Future Oncology Ahead of Print.
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Cancer Medicine by Alexandros G.Sfakianakis,Anapafseos 5 Agios Nikolaos,Crete 72100,Greece,tel :00302841026182 & 00306932607174
Δευτέρα 4 Απριλίου 2016
Prognostic significance of DSG3 in rectal adenocarcinoma treated with preoperative chemoradiotherapy
Age at Primary Malignancy Determines Survival in Adolescent and Young Adults That Develop a Secondary Thyroid Cancer
Journal of Adolescent and Young Adult Oncology , Vol. 0, No. 0.
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Psychometric Analysis of the Three-Factor Eating Questionnaire-R18V2 in Adolescent and Young Adult-Aged Central Nervous System Tumor Survivors
Journal of Adolescent and Young Adult Oncology , Vol. 0, No. 0.
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Inactivation of CYLD in intestinal epithelial cells exacerbates colitis-associated colorectal carcinogenesis - a short report
Abstract
Purpose
CYLD is a tumor suppressor that has been linked to the development of various human malignancies, including colon cancer. The tumor-suppressing function of CYLD is associated with its deubiquitinating activity, which maps to the carboxyl-terminal region of the protein. In the present study we evaluated the role of intestinal epithelial CYLD in colitis-associated cancer using a conditional mouse CYLD inactivation model.
Methods
In order to evaluate the role of CYLD in intestinal epithelial carcinogenesis, mice (IEC-Cyld Δ9 mice) that carry a mutation that eliminates the deubiquitinating domain of CYLD in intestinal epithelial cells (IEC) were generated by crossing Villin-Cre transgenic mice to previously generated mice carrying a loxP-flanked Cyld exon 9 (Cyld flx9 mice).
Results
We found that IEC-Cyld Δ9 mice did not present spontaneous intestinal abnormalities up to one year of age. However, upon challenge with a combination of genotoxic (AOM) and pro-inflammatory (DSS) agents we found that the number of adenomas in the IEC-Cyld Δ9 mice was dramatically increased compared to the control mice. Inactivation of CYLD in intestinal epithelial cells did not affect the classical nuclear factor-kappaB (NF-κB) and c-Jun kinase (JNK) activation pathways under physiological conditions, suggesting that these pathways do not predispose CYLD-deficient intestinal epithelia to colorectal cancer development before the onset of genotoxic and/or pro-inflammatory stress.
Conclusions
Our findings underscore a critical tumor-suppressing role for functional intestinal epithelial CYLD in colitis-associated carcinogenesis. CYLD expression and its associated pathways in intestinal tumors may be exploited for future prognostic and therapeutic purposes.
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TNF-α promotes breast cancer cell migration and enhances the concentration of membrane-associated proteases in lipid rafts
Abstract
Purpose
Tumor progression is associated with cell migration, invasion and metastasis. These processes are accompanied by the activation of specific proteases that are either linked to cellular membranes or are secreted into extracellular spaces. TNF-α is known to play an important role in various aspects of tumor progression. The aim of this work was to assess the effect of TNF-α on the migration of breast cancer cells and, in addition, to assess its association with the location of membrane-associated proteases in lipid rafts.
Methods
Wound scratch healing and Transwell migration assays were used to study the effect of TNF-α on the migration of both hormone-dependent and hormone-independent breast cancer-derived cells, i.e., MCF7 and MDA-MB-231, respectively. The expression and secretion of three matrix metalloproteases, MMP9, MMP2 and MT1-MMP, and two dipeptidyl peptidases, CD26 and FAP-α, was investigated using RT-PCR, Western blotting and gelatin zymography. In addition, activation of the MAPK/ERK signaling pathway was investigated by Western blotting.
Results
We found that a TNF-α-induced enhancement of breast cancer cell migration was accompanied by an increased secretion of MMP9, but not MMP2, into the culture media. We also found that TNF-α upregulated the expression of the dipeptidyl peptidases CD26 and FAP-α in a dose-dependent manner and, in addition, enhanced the concentration of all five proteases in lipid rafts in the breast cancer-derived cells tested, regardless of cell type. Furthermore, we found that TNF-α activated the MAPK/ERK signaling pathway by increasing the ERK1/2 phosphorylation level. Application of the MEK/ERK1/2 inhibitor U-0126 resulted in down-regulation of TNF-α-induced MMP9 secretion and abrogation of the enhanced concentration of proteases in the lipid rafts.
