scholarly journals Human Papillomavirus and Overall Survival After Progression of Oropharyngeal Squamous Cell Carcinoma

2014 ◽  
Vol 32 (30) ◽  
pp. 3365-3373 ◽  
Author(s):  
Carole Fakhry ◽  
Qiang Zhang ◽  
Phuc Felix Nguyen-Tan ◽  
David Rosenthal ◽  
Adel El-Naggar ◽  
...  
Keyword(s):  
Overall Survival ◽  
Human Papillomavirus ◽  
Disease Progression ◽  
Cancer Progression ◽  
Radiation Therapy Oncology Group ◽  
Treatment Protocol ◽  
Risk Of Death ◽  
Hpv Status ◽  
Increased Risk ◽  
Risk Of Cancer

Purpose Risk of cancer progression is reduced for patients with human papillomavirus (HPV) –positive oropharynx cancer (OPC) relative to HPV-negative OPC, but it is unknown whether risk of death after progression is similarly reduced. Patients and Methods Patients with stage III-IV OPC enrolled onto Radiation Therapy Oncology Group trials 0129 or RTOG 0522 who had known tumor p16 status plus local, regional, and/or distant progression after receiving platinum-based chemoradiotherapy were eligible for a retrospective analysis of the association between tumor p16 status and overall survival (OS) after disease progression. Rates were estimated by Kaplan-Meier method and compared by log-rank; hazard ratios (HRs) were estimated by Cox models. Tests and models were stratified by treatment protocol. Results A total of 181 patients with p16-positive (n = 105) or p16-negative (n = 76) OPC were included in the analysis. Patterns of failure and median time to progression (8.2 v 7.3 months; P = .67) were similar for patients with p16-positive and p16-negative tumors. After a median follow-up period of 4.0 years after disease progression, patients with p16-positive OPC had significantly improved survival rates compared with p16-negative patients (2-year OS, 54.6% v 27.6%; median, 2.6 v 0.8 years; P < .001). p16-positive tumor status (HR, 0.48; 95% CI, 0.31 to 0.74) and receipt of salvage surgery (HR, 0.48; 95% CI; 0.27 to 0.84) reduced risk of death after disease progression whereas distant versus locoregional progression (HR, 1.99; 95% CI, 1.28 to 3.09) increased risk, after adjustment for tumor stage and cigarette pack-years at enrollment. Conclusion Tumor HPV status is a strong and independent predictor of OS after disease progression and should be a stratification factor for clinical trials for patients with recurrent or metastatic OPC.

scholarly journals Tobacco Smoking and Increased Risk of Death and Progression for Patients With p16-Positive and p16-Negative Oropharyngeal Cancer

2012 ◽  
Vol 30 (17) ◽  
pp. 2102-2111 ◽  
Author(s):  
Maura L. Gillison ◽  
Qiang Zhang ◽  
Richard Jordan ◽  
Weihong Xiao ◽  
William H. Westra ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Tobacco Smoking ◽  
Oropharyngeal Cancer ◽  
Radiation Therapy Oncology Group ◽  
Phase Iii ◽  
Tobacco Exposure ◽  
Primary Tumors ◽  
Risk Of Death ◽  
Oropharynx Cancer ◽  
Increased Risk

Purpose Tobacco smoking is associated with oropharynx cancer survival, but to what extent cancer progression or death increases with increasing tobacco exposure is unknown. Patients and Methods Patients with oropharynx cancer enrolled onto a phase III trial of radiotherapy from 1991 to 1997 (Radiation Therapy Oncology Group [RTOG] 9003) or of chemoradiotherapy from 2002 to 2005 (RTOG 0129) were evaluated for tumor human papillomavirus status by a surrogate, p16 immunohistochemistry, and for tobacco exposure by a standardized questionnaire. Associations between tobacco exposure and overall survival (OS) and progression-free survival (PFS) were estimated by Cox proportional hazards models. Results Prevalence of p16-positive cancer was 39.5% among patients in RTOG 9003 and 68.0% in RTOG 0129. Median pack-years of tobacco smoking were lower among p16-positive than p16-negative patients in both trials (RTOG 9003: 29 v 45.9 pack-years; P = .02; RTOG 0129: 10 v 40 pack-years; P < .001). After adjustment for p16 and other factors, risk of progression (PFS) or death (OS) increased by 1% per pack-year (for both, hazard ratio [HR], 1.01; 95% CI, 1.00 to 1.01; P = .002) or 2% per year of smoking (for both, HR, 1.02; 95% CI, 1.01 to 1.03; P < .001) in both trials. In RTOG 9003, risk of death doubled (HR, 2.19; 95% CI, 1.46 to 3.28) among those who smoked during radiotherapy after accounting for pack-years and other factors, and risk of second primary tumors increased by 1.5% per pack-year (HR, 1.015; 95% CI, 1.005 to 1.026). Conclusion Risk of oropharyngeal cancer progression and death increases directly as a function of tobacco exposure at diagnosis and during therapy and is independent of tumor p16 status and treatment.

