly reduced overall survival (p < 0.004).
Conclusion
The ALPPS approach induces a considerable hypertrophic response in HCC patients and allows resection of intermediate-stage HCC, albeit at the cost of a 31 % perioperative mortality rate. The use of ALPPS for HCC remains prohibitive for most patients and should be performed only for a highly selected patient population younger than 60 years with low-grade fibrosis.
from Cancer via ola Kala on Inoreader http://ift.tt/220puxi
via IFTTT
TruSight Cancer Sequencing Panel reveals pharmacogenetic variants associated with sensitivity to chemotherapy in lung cancer
Abstract
Lung cancer is the most common cause of cancer death worldwide, and its prognosis and treatment response rate as well as the survival rate remain poor. In our study, we performed next generation sequencing (NGS) with cancer panel (Illumina) for 19 Bulgarian patients with both non-small cell lung cancer (NSCLC; 18 patients) and neuroendocrine tumor (1 patient) and focused on common polymorphisms which define proven or reported sensitivity to platinum-based therapy. We report reference SNP (rs)1042522 (TP53), rs2228001 (XPC), rs2227983 (EGFR), rs1799793, and rs13181 (ERCC2) single nucleotide polymorphism variants which have been detected in our patients in homozygous and/or heterozygous state. Therefore, we give important information to confirm the role of those polymorphisms in tumor resistance and recurrence after chemotherapy treatment. The results reveal that TruSight Cancer Panel could be a useful clinical tool for determining pharmacogenetic variants associated with the effect of chemotherapy.
from Cancer via ola Kala on Inoreader http://ift.tt/1YdUMMk
via IFTTT
miR-548d-3p/TP53BP2 axis regulates the proliferation and apoptosis of breast cancer cells
Abstract
Fast growth and hardly any apoptosis are important characteristics of breast cancer, which assure the spread via invasion and metastasis of breast cancer cells. Inhibition of fast proliferation and induction of apoptosis are critical way to cure this cancer. microRNAs (miRNAs) had been increasingly reported to be the critical regulator of tumorigenesis. In our study, we found that increasing copy number of miR-548d-2-3p is critically involved poor prognosis. We overexpressed miR-548d-3p in MDA-MB-231cells and found that the proliferation was promoted significantly, whereas the inhibition of miR-548d-3p repressed the proliferation of MDA-MB-231 cells and also induced the increase in apoptosis. Additionally, we found that miR-548d-3p downregulated the expression of TP53BP2 by directly targeting the 3′UTR. We also found that knockdown of TP53BP2 significantly resorted the proliferation and apoptosis regulated by miR-548d-3p inhibitor. Our study showed that miR-548d-3p/TP53BP2 pathway is critically involved in the proliferation and apoptosis of breast cancer cells and may be new therapeutic target of breast cancer cells.
High-level copy number of miR-548d-3p is critically involved in the low survival ratio. miR-548d-3p plays an important role on regulating the proliferation and apoptosis of breast cancer.
from Cancer via ola Kala on Inoreader http://ift.tt/1UmqXZH
via IFTTT
Gelsolin promotes cell growth and invasion through the upregulation of p-AKT and p-P38 pathway in osteosarcoma
Abstract
The gelsolin (GSN) has been involved in the regulation of tumor formation and development, but the biological role of GSN in the pathogenesis of osteosarcoma (OS) has not been well characterized. In this study, we show that high expression of GSN was observed in OS tissues and correlated with tumor size, advanced Enneking stage, and poor patient prognosis. Knockdown of GSN significantly inhibited cell proliferation and invasiveness in the OS cell lines. Furthermore, stable overexpression of GSN in OS cells resulted in a significant increase in cell growth and motility with the downregulation of p-AKT and p-P38 pathway. Finally, overexpression of GSN promoted growth of OS tumors in SCID mice. Taken together, these results provided the first evidence that GSN might contribute to OS cancer development and could be an attractive therapeutic target for patients with OS.