Conclusions
From our results we conclude that TNF-α-induced activation of the MAPK/ERK signaling pathway may promote breast cancer cell migration via both upregulation of MMP9, CD26 and FAP-α and concentration of these proteases, as also MT1-MMP and MMP2, in the lipid rafts. TNF-α may serve as a potential therapeutic target in breast cancers susceptible to TNF-α stimulation.
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Proof of principle for bevacizumab activity in desmoid-type fibromatosis
Abstract
Background
Desmoid-type fibromatosis (DF) is a rare disease, which often occurs in young adults. Medical treatment is an important option in the treatment algorithm of DF. Different chemotherapeutic regimens showed clinical activity in DF, but overall treatment tolerability remains poor for this patient cohort. Novel approaches investigated tyrosine kinase inhibitors in DF, but tolerability remained an issue.
Case presentation
We treated a patient with progressive DF after failure of chemotherapy for 1 year with singe agent bevacizumab. He achieved a symptomatic and radiologic response while attainning excellent tolerability.
Conclusions
This is the first report on single agent bevacizumab in DF, which showed both, good tolerability and efficacy in our patient, thereby warranting future trials in DF.
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In vitro and in vivo activity of melflufen (J1)in lymphoma
Abstract
Background
Melphalan has been used in the treatment of various hematologic malignancies for almost 60 years. Today it is part of standard therapy for multiple myeloma and also as part of myeloablative regimens in association with autologous allogenic stem cell transplantation. Melflufen (melphalan flufenamide ethyl ester, previously called J1) is an optimized derivative of melphalan providing targeted delivery of active metabolites to cells expressing aminopeptidases. The activity of melflufen has compared favorably with that of melphalan in a series of in vitro and in vivo experiments performed preferentially on different solid tumor models and multiple myeloma. Melflufen is currently being evaluated in a clinical phase I/II trial in relapsed or relapsed and refractory multiple myeloma.
Methods
Cytotoxicity of melflufen was assayed in lymphoma cell lines and in primary tumor cells with the Fluorometric Microculture Cytotoxicity Assay and cell cycle analyses was performed in two of the cell lines. Melflufen was also investigated in a xenograft model with subcutaneous lymphoma cells inoculated in mice.
Results
Melflufen showed activity with cytotoxic IC50-values in the submicromolar range (0.011-0.92 μM) in the cell lines, corresponding to a mean of 49-fold superiority (p < 0.001) in potency vs. melphalan. In the primary cultures melflufen yielded slightly lower IC50-values (2.7 nM to 0.55 μM) and an increased ratio vs. melphalan (range 13–455, average 108, p < 0.001). Treated cell lines exhibited a clear accumulation in the G2/M-phase of the cell cycle. Melflufen also showed significant activity and no, or minimal side effects in the xenografted animals.
Conclusion
This study confirms previous reports of a targeting related potency superiority of melflufen compared to that of melphalan. Melflufen was active in cell lines and primary cultures of lymphoma cells, as well as in a xenograft model in mice and appears to be a candidate for further evaluation in the treatment of this group of malignant diseases.
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Metastatic neuroblastoma in infants: are survival rates excellent only within the stringent framework of clinical trials?
Abstract
Introduction
SIOPEN INES protocol yielded excellent 5-year survival rates for MYCN-non-amplified metastatic neuroblastoma. Patients deemed ineligible due to lack or delay of MYCN status or late registration were treated, but not included in the study. Our goal was to analyse survival at 10 years among the whole population.
Materials and methods
Italian and Spanish metastatic INES patients' data are reported. SPSS 20.0 was used for statistical analysis.
Results
Among 98 infants, 27 had events and 19 died, while 79 were disease free. Five- and 10-year event-free survival (EFS) were 73 and 70 %, and overall survival (OS) was 81 and 74 %, respectively. MYCN status was significant for EFS, but not for OS in multivariate analysis.