Meta-analysis of the impact of human papillomavirus on cancer risk and overall survival in head and neck squamous cell carcinoma

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 6080-6080
Author(s):  
F. Dayyani ◽  
C. Etzel ◽  
M. Liu ◽  
C. Ho ◽  
S. M. Lippman ◽  
...  
Keyword(s):  
Overall Survival ◽  
Human Papillomavirus ◽  
Meta Analysis ◽  
Local Therapy ◽  
Forest Plot ◽  
Etiologic Factor ◽  
Hpv Dna ◽  
Hpv Status ◽  
Increased Risk ◽  
The Impact

6080 Background: Human papillomavirus (HPV) is an important etiologic factor in HNSCC and its prevalence has been reported in several independent studies. We conducted a meta-analysis to determine the prevalence of HPV, its impact on risk of developing HNSCC and overall survival (OS). Methods: Pubmed search terms “HPV” and “HNSCC” were used to identify 40 clinical and translational studies between the years 1980–2008 that reported the prevalence of HPV in HNSCC. Statistical software STATA 10.0 was used in the meta-analyses to identify the association of HPV and HNSCC risk and OS. Pooled adjusted odds ratio (OR) or hazard ratio (HR) were obtained using a random-effects model. The amount of heterogeneity between studies was estimated with both the Chi-squared based Q test and the I2 statistic model. Potential sources of publication bias were detected using funnel plots. OS between the trials was compared in forest plot. Results: A total of 6,794 patients (pts) were included. The prevalence of HPV among HNSCC pts was 24.2%; and 86.8% of all HPV(+) tumors were HPV16. Thirteen studies (n = 1933 pts) determined HPV status by serology and the remainder detected HPV DNA in tumor tissue by PCR. Overall, HPV positivity conferred an increased risk for HNSCC (OR = 1.43; 95% CI 1.04–1.82). Risk for HNSCC among HPV16(+) pts was 4.47 times that of HPV16(-) pts. The OS was improved in HPV(+) pts compared to HPV(-) pts (HR = 0.40; 0.27–0.53). In HPV16(+) pts the HR for OS was 0.41 and the survival benefit was even more pronounced in the subgroup of HPV16(+) oropharyngeal cancers (HR = 0.38;0.17–0.58). Conclusions: This meta-analysis provides further evidence supporting the role of HPV as an important causative agent in HNSCC and supports HPV(+) HNSCC as a separate biologic entity which likely should be treated differently than HPV(-) HNSCC. Additional analysis on treatment outcomes to systemic and local therapy is ongoing. No significant financial relationships to disclose.

scholarly journals The effect of adjuvant radiotherapy on overall survival in adults with intracranial ependymoma

2019 ◽  
Vol 7 (4) ◽  
pp. 391-399
Author(s):  
Roshan S Prabhu ◽  
Christopher D Corso ◽  
Matthew C Ward ◽  
John H Heinzerling ◽  
Reshika Dhakal ◽  
...  
Keyword(s):  
Overall Survival ◽  
Propensity Score ◽  
Adjuvant Radiotherapy ◽  
Subtotal Resection ◽  
National Cancer Database ◽  
Risk Of Death ◽  
Increased Risk ◽  
Intracranial Ependymoma ◽  
Male Sex ◽  
Grade 3