from Cancer via ola Kala on Inoreader http://ift.tt/1INSmlT
via IFTTT
The effects of bufadienolides on HER2 overexpressing breast cancer cells
Abstract
HER2 is a proto-oncogene frequently amplified in human breast cancer, its overexpression is correlated with tamoxifen resistance and decreased recurrence-free survival. Arenobufagin and bufalin are homogeneous bufadienolides of cardiac glycosides agents. In this research, we studied the effects of arenobufagin and bufalin on cellular survival and proliferation of HER2 overexpressing breast cancer cells and the mechanism under the results including the direct effect on HER2 downstream pathways. Our results showed that arenobufagin and bufalin could significantly inhibit the proliferation and survival of HER2 overexpressing breast cancer cells, along with the declination of SRC-1, SRC-3, nuclear transcription factor E2F1, phosphorylated AKT, and ERK. And the combination of each bufadienolide in low dose with tamoxifen could significantly enhance the inhibitory effect of tamoxifen on HER2 overexpressing breast cancer cells. All above suggest that arenobufagin and bufalin may be potential therapy adjuvants for HER2 overexpressing breast cancer therapy.
from Cancer via ola Kala on Inoreader http://ift.tt/1NqRfoI
via IFTTT
Prognostic value of the neutrophil-to-lymphocyte ratio for overall and disease-free survival in patients with surgically treated esophageal squamous cell carcinoma
Abstract
Although increasing evidence indicates that cancers are associated with inflammation, the prognostic role of the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) in patients with esophageal squamous cell carcinoma remains controversial. We determined the prognostic roles of NLR and PLR in patients with esophageal squamous cell carcinoma who underwent surgical treatment. We retrospectively reviewed 119 patients with esophageal squamous cell carcinoma who underwent surgical resection and complete lymph node dissection from 2004 to 2012. The preoperative NLR and PLR were measured. The patients included 112 (94.1 %) males (mean age, 63.64 ± 8.42 years) of whom 37 (31.1 %) were pathological stage I, 33 (27.7 %) were stage II, and 49 (41.2 %) were stage III. The median follow-up period was 28.68 months. Recurrence was reported in 48 (40.3 %) patients. Mean NLR and PLR were 2.35 ± 1.39 and 140.77 ± 70.47, respectively. A multivariate analysis revealed that NLR was a risk factor for disease-free survival (DFS) (hazard ratio [HR], 1.194; p = 0.031) and overall survival (OS) (HR, 1.230; p = 0.011), whereas PLR was not a risk factor for DFS or OS. The 3-year OS rates were 51.0 % in low-NLR (<2.97) patients and 17.4 % in high-NLR (≥2.97) patients (p = 0.007). Akaike's information criterion decreased when the NLR was included in the multivariate model compared to the multivariate model without NLR. A high NLR was a significant prognostic factor for OS and DFS in patients with surgically treated esophageal squamous cell carcinoma, whereas PLR showed no prognostic significance.
from Cancer via ola Kala on Inoreader http://ift.tt/1INSkdz
via IFTTT
Garcinol inhibits tumour cell proliferation, angiogenesis, cell cycle progression and induces apoptosis via NF-κB inhibition in oral cancer
Abstract
Garcinol, a polyisoprenylated benzophenone is extracted from the rind of the fruit of Garcinia indica, a plant found extensively in tropical regions. Its ability to inhibit tumour growth has been demonstrated in certain cancers. In this study, we evaluated the potential anti-tumour effects of garcinol on oral squamous cell carcinoma (OSCC) cells. Three OSCC cell lines (SCC-4, SCC-9 and SCC-25) were treated with garcinol for 48 h and its effect on growth and proliferation, clonogenic survival, cell cycle and apoptosis was studied by MTT, clonogenic assay, propidium iodide (PI) staining and annexin-V binding assay, respectively. The alteration in expression of NF-κB and COX-2 was studied by western blot analysis and that of VEGF by ELISA. Garcinol treatment significantly (p < 0.001) inhibited the growth and proliferation and colony formation of OSCC cells with a concomitant induction of apoptosis and cell cycle arrest. It did not show toxic effect on normal cells. It significantly (p < 0.05) reduced the expression of NK-κB and COX-2 expression in treated cells as compared to untreated controls besides inhibiting VEGF expression. It appears that garcinol exerts anti-proliferative, pro-apoptotic, cell-cycle regulatory and anti-angiogenic effects on oral cancer cells through inhibition of NF-κB and COX-2. Thus, garcinol may be developed as a potential chemopreventive and/or chemotherapeutic agent for treatment of oral squamous cell carcinoma.