Conclusions
The survival rates of patients who complied with all the inclusion criteria for INES trials are higher compared to those that included also not registered patients. Five-year EFS and OS for INES 99.2 were 87.8 and 95.7 %, while our stage 4s population obtained 78 and 87 %. Concerning 99.3, 5-year EFS and OS were 86.7 and 95.6 %, while for stage 4 we registered 61 and 68 %. MYCN amplification had a strong impact on prognosis and therefore we consider it unacceptable that many patients were not studied for MYCN and probably inadequately treated. Ten-year survival rates were shown to decrease: EFS from 73 to 70 % and OS from 81 to 74 %, indicating a risk of late events, particularly in stage 4s. Population-based registries like European ENCCA WP 11-task 11 will possibly clarify these data.
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Long-Term Survivor with Intrathecal and Intravenous Trastuzumab Treatment in Metastatic Breast Cancer
Abstract
We report the case of a woman with metastatic breast cancer receiving intrathecal trastuzumab (and intravenous trastuzumab for more than 7 years). She was diagnosed in 2001 with a duct invasive breast cancer T3N1M0 HER2 (human epidermal growth factor receptor 2)-positive +++ HR (hormone receptor) -negative. She received chemotherapy and then she had a mastectomy. Several metastases were discovered and treated from 2003 to 2008 with chemotherapy. In March 2010, brain metastases and a leptomeningeal carcinomatosis from her HER2-positive breast cancer appeared. From that moment on she received intravenous trastuzumab (6 mg/kg) every 3 weeks, intrathecal trastuzumab (21 mg) weekly for 16 injections and lapatinib. Intrathecal trastuzumab was stopped because of cerebrospinal fluid (CSF) clearing. Intrathecal trastuzumab was injected again from December 2013 for 14 injections. The relevance of treating leptomeningeal carcinomatosis with intrathecal trastuzumab administration is shown through this case report.
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Singing modulates mood, stress, cortisol, cytokine and neuropeptide activity in cancer patients and carers
Daisy Fancourt, Aaron Williamon, Livia A Carvalho, Andrew Steptoe, Rosie Dow and Ian Lewis
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Targeting persistent androgen receptor signaling in castration-resistant prostate cancer
Abstract
Castration-resistant prostate cancer (CRPC), the invariably lethal phenotype of advanced prostate cancer, represents a clinical state defined by disease progression despite reduction of testosterone to castrate levels (i.e., ≤50 ng/dL). Although resistant to androgen-deprivation therapy (i.e., LHRH agonists/antagonists), CRPC continues to depend on the androgen receptor (AR)-signaling pathway. Supporting the importance of AR-signaling in a castration-resistant state, the next-generation AR-signaling inhibitors enzalutamide and abiraterone have been shown to afford a survival benefit in men with metastatic CRPC. However, primary and secondary resistance mechanisms to these agents inevitably drive continued disease progression—often as a result of re-activation of AR-signaling. With increased understanding of the mechanisms underlying how continued AR-signaling occurs in spite of drugs like abiraterone and enzalutamide, a new wave of therapies is emerging designed to more effectively target AR-signaling. This review will focus on the more clinically relevant mechanisms of CRPC drug resistance and our ongoing efforts to develop drugs to target these mechanisms.