Abstract Background Adult intracranial ependymoma is rare, and the role for adjuvant radiotherapy (RT) is not well defined. Methods We used the National Cancer Database (NCDB) to select adults (age ≥ 22 years) with grade 2 to 3 intracranial ependymoma status postresection between 2004 and 2015 and treated with adjuvant RT vs observation. Four cohorts were generated: (1) all patients, (2) grade 2 only, (3) grade 2 status post–subtotal resection only, (4) and grade 3 only. The association between adjuvant RT use and overall survival (OS) was assessed using multivariate Cox and propensity score matched analyses. Results A total of 1787 patients were included in cohort 1, of which 856 patients (48%) received adjuvant RT and 931 (52%) were observed. Approximately two-thirds of tumors were supratentorial and 80% were grade 2. Cohorts 2, 3, and 4 included 1471, 345, and 316 patients, respectively. There was no significant association between adjuvant RT use and OS in multivariate or propensity score matched analysis in any of the cohorts. Older age, male sex, urban location, higher comorbidity score, earlier year of diagnosis, and grade 3 were associated with increased risk of death. Conclusions This large NCDB study did not demonstrate a significant association between adjuvant RT use and OS for adults with intracranial ependymoma, including for patients with grade 2 ependymoma status post–subtotal resection. The conflicting results regarding the efficacy of adjuvant RT in this patient population highlight the need for high-quality studies to guide therapy recommendations in adult ependymoma.

scholarly journals Human papillomavirus-driven immune deviation: challenge and novel opportunity for immunotherapy

2017 ◽  
Vol 5 (3) ◽  
pp. 69-82 ◽  
Author(s):  
Sigrun Smola ◽  
Connie Trimble ◽  
Peter L. Stern
Keyword(s):  
Human Papillomavirus ◽  
Immune System ◽  
Immune Escape ◽  
Hpv Vaccination ◽  
Suppressor Cells ◽  
Clinical Problem ◽  
Hpv Infection ◽  
Treatment Protocols ◽  
Increased Risk ◽  
Risk Of Cancer

It is now recognized that the immune system can be a key component of restraint and control during the neoplastic process. Human papillomavirus (HPV)-associated cancers of the anogenital tract and oropharynx represent a significant clinical problem but there is a clear opportunity for immune targeting of the viral oncogene expression that drives cancer development. However, high-risk HPV infection of the target epithelium and the expression of the E6/E7 oncogenes can lead to early compromise of the innate immune system (loss of antigen-presenting cells) facilitating viral persistence and increased risk of cancer. In these circumstances, a succession of interacting and self-reinforcing events mediated through modulation of different immune receptors, chemokine and cytokine responses (CCL20; CCL2; CCR2; IL-6; CCR7; IL-12) further promote the generation of an immune suppressive microenvironment [increased levels of Tregs, Th17, myeloid-derived suppressor cells (MDSCs) and PD-L1]. The overexpression of E6/E7 expression also compromises the ability to repair cellular DNA, leading to genomic instability, with the acquisition of genetic changes providing for the selection of advantaged cancer cells including additional strategies for immune escape. Therapeutic vaccines targeting the HPV oncogenes have shown some encouraging success in some recent early-phase clinical trials tested in patients with HPV-associated high-grade anogenital lesions. A significant hurdle to success in more advanced disease will be the local and systemic immune suppressive factors. Interventions targeting the different immunosuppressive components can provide opportunity to release existing or generate new and effective antitumour immunity. Treatments that alter the protumour inflammatory environment including toll-like receptor stimulation, inhibition of IL-6-related pathways, immune-checkpoint inhibition, direct modulation of MDSCs, Tregs and macrophages could all be useful in combination with therapeutic HPV vaccination. Future progress in delivering successful immunotherapy will depend on the configuration of treatment protocols in an insightful and timely combination.

scholarly journals Outcomes after Mastectomy and Lumpectomy in Octogenarians and Nonagenarians with Early-Stage Breast Cancer

2017 ◽  
Vol 83 (8) ◽  
pp. 887-894 ◽  
Author(s):  
Ameliay Merrill ◽  
Doris R. Brown ◽  
Heidi D. Klepin ◽  
Edward A. Levine ◽  
Marissa Howard-Mcnatt
Keyword(s):  
Breast Cancer ◽  
Overall Survival ◽  
Early Stage ◽  
Clinical Stage ◽  
Univariate Analysis ◽  
Local Treatment ◽  
Breast Conservation ◽  
Early Stage Breast Cancer ◽  
Risk Of Death ◽  
Increased Risk

