Molecular Carcinogenesis, EarlyView.
https://ift.tt/2MRcoQp
Cancer Medicine by Alexandros G.Sfakianakis,Anapafseos 5 Agios Nikolaos,Crete 72100,Greece,tel :00302841026182 & 00306932607174
Παρασκευή 22 Ιουνίου 2018
A452, an HDAC6‐selective inhibitor, synergistically enhances the anticancer activity of chemotherapeutic agents in colorectal cancer cells
KAP1 inhibits the Raf‐MEK‐ERK pathway to promote tumorigenesis in A549 lung cancer cells
Molecular Carcinogenesis, EarlyView.
https://ift.tt/2yzB257
Correction to: Fludarabine and rituximab with escalating doses of lenalidomide followed by lenalidomide/rituximab maintenance in previously untreated chronic lymphocytic leukaemia (CLL): the REVLIRIT CLL-5 AGMT phase I/II study
The original version of this article contained a mistake. The name of Tanja Nicole Hartman should have been Tanja Nicole Hartmann. The original article has been corrected.
https://ift.tt/2IhcltZ
Ionizing radiation-induced cellular senescence promotes tissue fibrosis after radiotherapy. A review
Publication date: Available online 22 June 2018
Source:Critical Reviews in Oncology/Hematology
Author(s): Hoang Quy Nguyen, Nhu Hanh To, Patricia Zadigue, Stéphane Kerbrat, Alexandre De La Taille, Sabine Le Gouvello, Yazid Belkacemi
Ionizing radiation-exposure induces a variety of cellular reactions, such as senescence and apoptosis. Senescence is a permanent arrest state of the cell division, which can be beneficial or detrimental for normal tissue via an inflammatory response and senescence-associated secretion phenotype. Damage to healthy cells and their microenvironment is considered as an important source of early and late complications with an increased risk of morbidity in patients after radiotherapy (RT). In addition, the benefit/risk ratio may depend on the radiation technique/dose used for cancer eradication and the irradiated volume of healthy tissues. For radiation-induced fibrosis risk, the knowledge of mechanisms and potential prevention has become a crucial point to determining radiation parameters and patients' intrinsic radiosensitivity. This review summarizes our understanding of ionizing radiation-induced senescent cell in fibrogenesis. This mechanism may provide new insights for therapeutic modalities for better risk/benefit ratios after RT in the new era of personalized treatments.
https://ift.tt/2MNA6gJ
Long non-coding RNA CRYBG3 blocks cytokinesis by directly binding G-actin
The dynamic interchange between monomeric globular actin (G-actin) and polymeric filamentous actin filaments (F-actin) is fundamental and essential to many cellular processes including cytokinesis and maintenance of genomic stability. Here we report that the long non-coding RNA LNC CRYBG3 directly binds G-actin to inhibit its polymerization and formation of contractile rings, resulting in M-Phase cell arrest. Knockdown of LNC CRYBG3 in tumor cells enhanced their malignant phenotypes. Nucleotide sequence 228-237 of the full-length LNC CRYBG3 and the ser14 domain of beta-actin are essential for their interaction, and mutation of either of these sites abrogated binding of LNC CRYBG3 to G-actin. Binding of LNC CRYBG3 to G-actin blocked nuclear localization of MAL, which consequently kept serum response factor (SRF) away from the promoter region of several immediate early genes, including JUNB and Arp3, which are necessary for cellular proliferation, tumor growth, adhesion, movement, and metastasis. These findings reveal a novel lncRNA-actin-MAL-SRF pathway and highlight LNC CRYBG3 as a means to block cytokinesis and treat cancer by targeting the actin cytoskeleton.