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FGFR3 promotes angiogenesis-dependent metastasis of hepatocellular carcinoma via facilitating MCP-1-mediated vascular formation
Abstract
The biological role of fibroblast growth factor receptor 3 (FGFR3) in tumor angiogenesis of hepatocellular carcinoma (HCC) has not been discussed before. Our previous work had indicated FGFR3 was overexpressed in HCC, and silencing FGFR3 in Hu7 cells could regulate tumorigenesis via down-regulating the phosphorylation level of key members of classic signaling pathways including ERK and AKT. In the present work, we explored the role of FGFR3 in angiogenesis-dependent metastasis by using SMMC-7721 and QGY-7703 stable cell lines. Our results indicated FGFR3 could regulate in vitro cell migration ability and in vivo lung metastasis ability of HCC, which was in accordance with increased angiogenesis ability in vitro and in vivo. Using the supernatant from SMMC-7721/FGFR3 cells, we conducted a human angiogenesis protein microarray including 43 angiogenesis factors and found that FGFR3 modulated angiogenesis and metastasis of HCC mainly by promoting the protein level of monocyte chemotactic protein 1 (MCP-1). Silencing FGFR3 by short hairpin RNA (shRNA) could reduce MCP-1 level in lysates and supernatant of QGY-7703 cells and SMMC-7721 cells. Silencing MCP-1 in QGY-7703 or SMMC-7721 cells could induce similar phenotypes compared with silencing FGFR3. Our results suggested FGFR3 promoted metastasis potential of HCC, at least partially if not all, via facilitating MCP-1-mediated angiogenesis, in addition to previously found cell growth and metastasis. MCP-1, a key medium between HCC cells and HUVECs, might be a novel anti-vascular target in HCC.
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Potential of sulfasalazine as a therapeutic sensitizer for CD44 splice variant 9-positive urogenital cancer
Abstract
Cancer stem-like cells (CSCs) with high expression of CD44 splice variant (CD44v) have an enhanced capacity for intracellular reduced glutathione synthesis and defense against reactive oxygen species, resulting in resistance to various therapeutic stresses. Sulfasalazine (SSZ), a drug used in the treatment of rheumatoid arthritis (RA), inhibits glutamate–cystine transport, and suppressed CD44v-dependent tumor growth and increased sensitivity to cytotoxic drugs in an in vivo study. Here, we present two cases of CD44v9-positive urogenital cancer with concomitant treatment with SSZ for RA. Patient 1 was a 62-year-old man who had received SSZ for RA beginning 2 months before the diagnosis of urinary bladder cancer. Although he had multiple metastases to the bladder, abdominal, left cervical and left axillary lymph nodes, and brain, complete response with multidisciplinary therapy was maintained for more than 2 years. Patient 2 was a 74-year-old man with castration-resistant prostate cancer who was diagnosed with RA during chemotherapy and a gradual increase in prostate-specific antigen (PSA) level. When SSZ was added, his PSA value (ng/mL) decreased from 12.93 to 5.58 in only 2 weeks and then quickly rebounded, whereas levels of neuron-specific enolase, a neuroendocrine differentiator and CSC marker, remained almost unchanged. We therefore speculate that SSZ treatment may represent a new adjuvant treatment option for patients with CD44v9-positive urogenital cancer.
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Dietary Patterns and Depression in Community-Dwelling Older Adults: State of the Evidence
Abstract
Depression is known to affect people's quality of life, and it should not be considered as a normal part of aging. Diet is a modifiable factor that may be associated with the likelihood of older adults becoming depressed. While some nutrients and specific food items, such as B vitamins or fish, have been explored, food is rarely eaten alone and may have a synergistic effect on health. Therefore, the study of dietary patterns, such as the Mediterranean pattern, is emerging. While evidence from longitudinal studies is still scarce, this synthesis of studies on the association of dietary patterns and depression in community-dwelling older adults suggests that dietary patterns may not be a strong predictor of late-life depression when social and biological factors are accounted for.
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Quantitative analysis of the BRAF V600E mutation in circulating tumor-derived DNA in melanoma patients using competitive allele-specific TaqMan PCR
Abstract
Background
BRAF V600E is a common mutation in melanoma, and BRAF inhibitors are effective in treating of BRAF mutation-positive melanoma. DNA carrying this mutation is released from melanoma cells into the circulation. As such, circulating tumor-derived DNA (ctDNA) in peripheral blood represents a novel biomarker for evaluating tumor features in cancer patients. However, ctDNA is present in the peripheral blood at very low levels, which makes the detection of specific mutations in this DNA a challenge. Competitive allele-specific TaqMan PCR (castPCR), a straightforward commercially available assay, is a sensitive technique for quantitating a small amount of DNA.