Prospective studies have shown equal outcomes after mastectomy or breast conservation in patients with invasive breast cancer; however, many of these studies excluded elderly patients. We identified patients in their eighties and nineties with clinical stage 0 to II breast cancer undergoing mastectomy or lumpectomy with or without radiation from the prospective sentinel lymph node database at Wake Forest Baptist Health and analyzed their treatment and survival. Of 92 patients, 24 (26.1%) underwent mastectomy, 22 (23.9%) lumpectomy with radiation, and 46 (50.0%) lumpectomy alone. Significant differences were noted in tumor size (P = 0.018), nodal status (P = 0.013), and stage (P = 0.011) between the groups. Only 7.6 per cent of patients had chemotherapy, whereas 51.1 per cent took antiestrogen therapy. Recurrence occurred in 11 patients. In univariate analysis, overall survival did not differ by surgery. Age was the only factor that increased risk of death (HR = 1.19, P = 0.028). In this age group, neither tumor factors nor the type of local treatment significantly influenced overall survival. Octogenarians and nonagenarians with early-stage breast cancer undergoing breast-conserving surgery with or without radiation have equivalent survival to patients having a mastectomy.

scholarly journals Downregulation of Cdc2/CDK1 Kinase Activity Induces the Synthesis of Noninfectious Human Papillomavirus Type 31b Virions in Organotypic Tissues Exposed to Benzo[a]pyrene

2010 ◽  
Vol 84 (9) ◽  
pp. 4630-4645 ◽  
Author(s):  
Samina Alam ◽  
Brian S. Bowser ◽  
Michael J. Conway ◽  
Mohd Israr ◽  
Eric J. Ryndock ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Cellular Proliferation ◽  
Kinase Activity ◽  
Specific Inhibitor ◽  
Cell Interaction ◽  
Epidemiological Studies ◽  
Cyclin Dependent Kinase ◽  
Hpv Status ◽  
Increased Risk ◽  
Control Virus

ABSTRACT Epidemiological studies suggest that human papillomavirus (HPV)-infected women who smoke face an increased risk for developing cervical cancer. We have previously reported that exposure of HPV-positive organotypic cultures to benzo[a]pyrene (BaP), a major carcinogen in cigarette smoke, resulted in enhanced viral titers. Since BaP is known to deregulate multiple pathways of cellular proliferation, enhanced virion synthesis could result from carcinogen/host cell interaction. Here, we report that BaP-mediated upregulation of virus synthesis is correlated to an altered balance between cell cycle-specific cyclin-dependent kinase (CDK) activity profile compared with controls. Specifically, BaP treatment increased accumulation of hyperphosphorylated retinoblastoma protein (pRb) which coincided with increased cdc2/CDK1 kinase activity, but which further conflicted with the simultaneous upregulation of CDK inhibitors p16INK4 and p27KIP1, which normally mediate pRb hypophosphorylation. In contrast, p21WAF1 and p53 levels remained unchanged. Under these conditions, CDK6 and CDK2 kinase activities were decreased, whereas CDK4 kinase activity remained unchanged. The addition of purvalanol A, a specific inhibitor of CDK1 kinase, to BaP-treated cultures, resulted in the production of noninfectious HPV type 31b (HPV31b) particles. In contrast, infectivity of control virus was unaffected by purvalanol A treatment. BaP targeting of CDK1 occurred independently of HPV status, since BaP treatment also increased CDK1 activity in tissues derived from primary keratinocytes. Our data indicate that HPV31b virions synthesized in the presence of BaP were dependent on BaP-mediated alteration in CDK1 kinase activity for maintaining their infectivity.

PERILOUS HIV BRINGS OUT DEADLY CANCERS

2020 ◽  
pp. 1-5
Author(s):  
Camila A Carlman ◽  
Bharat Mishra ◽  
Anita Patel
Keyword(s):  
Immune System ◽  
Hodgkin Lymphoma ◽  
Cancer Progression ◽  
Kaposi's Sarcoma ◽  
Cellular Proliferation ◽  
Kaposi’S Sarcoma ◽  
Hiv Patients ◽  
Non Hodgkin Lymphoma ◽  
Increased Risk ◽  
Risk Of Cancer

Human Immunodeficiency Virus (HIV) infection is both infectious and contagious disease. The people infected with HIV have an increased risk of cancer while comparing with uninfected people. Kaposi’s sarcoma, aggressive B-cell Non-Hodgkin Lymphoma & cervical cancer are the three types of cancers which are termed as “HIV –associated cancers”. Apart from these cancers, HIV patients are prone to cancers of anus, liver, lung, pharynx which are termed as “non-AIDS defining cancers”. Viral oncogenesis and cytokine induced growth contribute to the development of Kaposi sarcoma. Several virally encoded genes such as bcl-2, IL-6, cyclin-D, GPCR & interferon regulatory factor, plays key role in cellular proliferation and survival.  Infection with HIV weakens the immune system and reduces the body’s ability to fight against viral infections that may lead to cancer. Immunosuppression and inflammation in HIV patients also contribute to cancer progression. The complications of AIDS- related cancers include easy bleeding and bruising, tiredness, nausea, vomiting, poor appetite, mouth sores, hair loss etc. According to the data, HIV infected males are more susceptible to Kaposi’s sarcoma and Non- Hodgkin Lymphoma whereas females are more liable to cervical cancers. Early diagnosis and treatment options help to drop the risk of AIDS related cancers. The HAART therapy reduces the risk of cancer in HIV patients by lowering the amount of HIV circulating in blood, so that function of immune system to fight against the virus can be restored. Other treatment methods are chemotherapy, immunotherapy, radiation and surgery.