from Cancer via ola Kala on Inoreader http://ift.tt/1NqReRZ
via IFTTT
Gelsolin promotes cell growth and invasion through the upregulation of p-AKT and p-P38 pathway in osteosarcoma
Abstract
The gelsolin (GSN) has been involved in the regulation of tumor formation and development, but the biological role of GSN in the pathogenesis of osteosarcoma (OS) has not been well characterized. In this study, we show that high expression of GSN was observed in OS tissues and correlated with tumor size, advanced Enneking stage, and poor patient prognosis. Knockdown of GSN significantly inhibited cell proliferation and invasiveness in the OS cell lines. Furthermore, stable overexpression of GSN in OS cells resulted in a significant increase in cell growth and motility with the downregulation of p-AKT and p-P38 pathway. Finally, overexpression of GSN promoted growth of OS tumors in SCID mice. Taken together, these results provided the first evidence that GSN might contribute to OS cancer development and could be an attractive therapeutic target for patients with OS.
from Cancer via ola Kala on Inoreader http://ift.tt/1INSmlT
via IFTTT
The effects of bufadienolides on HER2 overexpressing breast cancer cells
Abstract
HER2 is a proto-oncogene frequently amplified in human breast cancer, its overexpression is correlated with tamoxifen resistance and decreased recurrence-free survival. Arenobufagin and bufalin are homogeneous bufadienolides of cardiac glycosides agents. In this research, we studied the effects of arenobufagin and bufalin on cellular survival and proliferation of HER2 overexpressing breast cancer cells and the mechanism under the results including the direct effect on HER2 downstream pathways. Our results showed that arenobufagin and bufalin could significantly inhibit the proliferation and survival of HER2 overexpressing breast cancer cells, along with the declination of SRC-1, SRC-3, nuclear transcription factor E2F1, phosphorylated AKT, and ERK. And the combination of each bufadienolide in low dose with tamoxifen could significantly enhance the inhibitory effect of tamoxifen on HER2 overexpressing breast cancer cells. All above suggest that arenobufagin and bufalin may be potential therapy adjuvants for HER2 overexpressing breast cancer therapy.
from Cancer via ola Kala on Inoreader http://ift.tt/1NqRfoI
via IFTTT
Prognostic value of the neutrophil-to-lymphocyte ratio for overall and disease-free survival in patients with surgically treated esophageal squamous cell carcinoma
Abstract
Although increasing evidence indicates that cancers are associated with inflammation, the prognostic role of the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) in patients with esophageal squamous cell carcinoma remains controversial. We determined the prognostic roles of NLR and PLR in patients with esophageal squamous cell carcinoma who underwent surgical treatment. We retrospectively reviewed 119 patients with esophageal squamous cell carcinoma who underwent surgical resection and complete lymph node dissection from 2004 to 2012. The preoperative NLR and PLR were measured. The patients included 112 (94.1 %) males (mean age, 63.64 ± 8.42 years) of whom 37 (31.1 %) were pathological stage I, 33 (27.7 %) were stage II, and 49 (41.2 %) were stage III. The median follow-up period was 28.68 months. Recurrence was reported in 48 (40.3 %) patients. Mean NLR and PLR were 2.35 ± 1.39 and 140.77 ± 70.47, respectively. A multivariate analysis revealed that NLR was a risk factor for disease-free survival (DFS) (hazard ratio [HR], 1.194; p = 0.031) and overall survival (OS) (HR, 1.230; p = 0.011), whereas PLR was not a risk factor for DFS or OS. The 3-year OS rates were 51.0 % in low-NLR (<2.97) patients and 17.4 % in high-NLR (≥2.97) patients (p = 0.007). Akaike's information criterion decreased when the NLR was included in the multivariate model compared to the multivariate model without NLR. A high NLR was a significant prognostic factor for OS and DFS in patients with surgically treated esophageal squamous cell carcinoma, whereas PLR showed no prognostic significance.