Methods
The level of BRAF V600E ctDNA was quantified by castPCR in 26 consecutive plasma samples from six melanoma patients.
Results
The castPCR assay was performed using a mixture of BRAF V600E DNA and BRAF wild DNA and found to be able to detect BRAF V600E at a fractional abundance of ≥0.5 % in 2- to 10-ng samples of genomic DNA. Cell-free DNA was then extracted from peripheral blood samples collected from six patients with melanoma harboring the BRAF V600E mutation. BRAF V600E ctDNA was detected in three patients, at a fractional abundance of between 1.28 and 58.0 % of total BRAF cell-free DNA. The abundance of BRAF V600E ctDNA correlated with tumor burden, as determined by computed tomography imaging. In two cases, an increase in the level of BRAF V600E ctDNA preceded exacerbation of clinical symptoms.
Conclusion
The castPCR assay can detect and quantitate small amounts of BRAF V600E ctDNA in samples containing large amounts of BRAF wild cell-free DNA. Thus, we suggest that the castPCR assay is suitable for monitoring ctDNA in the plasma of melanoma patients.
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Lentivirus-Mediated Knockdown of CTHRC1 Inhibits Osteosarcoma Cell Proliferation and Migration
Cancer Biotherapy & Radiopharmaceuticals , Vol. 0, No. 0.
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Genital invasion or perigenital spread may pose a risk of marginal misses for Intensity Modulated Radiotherapy (IMRT) in anal cancer
While intensity modulated radiotherapy (IMRT) in anal cancer is feasible and improves high-dose conformality, the current RTOG/AGITG contouring atlas and planning guidelines lack specific instructions on how t...
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Bone morphogenetic protein signaling in musculoskeletal cancer
Abstract
Purpose
Bone morphogenetic proteins (BMPs) belong to the transforming growth factor-β (TGF-β) superfamily of proteins; they were initially named after their ability to induce ectopic bone formation. Published studies have proved BMPs' role in a variety of biological processes such as embryogenesis and patterning of body axes, and maintaining adult tissue homeostasis. Other studies have focused on BMPs properties, functions and possible involvement in skeletal diseases, including cancer.
Methods
A literature search mainly paying attention to the role of BMPs in musculoskeletal tumors was performed in electronic databases.
Results
This article discusses BMPs synthesis and signaling, and summarizes their prominent roles in the skeletal system for the differentiation of osteoblasts, osteocytes and chondrocytes.
Conclusions
The review emphasizes on the role of BMP signaling in the initiation and progression of musculoskeletal cancer.
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Axillary reverse mapping in patients with breast cancer: Is it oncologically safe?
Background
Axillary reverse mapping (ARM) is a technique used to identify the lymphatics draining the arm. The aim of this study was to examine the prevalence and predictors of ARM node metastases in breast cancer patients undergoing an axillary lymph node dissection (ALND).
Methods
A total of 87 patients were enrolled in this study. Patent V Blue dye was injected in the upper arm for ARM node localization. All patients had an ALND with the identified ARM node removed and sent separately for histologic analysis.
Results
Of 67 (77%) patients in whom an ARM node was identified, 49 (73%) were negative and 18 (27%) were positive for metastases on final histopathology. Positive ARM node status was significantly associated with advanced axillary disease, and larger primary cancers. Patients requiring a completion ALND due to a positive sentinel lymph node biopsy (SLNB) with non-suspicious ARM nodes during surgery did not have ARM node metastases.
Conclusions
There is a high risk of ARM node involvement, approximately a quarter, in patients with preoperatively known lymph node metastases from breast cancer. However, it may be safe to preserve a clinically non-suspicious ARM node in patients with a positive SLNB who require a completion ALND. J. Surg. Oncol. © 2016 Wiley Periodicals, Inc.
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Clinical and radiological features of synchronous pure ground-glass nodules observed along with operable non-small cell lung cancer
Background
It is common to observe synchronous pure ground-glass nodules (PGN) along with operable primary tumor on initial CT scans while clinical and radiological features of these PGNs remain unclear.