https://ift.tt/2K3TNmq
Induction of Thioredoxin-Interacting Protein by Histone Deacetylase Inhibitor, Entinostat, Is Associated with DNA Damage and Apoptosis in Esophageal Adenocarcinoma
In 2017, an estimated 17,000 individuals were diagnosed with esophageal adenocarcinoma (EAC) and less than 20% will survive 5 years. PET-avidity is indicative of high glucose utilization and is nearly universal in EAC. TXNIP blocks glucose uptake and exhibits pro-apoptotic functions. Higher expression in EAC has been associated with improved disease-specific survival, lack of lymph node involvement, reduced perineural invasion, and increased tumor differentiation. We hypothesized that TXNIP may act as a tumor suppressor that sensitizes EAC cells to standard chemotherapeutics. EAC cell lines and a Barrett's epithelial cell line were used. qRT-PCR, immunoblot, and immunofluorescence techniques evaluated gene expression. TXNIP was stably over-expressed or knocked down using lentiviral RNA transduction techniques. Murine xenograft methods examined growth following over-expression of TXNIP. Apoptosis and DNA damage were measured by Annexin V and H2AX assays. Activation of the intrinsic apoptosis was quantitated with green fluorescence protein-caspase 3 reporter assay. In cultured cells and an esophageal tissue array, TXNIP expression was higher in Barrett's epithelia and normal tissue compared to EAC. Constitutive over-expression of TXNIP decreased proliferation, clonogenicity, and tumor xenograft growth. TXNIP overexpression increased whereas knockdown abrogated DNA damage and apoptosis following cisplatin treatment. An HDAC-inhibitor, entinostat (currently in clinical trials), upregulated TXNIP and synergistically increased cisplatin-mediated DNA damage and apoptosis. TXNIP is a tumor suppressor that is down-regulated in EACC. Its re-expression dramatically sensitizes these cells to cisplatin. Our findings support phase I/II evaluation of 'priming' strategies to enhance the efficacy of conventional chemotherapeutics in EAC.
https://ift.tt/2tlGAv7
Recombinant MDA-7/IL-24 suppresses prostate cancer bone metastasis through down regulation of the Akt/Mcl-1 pathway
Prostate cancer (PC) is a principal cause of cancer-associated morbidity in men. Although 5-year survival of patients with localized PC approaches 100 percent, survival decreases precipitously after metastasis. Bone is the preferred site for disseminated PC cell colonization, altering the equilibrium of bone homeostasis resulting in weak and fragile bones. Currently, no curative options are available for PC bone metastasis. MDA-7/IL-24 is a well-studied cytokine established as a therapeutic in a wide-array of cancers upon delivery as a gene therapy. In this study, we explored the potential anti-cancer properties of MDA-7/IL-24 delivered as a recombinant protein. Using bone metastasis experimental models, animals treated with recombinant MDA-7/IL-24 had significantly less metastatic lesions in their femurs as compared to controls. The inhibitory effects of MDA-7/IL-24 on bone metastasis resulted from PC-selective killing and inhibition of osteoclast differentiation, which is necessary for bone resorption. Gain- and loss-of-function genetic approaches document that pro-survival Akt and Mcl-1 pathways are critically important in the anti-bone metastatic activity of MDA-7/IL-24. Our previous findings showed that MDA-7/IL-24 gene therapy plus Mcl-1 inhibitors cooperate synergistically. Similarly, an Mcl-1 small molecule inhibitor synergized with MDA-7/IL-24 and induced robust anti-bone metastatic activity. These results expand the potential applications of MDA-7/IL-24 as an anti-cancer molecule and demonstrate that purified recombinant protein is non-toxic in pre-clinical animal models and has profound inhibitory effects on bone metastasis, which can be enhanced further when combined with an Mcl-1 inhibitory small molecule.
https://ift.tt/2yA0NCt
A difficult situation – balancing critical anticoagulation versus the risk of permanent neurologic deficit: a case report
Anticoagulation is the mainstay of treatment for pulmonary embolism. However, if bleeding unfortunately occurs, the risks and benefits of anticoagulation present a challenge. Management of one hemorrhagic comp...
https://ift.tt/2K8BMiW
Anterior hypopituitarism in a patient with amyloidosis secondary to Crohn’s disease: a case report
Amyloid infiltration of endocrine glands has been reported, mostly in the thyroid, pancreas, adrenals, and testes, but affected patients do not frequently exhibit overt endocrine insufficiency. Here we report ...
https://ift.tt/2K1xXjI
Statistical motion modelling for robust evaluation of clinically delivered accumulated dose distributions after curative radiotherapy of locally advanced prostate cancer
Planned doses are used as surrogate for the actually delivered dose in radiotherapy. We have estimated the delivered dose in a dose-escalation trial of locally advanced prostate cancer by statistical dose-accumulation and by DVH-summation, and compared to planned dose.
https://ift.tt/2yzOiXx
Nationwide Japanese Prostate Cancer Outcome Study of Permanent Iodine-125 Seed Implantation (J-POPS): first analysis on survival
Abstract
Background
Investigating oncological outcomes in patients registered in the Japanese Prostate Cancer Outcome Study of Permanent Iodine-125 Seed Implantation (J-POPS) in terms of biochemical relapse-free survival (bRFS) by the Phoenix and the newly developed J-POPS definitions, exploration of predictive factors for bRFS, and preliminary verification of pitfalls of prostate-specific antigen (PSA) failure definitions.