from Cancer via ola Kala on Inoreader http://ift.tt/1INSkdz
via IFTTT
Garcinol inhibits tumour cell proliferation, angiogenesis, cell cycle progression and induces apoptosis via NF-κB inhibition in oral cancer
Abstract
Garcinol, a polyisoprenylated benzophenone is extracted from the rind of the fruit of Garcinia indica, a plant found extensively in tropical regions. Its ability to inhibit tumour growth has been demonstrated in certain cancers. In this study, we evaluated the potential anti-tumour effects of garcinol on oral squamous cell carcinoma (OSCC) cells. Three OSCC cell lines (SCC-4, SCC-9 and SCC-25) were treated with garcinol for 48 h and its effect on growth and proliferation, clonogenic survival, cell cycle and apoptosis was studied by MTT, clonogenic assay, propidium iodide (PI) staining and annexin-V binding assay, respectively. The alteration in expression of NF-κB and COX-2 was studied by western blot analysis and that of VEGF by ELISA. Garcinol treatment significantly (p < 0.001) inhibited the growth and proliferation and colony formation of OSCC cells with a concomitant induction of apoptosis and cell cycle arrest. It did not show toxic effect on normal cells. It significantly (p < 0.05) reduced the expression of NK-κB and COX-2 expression in treated cells as compared to untreated controls besides inhibiting VEGF expression. It appears that garcinol exerts anti-proliferative, pro-apoptotic, cell-cycle regulatory and anti-angiogenic effects on oral cancer cells through inhibition of NF-κB and COX-2. Thus, garcinol may be developed as a potential chemopreventive and/or chemotherapeutic agent for treatment of oral squamous cell carcinoma.
from Cancer via ola Kala on Inoreader http://ift.tt/1NqReRZ
via IFTTT
Translation failure and medical reversal: Two sides to the same coin
Publication date: January 2016
Source:European Journal of Cancer, Volume 52
Author(s): Vinay Prasad
Translation failure occurs when the results of preclinical, observational and/or early phase studies fail to predict the results of well done (i.e. appropriately controlled, adequately powered, and properly conducted) phase III or randomised clinical trials.Some failures occur when promising basic science findings fail to replicate in human studies, while others happen when promising uncontrolled trial data show an exaggerated effect that vanishes in the setting of a randomised trial.Medical reversals occur when the results of preclinical, observational and/or early phase studies fail to predict the results of subsequent randomized clinical trials, but the practice has already gained widespread acceptance. Oncologic examples include bevacizumab and the use of autologous stem cell transplant in metastatic breast cancer.In a well-intentioned effort to reduce the rate of translation failure, oncologists must be careful that changes to regulatory processes and clinical trial design do not actually work to increase the approval of ineffective compounds. By trying to cure translation failure, we should be careful to avoid medical reversal. The rise of surrogate end-points and role of hard-wired bias in oncology trials suggest that we may be currently ignoring the simple fact that translation failure and medical reversal are two sides to the same coin.