Methods
We included patients with primary tumor and PGNs detected between June 2010 and December 2013 retrospectively. The radiographic manifestations of all PGNs, pathologic findings of resected PGNs, and follow-up outcomes of unresected PGNs were analyzed to determine the predictors of malignant PGNs.
Results
Overall, 84 PGNs in 71 patients were included, of which 41 were resected at primary surgery and 43 were followed up. In resected group, there were 17 carcinomatous PGNs, 11 atypical adenomatous hyperplasia, and 13 benign lesions. In a follow-up group, 7 out of 43 PGNs grew, out of which four PGNs were diagnosed as adenocarcinoma and the remaining three PGNs were still followed up. In univariate analysis, size (P < 0.001), air bronchogram (P = 0.001), bubble lucency (P = 0.038), and pleural tag (P = 0.004) were the factors for malignant potential of PGNs. Multivariate analysis showed that size was an independent risk factor (P = 0.005), and the cut-off value was 9.4 mm.
Conclusions
The initial size and imaging signs may be useful in assessing the malignant potential of synchronous PGNs before surgery. J. Surg. Oncol. © 2016 Wiley Periodicals, Inc.
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The feasibility of indocyanine green fluorescence imaging for identifying and assessing the perfusion of parathyroid glands during total thyroidectomy
Background
There are limited adjuncts available for identifying and assessing the viability of parathyroid glands (PGs) during total thyroidectomy (TT). The aim of this study is to determine the feasibility of indocyanine green (ICG) imaging in identifying and assessing perfusion of PGs during TT.
Methods
ICG was administered in patients undergoing TT and fluorescence of PGs was assessed. A grading scale was developed for assessing degree of ICG uptake. Patients were evaluated for hypocalcemia and hypoparathyroidism on post-operative day (POD) #1.
Results
Twenty-seven patients underwent TT with ICG imaging for multinodular goiter (n = 13), thyroid cancer (n = 10), and Graves' disease (n = 4). Eight-five PGs were identified visually, 71 (84%) of which showed ICG fluorescence. False negative rate was 6%. Post-operatively, three patients (11%) had a serum calcium value <8 mg/dl. ICG uptake after TT correlated with post-operative PTH levels: mean POD#1 PTH of those patients with at least two PGs exhibiting <30% fluorescence was 9 pg/ml; whereas those with fewer than two demonstrating <30% fluorescence had a POD#1 PTH of 19.5 pg/ml (P = 0.05).
Conclusion
ICG imaging of PGs during TT is feasible. ICG might be a useful adjunct in identifying those patients at risk for post-thyroidectomy hypoparathyroidism. J. Surg. Oncol. © 2016 Wiley Periodicals, Inc.
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Prophylactic pasireotide administration following pancreatic resection reduces cost while improving outcomes
Background and Objectives
Pasireotide decreases leak rates after pancreatic resection, though significant drug cost may be prohibitive. We conducted a cost-effectiveness analysis to determine whether prophylactic pasireotide possesses a reasonable cost profile.
Methods
A cost-effectiveness model compared pasireotide administration after pancreatic resection versus usual care, populated by probabilities of clinical outcomes from a randomized trial and hospital costs (2013 US$) from a university pancreatic disease center. Sensitivity analyses were performed to identify influential clinical components of the model.
Results
With the cost of pasireotide included, per patient costs of pancreatectomy, including those for readmission, were lower in the intervention arm (41,769 versus 42,159$; net savings of 390$, or 1%). This was associated with a 56% reduction in pancreatic fistula/pancreatic leak/abscess (PF/PL/A; 21.9–9.2%). Pasireotide cost would need to increase by over 15.4% to make the intervention strategy more costly than usual care. Sensitivity analyses exploring variability of key model inputs demonstrated that the three strongest drivers of cost were (i) cost of pasireotide; (ii) probability of readmission; and (iii) probability of PF/PL/A.
Conclusions
Prophylactic pasireotide administration following pancreatectomy is cost savings, reducing expensive post-operative sequealae (major complications and readmissions). Pasireotide should be utilized as a cost-saving measure in pancreatic resection. J. Surg. Oncol. © 2016 Wiley Periodicals, Inc.
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