Methods
Between July 2005 and June 2007, 2316 clinically localized patients underwent permanent seed implantation. The primary endpoint was bRFS. One of the secondary endpoints was overall survival (OS).
Results
The median age was 69 and performance status was 0 in 99.1% of participants. The median biologically effective dose (BED) was about 180 Gy2. During a median follow-up of 60.0 months, 8.4 and 5.9% had PSA failure by the Phoenix and the J-POPS definitions, respectively. The 5-year bRFSs based on the Phoenix and the J-POPS definitions were 89.1 and 91.6%, respectively. The 5-year OS was 97.3%. According to multivariate analyses, only age affected bRFS based on the Phoenix definition, whereas the risk group and BED independently affected bRFS based on the J-POPS definition. A spontaneous PSA decrease was seen in 91.1% of participants after PSA failure based on the Phoenix definition alone, but in only 22.2% after PSA failure based on the J-POPS definition alone.
Conclusion
The world's largest registration study, J-POPS, consisted of patients with longevity, and a highly quality-controlled BED resulted in excellent bRFS and OS. The high likelihood of PSA bounce by the Phoenix definition should be taken into account, especially in younger patients.
Clinical trial information
NCT00534196.
https://ift.tt/2K9zAaT
Abdominal DIBH reduces the cardiac dose even further: a prospective analysis
Deep inspiration breath hold (DIBH) can be performed using different breathing maneuvers, such as DIBH with a thoracic breathing maneuver (T-DIBH) and DIBH with an abdominal breathing maneuver (A-DIBH). Dosime...
https://ift.tt/2lulSos
Approval Expanded for Venetoclax in Chronic Lymphocytic Leukemia
FDA expanded the approval of venetoclax (Venclexta) for people with chronic lymphocytic leukemia (CLL) to include those whose cancer has progressed after previous treatment, regardless of whether their cancer cells have the deletion 17p gene alteration.
https://ift.tt/2IgHyNy
Anesthetic management without perioperative platelet transfusion for cervical laminectomy and laminoplasty in a case of May–Hegglin anomaly
Abstract
May–Hegglin anomaly (MHA) is an inherited autosomal dominant disorder characterized by giant platelets and inclusion bodies in granulocytes, and thrombocytopenia. There is no consensus on the perioperative management of this disorder. We report a case involving a patient with MHA who was perioperatively managed without platelet transfusion for cervical laminectomy and laminoplasty. In our case, the platelet count was measured to be 0.6 × 104/µL using an automatic blood cell counter. Peripheral blood smear and genetic test analyses were performed, leading to a definitive diagnosis of MHA. However, clot retraction, serotonin release, and platelet aggregation were normal. Total intravenous anesthesia with propofol and remifentanil, in combination with intermittent injection of fentanyl, was administered. The total blood loss volume was 300 mL, and perioperative course was uneventful. Visual platelet count and platelet function were preserved in this case, although platelet or red blood cell transfusion was not performed. No bleeding tendency was observed during perioperative management.
https://ift.tt/2yBo5ry
Anxiety and depression in women with breast cancer: Social and clinical determinants and influence of the social network and social support (DAMA cohort)
Source:Cancer Epidemiology, Volume 55
Author(s): R. Puigpinós-Riera, A. Graells-Sans, G. Serral, X. Continente, X. Bargalló, M. Domènech, M. Espinosa-Bravo, J. Grau, F. Macià, R. Manzanera, M. Pla, M.J. Quintana, M. Sala, E. Vidal
BackgroundAnxiety and depression are the most prevalent mental health pathologies among women with breast cancer. Social, clinical and contextual variables may influence emotional stress among women with breast cancer.The aim of this work is to study anxiety and depression in a cohort of women diagnosed with breast cancer between 2003 and 2013 in Barcelona. We evaluate social and clinical determinants.MethodsWe performed a mixed cohort study (prospective and retrospective) using a convenience sample of women diagnosed with breast cancer. The information sources were the Hospital Anxiety and Depression questionnaire and hospital medical records. Dependent variables were anxiety and depression; independent variables were social class, age, employment status, tumour stage at diagnosis, time since diagnosis, social network and social support. We performed a descriptive analysis, a bivariate analysis, and a multivariate logistic regression analysis.ResultsA total of 1086 (48.6%) women had some degree of anxiety-related problem. As for depression. In the case of depression, 225 (15%) women had some degree of depression-related problem. Low emotional support and social isolation were clear risk factors for having more anxiety and depression. Low social class was also a risk factor, and age also played a role.DiscussionOur results show that women long period of cancer survival have high prevalences of anxiety than depression, and this prevalence of anxiety is higher than the general population. In addition, we found inequalities between social classes and the isolation and social support are worse too in low social class.