from Cancer via ola Kala on Inoreader http://ift.tt/21YYsWX
via IFTTT
Induction or consolidation chemotherapy for unresectable stage III non-small-cell lung cancer patients treated with concurrent chemoradiation: a randomised phase II trial GFPC – IFCT 02-01
Publication date: January 2016
Source:European Journal of Cancer, Volume 52
Author(s): Pierre Fournel, Alain Vergnenégre, Gilles Robinet, Hervé Léna, Radj Gervais, Hervé Le Caer, Pierre-Jean Souquet, Jean-Michel Chavaillon, Marie-Cécile Bozonnat, Jean-Pierre Daurès, Christos Chouaid, Isabelle Martel-Lafay
PurposeThe objective of this randomised phase II study was to evaluate the impact in terms of response and toxicities of induction or consolidation chemotherapy respectively before or after concurrent chemoradiotherapy in unresectable stage III non-small-cell lung cancer.Patients and methodsIn the induction arm, patients received induction chemotherapy with cisplatin (80 mg/m2) and paclitaxel (200 mg/m2) on days 1 and 29 followed by a concurrent chemoradiotherapy (66 Gy in 33 fractions, cisplatin 80 mg/m2 days 1, 29 and 57, vinorelbine 15 mg/m2 days 1, 8, 29, 36, 57 and 64). In consolidation arm, the same concurrent chemoradiotherapy began on day 1 followed by two cycles of cisplatin and paclitaxel.ResultsOne hundred twenty seven patients were randomised. The intent to treat response rates in induction and consolidation arms were 58% and 56% respectively. Median survival was 19.6 months in induction arm and 16.3 months in consolidation arm and 4-year survival rates were 21% and 30% respectively. Haematologic and non-haematologic toxicities were similar in both arms, except grade 3/4 oesophagitis, more frequent in consolidation arm than in induction arm (17% versus 10%).ConclusionCisplatin-based chemotherapy as induction or consolidation with concurrent chemoradiotherapy can be administrated safely. Response rates were similar in both arms with a trend in favour for consolidation arm for long-term survival.
from Cancer via ola Kala on Inoreader http://ift.tt/21YYqOP
via IFTTT
Nicotine induces self-renewal of pancreatic cancer stem cells via neurotransmitter-driven activation of sonic hedgehog signalling
Publication date: January 2016
Source:European Journal of Cancer, Volume 52
Author(s): Mohammed H. Al-Wadei, Jheelam Banerjee, Hussein A.N. Al-Wadei, Hildegard M. Schuller
A small subpopulation of pancreatic cancer cells with characteristics of stem cells drive tumour initiation, progression and metastasis. A better understanding of the regulation of cancer stem cells may lead to more effective cancer prevention and therapy. We have shown that the proliferation and migration of pancreatic cancer cell lines is activated by the nicotinic receptor-mediated release of stress neurotransmitters, responses reversed by γ-aminobutyric acid (GABA). However, the observed cancer inhibiting effects of GABA will only succeed clinically if GABA inhibits pancreatic cancer stem cells (PCSCs) in addition to the more differentiated cancer cells that comprise the majority of cancer tissues and cell lines. Using PCSCs isolated from two pancreatic cancer patients by cell sorting and by spheroid formation assay from pancreatic cancer cell line Panc-1, we tested the hypothesis that nicotine induces the self-renewal of PCSCs. Nicotinic acetylcholine receptors (nAChRs) α3, α4, α5 and α7 were expressed and chronic exposure to nicotine increased the protein expression of these receptors. Immunoassays showed that PCSCs produced the stress neurotransmitters epinephrine and norepinephrine and the inhibitory neurotransmitter GABA. Chronic nicotine significantly increased the production of stress neurotransmitters and sonic hedgehog (SHH) while inducing Gli1 protein and decreasing GABA. GABA treatment inhibited the induction of SHH and Gli1. Spheroid formation and 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazoliumbromide assays showed significant nicotine-induced increases in self renewal and cell proliferation, responses blocked by GABA. Our data suggest that nicotine increases the SHH-mediated malignant potential of PCSCs and that GABA prevents these effects.
from Cancer via ola Kala on Inoreader http://ift.tt/1MatTC3
via IFTTT
Cancer incidence among Asian American populations in the United States, 2009-2011
Abstract
Cancer incidence disparities exist among specific Asian American populations. However, the existing reports exclude data from large metropoles like Chicago, Houston, and New York. Moreover, incidence rates by subgroup have been underestimated due to the exclusion of Asians with unknown subgroup. Cancer incidence data for 2009 to 2011 for eight states accounting for 68% of the Asian American population were analyzed. Race for cases with unknown subgroup was imputed using stratified proportion models by sex, age, cancer site, and geographic regions. Age-standardized incidence rates were calculated for 17 cancer sites for the six largest Asian subgroups. Our analysis comprised 90,709 Asian and 1,327,727 non-Hispanic white cancer cases. Asian Americans had significantly lower overall cancer incidence rates than non-Hispanic whites (336.5 per 100,000 and 541.9 for men, 299.6 and 449.3 for women, respectively). Among specific Asian subgroups, Filipino men (377.4) and Japanese women (342.7) had the highest overall incidence rates while South Asian men (297.7) and Korean women (275.9) had the lowest. In comparison to non-Hispanic whites and other Asian subgroups, significantly higher risks were observed for colorectal cancer among Japanese, stomach cancer among Koreans, nasopharyngeal cancer among Chinese, thyroid cancer among Filipinos, and liver cancer among Vietnamese. South Asians had remarkably low lung cancer risk. Overall, Asian Americans have a lower cancer risk than non-Hispanic whites, except for nasopharyngeal, liver and stomach cancers. The unique portrayal of cancer incidence patterns among specific Asian subgroups in this study provides a new baseline for future cancer surveillance research and health policy. This article is protected by copyright. All rights reserved.