Expression of Phosphorylated Signal Transducer and Activator of Transcription 5 (pSTAT5) Is Associated with An Increased Risk of Death In Acute Myeloid Leukemia.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1675-1675
Author(s):  
Anna Brady ◽  
Sarah Gibson ◽  
Lisa Rybicki ◽  
Eric Hsi ◽  
Edward Copelan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Overall Survival ◽  
Prognostic Factors ◽  
Myeloid Leukemia ◽  
Signal Transducer ◽  
Newly Diagnosed ◽  
Risk Of Death ◽  
Increased Risk ◽  
History Of ◽  
Acute Myeloid

Abstract Abstract 1675 Background: Acute myeloid leukemia (AML) is characterized by rapid growth, resistance to therapy, and poor overall survival. Clinical and biologic prognostic markers can help define pathogenesis, guide treatment, and identify novel therapies. Phosphorylated signal transducer and activator of transcription 5 (pSTAT5) is one such potential marker. The transcription factor STAT5 regulates many aspects of cell growth, survival, and differentiation. Constitutive activation of STAT5 (by phosphorylation) has been identified in a number of malignancies, including AML. We investigated whether the level of pSTAT5 expression correlates with complete remission (CR) rates, progression-free survival (PFS), and overall survival (OS) in patients (pts) with newly diagnosed AML. Methods: From 1999 to 2005, all adult pts with newly diagnosed AML (WHO criteria) receiving induction chemotherapy and with an available diagnostic bone marrow biopsy performed at our institution were evaluated. B5-fixed bone marrow core biopsies were reviewed for areas with the highest concentration of blasts. A tissue microarray was constructed using 1 mm cores. The cores were arrayed in duplicate in the majority of samples. Immunohistochemistry was performed for pSTAT5 with anti-pSTAT5 a/b Y695/99 mouse monoclonal antibody (AX1; Advantex Bioreagents) using automated stainers and heat-induced epitope retrieval. In each case, five hundred blasts were counted. The percentage of cells staining positive for pSTAT5 expression was determined by a pathologist blinded to clinical results. Standard metaphase karyotypes were classified into cytogenetic (CG) risk groups by CALGB criteria. Cox proportional hazards analysis was used to identify univariate and multivariate prognostic factors for CR, PFS, and OS, including age at diagnosis, history of an antecedent hematologic disorder (AHD), WBC at diagnosis, pSTAT5 expression, and CG risk group. Results: Adequate tissue and clinical data were available in 112 pts. The median age was 57 years, and median WBC at diagnosis 12.0 K/ μL. Twenty six percent of pts had favorable CG, 41% intermediate risk, 27% high risk, and 6% other (unknown or could not be classified). Nineteen percent of pts had an AHD. pSTAT5 expression was absent in 58% of pts. The remainder of the pts had: 1–5% pSTAT5 (25% of pts), 10% pSTAT5 (11% of pts), 20% pSTAT5 (4% of pts), 30% pSTAT5 (1% of pts), and 50% pSTAT5 (2% of pts). Seventy percent of all pts achieved a CR following induction chemotherapy. Sixty-four percent of pts received post-remission chemotherapy, 3.6% an autologous transplant, and 13.6% an allogeneic transplant in first CR. Median PFS and OS were 9.6 months and 16.0 months, respectively. On univariate analysis, age, history of AHD, WBC at diagnosis, CG risk, and any pSTAT5 expression were prognostic factors for PFS and OS. In multivariable analyses controlling for the above prognostic factors, pSTAT5 expression > 0 was also significantly associated with an increased risk of death (HR 1.96, 95% CI 1.19–3.23, p=0.008), progression or death (HR 1.64, 95% CI 1.01–2.66, p=0.046), and relapse after achieving CR (HR 2.31, 95% CI 1.16–4.63, p=0.018). pSTAT5 expression was not a predictor of achievement of CR. Conclusions: pSTAT5 expression in newly diagnosed adults with AML is associated with a decreased PFS, decreased OS, and increased risk of relapse. Validation of its prognostic value requires additional study. Agents targeting this signaling pathway might improve the outcome of pts with AML. Disclosures: No relevant conflicts of interest to declare.