https://ift.tt/2K0u924
Retraction Note to: Monitoring of vecuronium-induced neuromuscular block at the sternocleidomastoid muscle in anesthetized patients
The Editor-in-Chief has retracted this article [1] because the three studies included in the meta-analysis [2,3 and 4] (cited as references 16, 17 and 18) have been retracted due to concerns regarding the data, which has rendered the results of this meta-analysis invalid.
https://ift.tt/2K0Pdpj
Cancers, Vol. 10, Pages 213: Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers
Cancers, Vol. 10, Pages 213: Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers
Cancers doi: 10.3390/cancers10070213
Authors: Maria Lina Tornesello Clorinda Annunziata Anna Lucia Tornesello Luigi Buonaguro Franco Maria Buonaguro
Viral oncogenesis is a multistep process largely depending on the complex interplay between viruses and host factors. The oncoviruses are capable of subverting the cell signaling machinery and metabolic pathways and exploit them for infection, replication, and persistence. Several viral oncoproteins are able to functionally inactivate the tumor suppressor p53, causing deregulated expression of many genes orchestrated by p53, such as those involved in apoptosis, DNA stability, and cell proliferation. The Epstein–Barr virus (EBV) BZLF1, the high-risk human papillomavirus (HPV) E6, and the hepatitis C virus (HCV) NS5 proteins have shown to directly bind to and degrade p53. The hepatitis B virus (HBV) HBx and the human T cell lymphotropic virus-1 (HTLV-1) Tax proteins inhibit p53 activity through the modulation of p300/CBP nuclear factors, while the Kaposi's sarcoma herpesvirus (HHV8) LANA, vIRF-1 and vIRF-3 proteins have been shown to destabilize the oncosuppressor, causing a decrease in its levels in the infected cells. The large T antigen of the Merkel cell polyomavirus (MCPyV) does not bind to p53 but significantly reduces p53-dependent transcription. This review describes the main molecular mechanisms involved in the interaction between viral oncoproteins and p53-related pathways as well as in the development of therapeutic strategies targeting such interactions.
https://ift.tt/2JY1ydP
Successful treatment of invasive mucormycosis with isavuconazole in pediatric patients
Pediatric Blood &Cancer, EarlyView.
https://ift.tt/2MLgIRg
Racial and ethnic disparities in travel for head and neck cancer treatment and the impact of travel distance on survival
Cancer, EarlyView.
https://ift.tt/2KbpB59
Cancers, Vol. 10, Pages 212: Understanding Intratumor Heterogeneity and Evolution in NSCLC and Potential New Therapeutic Approach
Cancers, Vol. 10, Pages 212: Understanding Intratumor Heterogeneity and Evolution in NSCLC and Potential New Therapeutic Approach
Cancers doi: 10.3390/cancers10070212
Authors: Taichiro Goto Yosuke Hirotsu Kenji Amemiya Hitoshi Mochizuki Masao Omata
Advances in innovative technology, including next-generation sequencing, have allowed comprehensive genomic analysis and the elucidation of the genomic aspect of intratumor heterogeneity (ITH). Moreover, models of the evolution of the cancer genome have been proposed by integrating these analyses. Cancer has been considered to accumulate genetic abnormalities for clonal evolution in time and space, and these evolutionary patterns vary depending on the organs of primary sites. Selection pressure is an important determinant of such evolutionary patterns. With weak selection pressure, more diverse clones coexist, and heterogeneity increases. Heterogeneity is maximized when there is no selection pressure; in other words, neutral evolution occurs. Some types of cancer such as lung cancer evolve in conditions that have maintained close to neutral evolution and produce diverse variants. This ITH is a key factor contributing to the lethal outcome of cancer, therapeutic failure, and drug resistance. This factor reaffirms the complexity and subtle adaptability of cancer. It is expected that further understanding of ITH and cancer genome evolution will facilitate the development of new therapeutic strategies to overcome ITH.
