105 research outputs found
Is the Delphi's Oracle Pertinent to Patients With Resectable and Borderline Resectable Pancreatic Ductal Adenocarcinoma?
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Retroperitoneal lymphangioma: A report of 2 cases and a review of the literature regarding the differential diagnoses of retroperitoneal cystic masses
No full textCystic lymphangioma is a type of benign tumor originating from the lymph vessels. The tumor commonly occurs in childhood, in the head or neck regions, and retroperitoneal localization and presentations in adulthood are rare. Determining a pre-operative diagnosis is often challenging, and in the majority of cases, a diagnosis is only possible subsequent to the histological examination of the surgical specimen. A radical resection is the recommended treatment for cystic lymphangioma, and recurrence is usually due to an incomplete excision of the mass. The present study reports 2 cases of cystic lymphangioma, localized in the pancreatic gland and duodenal wall respectively, which were treated with surgical resection. The study also briefly reviews the literature regarding the differential diagnosis of retroperitoneal cystic masses
Clinical impact of nonselective beta-blockers on survival in patients with pancreatic cancer- revival of well known drugs?
No full textBackground: Basic research has suggested that adrenergic activation can promote PDAC growth. Here we investigate the impact of Beta- blockers (BB) in resected PDAC patients.
Method: Patients from two European pancreatic centers after resection of PDAC between 2002 and 2012 (n1⁄4595) were studied. 159 patients received BB. Seventeen patients with non-selective-BB (NSBB) were compared to 85 patients receiving no-BB (NBB) using a matched-pair analysis (1:5 scenario). 142 patients with beta1-selective agents (SB1B) were also studied. Univariate and multivariate survival analysis (Cox) was performed. Microtumors from PDAC were generated and treated with SB1B, beta2-selective blockers (SB2B; ICI118,551) and NSBB (propranolol) in addition to GEM.
Results: The median age was 70 years (22-88 years). For patients receiving any beta-blocker, the median OS was 25 vs. 21 mo for NBB (p1⁄40.0084). The median OS of patients receiving UBB was 40 vs. 23 mo for NBB (p1⁄40.0007) and 21 mo for patients with SB1B (p1⁄40.0396). Hyper- tension (HPT) was associated with decreased OS across all groups. Even among patients with HPT, a longer median OS was observed among UBB compared with NBB (40 vs 19 mo; p1⁄40.041). Microtumors when treated using NSBB or SB2B in addition to GEM showed a significantly lower re- sidual metabolic activity (p1⁄40.032).
Conclusion: For the first time a matched pair analysis comparing administration of NSBB to SB1B and NBB in PDAC patients is presented. UBB almost doubled OS in PDAC in an adjuvant setting, while SB1B did not show a difference. This data implicates that targeted therapy of the adrenergic beta2-pathway might be a promising therapeutic strategy in the treatment PDAC
GEMOX AS FIRST-LINE CHEMOTHERAPY IN ADVANCED PANCREATIC CANCER (APC): A MONOINSTITUTIONAL EXPERIENCE
No full textBackground: To date, gemcitabine (GEM) remains the cornerstone of chemotherapy (CHT) for APC. According to GERCOR and GISCAD phase III trials the combination of GEM and oxaliplatin (GEMOX) has proven superior to GEM alone in terms of response rate (RR), time to progression (TTP) and clinical benefit rate (CBR).
Methods: We conducted a retrospective analysis on 19 patients (pts) affected with histologically-confirmed APC, in order to determine the impact of GEMOX as first-line chemotherapy in terms of objective responses (OR) and TTP, using the Kaplan-Meier method. Among the 19 pts considered there were 15 males and 4 females (median age at diagnosis of 60.84 yrs; ECOG 0-2). The staging, according to AJCC criteria, was: IIB in 1 case, III in 5 cases and IV in the 13 remaning cases. The only metastatic site was the liver (in 13/19 pts). Ten of the 19 pts underwent surgical treatment prior to CHT: 2 radically resected (R0) subsequently treated with GEMOX after recurrence, 4 with positive margins (R1) and 4 surgically palliated. All pts received GEM 1000 mg/m2/d1 + oxaliplatin 100 mg/m2/d2 every 2 weeks. The median number of cycles was 5.89.
Results: Among the 19 pts, 3 had a partial response (PR, 15.69%), 6 had stable disease (SD, 31.57%); no complete response was observed and 10 pts had progressive disease (PD, 52.63%). The overall disease control rate (DCR: PR + SD) was 47.37% while the OR were 15.69%. The median survival observed was 9.03 months (95% C.I. 5.15-12.91) and the median TTP was 6.13 months (95% C.I. 2.81-9.46). The main toxicities were: leuco-piastrinopenia, diarrhoea, nausea, fever and peripheral neuropathy; 3 pts discontinued the treatment due to grade 3-4 neurotoxicity.