from Cancer via ola Kala on Inoreader http://ift.tt/1mi6A4v
via IFTTT
Menopausal hormone therapy use and risk of primary liver cancer in the Clinical Practice Research Datalink
Abstract
Primary liver cancer occurs less commonly among women than men in almost all countries. This discrepancy has suggested that hormone levels and/or exogenous hormone use could have an effect on risk, although prior studies have reached inconsistent conclusions. Thus, the current study was conducted to examine the relationship between menopausal hormone therapy (MHT) use and development of liver cancer. A nested case-control study was conducted within the United Kingdom's Clinical Practice Research Datalink (CPRD). Controls were matched, at a 4-to-1 ratio, to women diagnosed with primary liver cancer between 1988 and 2011. A second match, based on whether the cases and controls had diabetes, was also conducted. Odds ratios (OR) and 95% confidence intervals (95%CI) for associations of MHT with liver cancer were estimated using conditional logistic regression adjusted for known risk factors. In the overall match, 339 women with liver cancer were matched to 1318 controls. MHT use was associated with a significantly lower risk of liver cancer (ORadj=0.58, 95%CI=0.37-0.90) especially among users of estrogen-only MHT (ORadj=0.44, 95%CI=0.22-0.88) and among past users (ORadj=0.53, 95%CI=0.32-0.88). Among the matched cases (n=58) and controls (n=232) with diabetes, the odds ratios were similar to the overall analysis (ORadj=0.57, 95%CI=0.09-3.53), but did not attain statistical significance. In the current study, MHT use, especially estrogen-only MHT use, was associated with a significantly lower risk of liver cancer. These results support the need of further investigation into whether hormonal etiologies can explain the variation in liver cancer incidence between men and women. This article is protected by copyright. All rights reserved.
from Cancer via ola Kala on Inoreader http://ift.tt/1MarJlS
via IFTTT
Age-specific prevalence of HPV16/18 genotypes in cervical cancer: a systematic review and meta-analysis
Abstract
The prevalence of HPV16/18 in cervical cancer has been reported to decline with age in some papers. However, whether this decline in proportion of cancers positive for HPV16/18 is consistently observed across studies remains to be elucidated. Thus, the aim of our study was to identify papers reporting data on age-specific prevalence of HPV16/18 in cervical cancer and to summarize the results. We employed MEDLINE and Embase for a systematic literature search and thereby identified a total of 644 papers published in the period 1999-2015 of which 15 papers, reporting cross-sectional data, were included for review (11,526 cervical cancers). The prevalence of HPV16/18 in cervical cancer declined significantly with age (ρ =-0.83, p=0.04) from 74.8% (95% CI 67.6 – 80.8) in women aged 30-39 years to 56.8% (95% CI 43.9 – 68.8) in women ≥70 years. As the HPV16/18 positive cancers are prevented in fully vaccinated cohorts, the age-specific epidemiology of cervical cancer is anticipated to change, with a shift in peak incidence rate to older ages. It will be important for integrated vaccination and screening strategies to consider predicted change in the age-specific epidemiology of cervical cancer. This article is protected by copyright. All rights reserved.
from Cancer via ola Kala on Inoreader http://ift.tt/1MarJSO
via IFTTT
Εγγραφή σε:
Αναρτήσεις (Atom)