https://ift.tt/2yxDSHJ
Refractory Septic Shock due to Underlying Immunocompromised Disease: A Case of Fatal Peripheral T-Cell Lymphoma Not Otherwise Specified in a Young Hispanic Woman
Peripheral T-cell lymphoma not otherwise specified (PTCL-NOS) is known as an unclassified group of non-Hodgkin lymphomas. PTCL-NOS is a subtype of peripheral T-cell lymphoma that accounts for 3% of all lymphomas in the United States. PTCL-NOS commonly presents as a disseminated disease, B symptoms (fever, night sweats, and weight loss), generalized lymphadenopathy, bone marrow infiltration, and extranodal involvement. Other rare and possible manifestations include peripheral eosinophilia, pruritus, or hemophagocytic syndrome. This type of lymphoma is aggressive in nature and carries a high mortality rate. There is no established standard-of-care treatment protocol for PTCL-NOS, several chemotherapy drug combinations are frequently used as a frontline treatment with an overall 5-year survival rate of 25%. We present a case of a 35-year old Hispanic woman who initially presented with a chief complaint of bilateral lower extremity swelling due to hypoalbuminemia and new-onset hyperkeratotic skin of the palms and soles.
Case Rep Oncol 2018;11:404–411
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Genomic Profiling Reveals Medullary Thyroid Cancer Misdiagnosed as Lung Cancer
Mutations or other alterations in the RET gene have been implicated in a variety of malignancies – most commonly thyroid, but also chronic myelomonocytic leukemia, acute myeloid leukemia, and lung, breast, pancreatic, and colon cancers. Here we present a case of a gentlemen initially diagnosed with and treated for non-small cell lung adenocarcinoma. Genomic profiling of his tumor specimen revealed a RET point mutation with a known association with medullary thyroid cancer (MTC). Further pathological and molecular diagnostic evaluation confirmed a diagnosis of MTC, leading to a change in treatment from standard chemotherapy for non-small cell lung cancer to targeted therapy against RET and potential implications regarding inherited cancer risk for his offspring. The patient experienced a clinical response to treatment and several months of improved quality of life. This case illustrates the capacity of genomic profiling to uncover molecular drivers of disease and help ensure proper diagnosis and management of cancer.
Case Rep Oncol 2018;11:399–403
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Rapid disease progression in a patient with mismatch repair-deficient and cortisol secreting adrenocortical carcinoma treated with pembrolizumab
Publication date: Available online 21 June 2018
Source:Seminars in Oncology
Author(s): R.T. Casey, O. Giger, I. Seetho, A. Marker, D. Pitfield, L.H. Boyle, M. Gurnell, A. Shaw, M. Tischowitz, E.R. Maher, V.K. Chatterjee, T. Janowitz, G. Mells, P. Corrie, B.G. Challis
Context: Metastatic adrenocortical carcinoma (ACC) is an aggressive malignancy with a poor prognosis and limited therapeutic options. A subset of ACC is due to Lynch syndrome, an inherited tumor syndrome resulting from germline mutations in mismatch repair (MMR) genes. It has been demonstrated that several cancers characterized by MMR-deficiency are sensitive to immune checkpoint inhibitors that target PD-1. Here, we provide the first report of PD-1 blockade with pembrolizumab in a patient with Lynch syndrome and progressive cortisol-secreting metastatic ACC.Case report: A 58-year old female with known Lynch syndrome who presented with severe Cushing's syndrome was diagnosed with a cortisol-secreting ACC. Three months following surgical resection and adjuvant mitotane therapy the patient developed metastatic disease and persistent hypercortisolemia. She commenced pembrolizumab, but her second cycle was delayed due to a transient transaminitis. Computed tomography performed after twelve weeks and 2 cycles of pembrolizumab administration revealed significant disease progression and treatment was discontinued. Seven weeks later, the patient became jaundiced and died rapidly with fulminant liver failure.Conclusion: Treatment of MMR-deficient cortisol-secreting ACC with pembrolizumab may be ineffective due to supra-physiological levels of circulating corticosteroids, which may in turn mask severe drug-induced organ damage.