Conclusions: In our experience GEMOX gives an improved control of APC in terms of OR and TTP, with acceptable toxicity. The OS is in accordance to literature as well as the other data
Gemox in combination witherlotinib (E) in pancreatic cancer (PC).
No full textContext: We report a case of clinical benefit and metabolic response to GEMOX and E.
Case report: In November 2007 a 48-year-old woman was admitted to the our Oncology Unit for a suspected PC with a doubtful lung lesion on the basis of a CT carried out following the appearance of the abdominal pain and alteration of CA19.9 (1719 U/mL).
A biopsy of pancreatic lesion documented an infiltrating pancreatic ductal adenocarcinoma.
In December patient underwent exploratory laparotomy but due to the infiltration of the main vascular structures only a diagnostic laparotomy was possible. The clinical conditions were compromised (ECOG 2). CA19.9 was 21.890 U/mL.
The patient started on a chemotherapy (CHT) with gemcitabine 1000 mg/m2/d1 and oxaliplatin 100 mg/m2/d2 every 2 weeks (GEMOX).
After 3 cycles of CHT a CT showed a reduction in size of the pancreatic lesion (4.4 x 3.3 cm to 2.8 x 2.6 cm), a doubtful liver lesion, a stable lung lesion and multiple bone thickening lesions. CA19.9 was 8,942 U/mL.
In February a PET showed a hyperfixation of tracer in pancreatic head, left lung and at the level of multiple segments of bone compatible with secondary lesions. The clinical conditions worsened.
Therefore patient started on GEMOX combined with E 100 mg daily and also Zoledronic acid.
After 6 cycles of CHT, a CT showed an important reduction of the lung lesion, compatible with a primary neoplasm; the bone lesions were stable and the pancreatic lesion was further reduced.
A subsequent PET showed a minimal residual disease at the bone level only. The clinical conditions improved significantly (ECOG 0). CA 19.9 was 1382 U/mL.
Conclusion: This is the first case reported in literature in which was used the combination of GEMOX and E
Metastatic pancreatic cancer: is gemcitabine still the best standard treatment?
No full textPancreatic ductal adenocarcinoma is the fourth cause of death in the Western world. Surgery remains the only treatment offering an advantage in terms of overall survival (5-year survival range, 15-25%), but unfortunately only 10-20% of patients present resectable disease at the time of diagnosis. Hence chemotherapy, possibly combined with radiation therapy, remains the only treatment option aimed at palliation of symptoms and ensuring a better quality of life. Notwithstanding the efforts to find more effective therapies for the treatment of pancreatic cancer, significant results have not yet been achieved. Increasing interest has focused on integrated treatments, i.e. chemotherapy combined with targeted therapies, and a better selection of patients. This study examines the principal clinical trials that will help give clinicians an overview of the progress made in the systemic therapy for advanced pancreatic cancer patients in recent years
Advanced pancreatic cancer (apc); a Monocenter experience in 53 patients. It is possible a second line treatment?
No full textMassively Parallel Sequencing Analysis of Genetic Alterations Carried by Pancreatic Adenocarcinoma
No full textContext: Pancreatic cancer (PC) is characterized by a 5 year survival rate of 4%. The molecular mechanisms involved in the high tumorigenicity of PC are not yet well-known.
Methods: PC samples from 7 localized and advanced cases of pancreatic adenocarcinomas were collected by ultrasound-guided biopsy. Whole transcriptome RNA libraries were sequenced at 75x2 bp on a HiScanSQ Illumina platform. An average of 4,5x107 reads per sample were generated, with a mean read depth of 40. Sequences were mapped to the human genome (build hg19) and the single nucleotide variants (SNVs) were detected with SNVMix2 tool. The SNVs were compared with genetic variations databanks (dbSNP, 1000genomes, Cosmic) in order to highlight the novel variants. The non-synonimous SNVs were considered at the protein level and analyzed with SNPs&GO, in order to predict whether a variation is disease-related or neutral.
Results: Pancreatic adenocarcinomas exhibited a mean of 139 (range: 65-252) non-synonimous SNVs, of which 12 on average are potentially disease-related. We found mutations in oncogenes and tumor suppressor genes known to be related to pancreatic tumors, as 4/7 patients exhibited KRAS oncogenic variants (p.G12D, R or V) two of which carried also mutations either in SMAD4 or PIK3CA, one patient showed both TP53 and CDKN2A inactivating mutations and one a mutation in SMARCA4. Novel disease-related SNVs were found in genes regulating cell cycle progression and proliferation, apoptosis, TGFbeta and Integrin-signaling, epithelial to mesenchimal transition and nucleotide excision repair. Of interest some genes were mutated in multiple patients, as CBLC that regulates intracellular signalling by multiple tyrosine kinase genes.
Conclusions: Next generation sequencing analysis, through the identification of the oncogenic alterations carried by tumor cells, can improve the understanding of pancreatic carcinogenesis and highlight new biomarkers for early diagnosis and potential therapeutic targets in pancreatic cancer
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