Prognostic Impact of Comorbidities In A Cohort of 788 MDS Patients Based On A CIRS-G Derived Score. A MDS Piedmont Registry Prospective Study

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1729-1729
Author(s):  
Emanuela Messa ◽  
Daniela Gioia ◽  
Claudia Bertassello ◽  
Gianni Ciccone ◽  
Bernardino Allione ◽  
...  
Keyword(s):  
Overall Survival ◽  
Multivariate Analysis ◽  
Prognostic Impact ◽  
Risk Of Death ◽  
Number Of Patients ◽  
Increased Risk ◽  
Risk Patients ◽  
Progression Risk ◽  
Cox Analysis ◽  
Severe Grade

Abstract Abstract 1729 Background: Management of neoplastic patients is strongly influenced by comorbidities, especially in more advanced ages. Due to that, comorbidities evaluation is a critical issue in the global assessment of patients (pts) affected by myelodysplastic syndromes (MDS). Until now, there is no agreement on which comorbidity index (CI) is more suitable in this setting and different CI has been proposed. Recently a new MDS-specific score (MDS-CI) has been published by Della Porta et al., while the majority of CI in use has been developed in geriatric oncology setting. One of the most useful is Cumulative Illness Rating Scale of Geriatrics (CIRS-G). Aim of our study: Aim of our study was to test the usefulness of the conventional and easy to apply CIRS-G score among a cohort of MDS pts enrolled in the MDS Piedmont Registry from 1999 to 2010 in predicting OS and leukemic progression. Materials and methods: 788 patients from the MDS Piedmont Registry with CIRS-G evaluation at diagnosis were included in our statistical analysis. 78% of the patients were low and Int-1 IPSS risk, the remaining 22% were Int-2-high risk. The majority of patients (69%) carried an histological diagnosis of non RAEB MDS according to WHO classification, the remaining 31% were RAEB I-II. Age stratification was as follows: 10% up to 60, 23% from 61 to 70, 43% from 71 to 80, 24% over 80 years. Comorbidities with score up to 2 were considered mild while the ones with values higher than 2 were considered severe. We evaluated the global impairment of each patient creating two comorbidity scores based on the number of mild comorbidities (mild comorbidities score, MCS) and severe comorbidities (severe comorbidities score, SCS). Results: The majority of our patients showed only mild comorbidities and the comorbidities with the greater number of patients carrying severe grade of impairment are the cardiac (25%), hypertensive (30%) and endocrinological (20%) ones. COX analysis did not show an impact of comorbidities on leukemic progression risk while there is a statistically significant impact on overall survival of respiratory, renal, urological and osteo-muscular comorbidities (HR respectively of 1,18; 1,3; 1,3; 1,16). There is a trend of increased risk of non MDS related death in patients with severe grade of each comorbidity. Then we set up a Fine and Gray regression model in order to evaluate the global impact of comorbidities on leukemic progression and overall survival according to SCS and MCS. Neither SCS nor MCS showed an impact on the leukemic progression risk. Considering overall survival (OS), MCS showed a HR of 1,12 (p= 0,009) and moreover SCS has a strong impact on the risk of death (HR 1,59; p= 0,000). MCS remains statistically significant in low IPSS risk patients (p<0,001) while there is no influence of MCS on OS considering high IPSS risk patients (p=0,244). COX analysis stratifying pts for performance status (PS) and age classes confirmed the results obtained in the whole population. We performed a multivariate analysis and confirmed that SCS score (p=0,0006), age and IPSS (all p<0,0001) but not PS (p=0,22) are independent prognostic factors in OS prediction. Conclusions: Our data based on a prospective evaluation of 788 MDS patients enrolled in the MDS Piedmont Registry showed that CIRS-G evaluation is a suitable and easy to apply method useful in patients evaluation at diagnosis and during disease management. In our multivariate analysis IPSS is the most useful tool for leukemic progression evaluation, while SCS score (derived from CIRS-G evaluation) and age are the most important variables able to predict overall survival while PS at diagnosis does not add any useful information for this evaluation. Disclosures: No relevant conflicts of interest to declare.

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