https://ift.tt/2Kd33kx
Long-Term Disease-Free Survival of a Patient with Oligometastatic Nasopharyngeal Carcinoma Treated with Radiotherapy Alone
Distant metastases in nasopharyngeal carcinoma are fairly common. While the mainstay of treatment for metastatic nasopharyngeal carcinoma remains chemotherapy, it is now increasingly recognised that metastatic cases are a heterogenous group and can be stratified into oligometastatic cases versus those with widespread metastases, the former potentially benefiting more from local therapy. In this report, we describe a case of nasopharyngeal carcinoma with a solitary vertebral metastasis successfully treated with high-dose palliative radiotherapy alone, resulting in a long-term disease-free interval of more than 8 years at the time of writing. To our knowledge, this is the first report of a long-term survivor of metastatic nasopharyngeal carcinoma with oligometastatic bone disease who had received no chemotherapy. In view of this case, there may be potential for other patients with oligometastases from nasopharyngeal carcinoma to be treated solely with local therapy, thereby sparing them the toxicities of chemotherapy.
Case Rep Oncol 2018;11:392–398
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Indocyanine Green Fluorescence Imaging for Sentinel Lymph Node Detection in Colorectal Cancer: A Systematic Review
Publication date: Available online 21 June 2018
Source:European Journal of Surgical Oncology
Author(s): Gabriel Liberale, Ali Bohlok, Anne Bormans, Fikri Bouazza, Maria Gomez Galdon, Issam El Nakadi, Pierre Bourgeois, Vincent Donckier
Indocyanine green fluorescence-imaging (ICG-FI) has emerged as a potential tool for increasing the accuracy of staging of patients with primary colorectal cancer (CRC) through the detection of sentinel lymph nodes (SLNs). Here, we report the results of a systematic review of the available literature in the clinical setting of ex vivo and in vivo ICG-FI for the detection of SLNs in primary colorectal cancer. PubMed, Scopus, and Cochrane literature databases were searched for original articles on the use of ICG in the setting of clinical studies of CRC. Eighty studies were identified and screened, 23 were assessed for eligibility and 10 were included for review. Both ex vivo and in vivo ICG-FI are reported to be feasible for the detection of SLNs in CRC. The reported sensitivity of both techniques remains low, varying from 0% to 100% for the in vivo technique and 57% for the ex vivo technique. ICG-FI has not yet been shown to perform better than the standard blue dye technique. In addition, large variability among reported studies in terms of techniques used (ICG dose, type of injection), type of pathologic analyses performed (HE, IHC, serial section), and definition of positive LN status for sensitivity calculations made them difficult to compare directly. ICG-FI is a promising technique for the detection of SLNs in the setting of CRC but more work needs to be done to clearly define protocols and indications for its use and to test its efficacy in larger patient populations.
https://ift.tt/2JYjp4i
A model prediction of long-term prognosis in patients with centrally located hepatocellular carcinoma undergoing hepatectomy
Publication date: Available online 21 June 2018
Source:European Journal of Surgical Oncology
Author(s): Yang Yantong, Liu Shan, Chu Zhijie, Zheng Youwei
Background and ObjectivesThe prognostic prediction for centrally located hepatocellular carcinoma (CL-HCC) after hepatectomy has not been well established. We aimed to develop prognostic nomograms for patients undergoing hepatectomy for CL-HCC.MethodsA cohort of 380 patients who underwent curative hepatectomy for CL-HCC at our hospital between 2009 and 2015 were retrospectively studied. We randomly divided the subjects into training (n = 210) and validation (n = 170) groups. Univariate and multivariate survival analysis were used to identify prognostic factors. Visually orientated nomograms were constructed using Cox proportional hazards models. The performance of the nomogram was evaluated by the area under the ROC curve (AUC), calibration curve and compared with the conventional staging systems.ResultsThe statistical nomogram for OS built on the basis of ALBI grade, tumor number, tumor size, classification, hepatectomy methods, capsule formation and microvascular invasion (MVI) had good calibration and discriminatory abilities, with AUC of 0.746 (65-month survival). The nomogram for DFS was based on tumor number, tumor size, classification, HBV-DNA load, capsule formation and MVI, with AUC of 0.733 (65-month survival). These nomograms showed satisfactory performance in the validation cohort (AUC, 0.733 for 65-month OS; and 0.702 for 65-month DFS). The AUC of our nomograms were greater than those of conventional staging systems in the validation cohort.ConclusionThe established nomograms might be useful for estimating survival for patients with CL-HCC after liver resection.
https://ift.tt/2IeNwhW
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