Publications by authors named "Luca Sacco"

6 Publications

  • Page 1 of 1

Endoscopic management of intramural spontaneous duodenal hematoma: A case report.

World J Gastroenterol 2022 May;28(20):2243-2247

Gastroenterology and Endoscopy Unit, Ospedale G. Mazzini, Teramo 64100, Italy.

Background: Intramural duodenal hematoma is a rare condition described for the first time in 1838. This condition is usually associated with blunt abdominal trauma in children. Other non-traumatic risk factors for spontaneous duodenal haematoma include several pancreatic diseases, coagulation disorders, malignancy, collagenosis, peptic ulcers, vasculitis and upper endoscopy procedures. In adults the most common risk factor reported is anticoagulation therapy. The clinical presentation may vary from mild abdominal pain to acute abdomen and intestinal obstruction or gastrointestinal bleeding.

Case Summary: The aim of this case summary is to show a case of intramural spontaneous hematoma with symptoms of intestinal obstruction that was properly drained endoscopically by an innovative system lumen-apposing metal stent Hot AXIOS™ stent (Boston Scientific Corp., Marlborough, MA, United States).

Conclusion: Endoscopic lumen-apposing metal stent Hot AXIOS™ stent is a safe and feasible treatment of duodenal intramural hematoma in our case.
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http://dx.doi.org/10.3748/wjg.v28.i20.2243DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9157618PMC
May 2022

Genetically driven CD39 expression shapes human tumor-infiltrating CD8 T-cell functions.

Int J Cancer 2020 11 8;147(9):2597-2610. Epub 2020 Jul 8.

Department of Internal Clinical, Anaesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.

In our study, we investigated the role of CD39 on tumor-infiltrating CD8 T lymphocytes (CD8 TILs) in colorectal, head and neck and pancreatic cancers. Partially confirming recent observations correlating the CD39 expression with T-cell exhaustion, we demonstrated a divergent functional activity in CD39 CD8 TILs. On the one hand, CD39 CD8 TILs (as compared to their CD39 counterparts) produced significantly lower IFN-γ and IL-2 amounts, expressed higher PD-1, and inversely correlated with perforin and granzyme B expression. On the other, they displayed a significantly higher proliferative capacity ex vivo that was inversely correlated with the PD-1 expression. Therefore, CD39 CD8 TILs, including those co-expressing the CD103 (a marker of T resident memory [TRM] cells), were defined as partially dysfunctional T cells that correlate with tumor patients with initial progression stages. Interestingly, our results identified for the first time a single nucleotide polymorphism (SNP rs10748643 A>G), as a genetic factor associated with CD39 expression in CD8 TILs. Finally, we demonstrated that compounds inhibiting CD39-related ATPases improved CD39 CD8 T-cell effector function ex vivo, and that CD39 CD8 TILs displayed effective suppression function in vitro. Overall these data suggest that the SNP analysis may represent a suitable predictor of CD39 CD8 T-cell expression in cancer patients, and propose the modulation of CD39 as a new strategy to restore partially exhausted CD8 TILs.
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http://dx.doi.org/10.1002/ijc.33131DOI Listing
November 2020

Intrapancreatic accessory spleen false positive to 68Ga-Dotatoc: case report and literature review.

World J Surg Oncol 2019 Jul 9;17(1):117. Epub 2019 Jul 9.

Department of Surgical Sciences, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.

Background: Intrapancreatic accessory spleen (IPAS) is an uncommon finding of pancreatic mass. Differential diagnosis with pancreatic tumor, especially with non-functional neuroendocrine tumor (NF-NET), may be very hard and sometimes it entails unnecessary surgery. A combination of CT scan, MRI, and nuclear medicine can confirm the diagnosis of IPAS. 68-Ga-Dotatoc PET/CT is the gold standard in NET diagnosis and it can allow to distinguish between IPAS and NET.

Case Presentation: A 69-year-old man was admitted to our hospital for an incidental nodule in the tail of the pancreas with focal uptake of 68-Ga-dotatate at PET/CT. NET was suspected and open distal splenopancreatectomy was performed. Pathologic examination revealed an IPAS.

Conclusion: This is the second IPAS case in which a positive 68Ga-Dotatoc uptake led to a false diagnosis of pancreatic NET. Here is a proposal of a literature review.
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http://dx.doi.org/10.1186/s12957-019-1660-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6617599PMC
July 2019

Wnt3a/β-Catenin Signaling Conditions Differentiation of Partially Exhausted T-effector Cells in Human Cancers.

Cancer Immunol Res 2018 08 17;6(8):941-952. Epub 2018 Jul 17.

Dipartimento di Medicina Interna e Specialità Mediche, "Sapienza" Università di Roma, Policlinico Umberto I, Rome, Italy.

In this study, we investigated the role of the Wnt/β-catenin signaling pathway in antitumor immune responses. We report that the concentration of secreted Wnt3a was significantly higher in conditioned medium from tumor or nontumor tissues obtained from all hepatocellular carcinoma or colorectal cancer patients tested, than in serum of healthy donors or patients. In addition, both Wnt3a and β-catenin were overexpressed by tumor-infiltrating and nontumor-infiltrating CD4 or CD8 T cells. The majority of these T cells expressed a dysfunctional effector memory EomesT-betphenotype that we defined as partially exhausted, because they performed effector functions (in terms of interferon-γ and tumor necrosis factor-α production, as well as CD107a mobilization) despite their PD-1 expression. Wnt3a/β-catenin signaling in T naïve cells recapitulated the T-cell setting Indeed, the differentiation of cultured T naïve cells was arrested, producing cells that resembled the EomesT-betβ-catenin T cells with moderate effector functions that infiltrated tumor and nontumor areas. Wnt3a blockade improved the capacity of T naïve cells to differentiate into effector cells However, Wnt3a blockade did not affect the function and phenotype of differentiated, partially exhausted, tumor-infiltrating T cells Taken together, our data suggest that Wnt3a blockade halts the capacity of Wnt/β-catenin signaling to inhibit the differentiation of T naïve cells, but it does not restore the dysfunction of differentiated T cells, in the tumor setting. .
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http://dx.doi.org/10.1158/2326-6066.CIR-17-0712DOI Listing
August 2018

Regulatory T cells with multiple suppressive and potentially pro-tumor activities accumulate in human colorectal cancer.

Oncoimmunology 2016 Jul 25;5(7):e1175800. Epub 2016 Apr 25.

Dipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, Rome, Italy; Istituto Pasteur-Fondazione Cenci Bolognetti, Rome, Italy.

Tregs can contribute to tumor progression by suppressing antitumor immunity. Exceptionally, in human colorectal cancer (CRC), Tregs are thought to exert beneficial roles in controlling pro-tumor chronic inflammation. The goal of our study was to characterize CRC-infiltrating Tregs at multiple levels, by phenotypical, molecular and functional evaluation of Tregs from the tumor site, compared to non-tumoral mucosa and peripheral blood of CRC patients. The frequency of Tregs was higher in mucosa than in blood, and further significantly increased in tumor. Ex vivo, those Tregs suppressed the proliferation of tumor-infiltrating CD8(+) and CD4(+) T cells. A differential compartmentalization was detected between Helios(high) and Helios(low) Treg subsets (thymus-derived versus peripherally induced): while Helios(low) Tregs were enriched in both sites, only Helios(high) Tregs accumulated significantly and specifically in tumors, displayed a highly demethylated TSDR region and contained high proportions of cells expressing CD39 and OX40, markers of activation and suppression. Besides the suppression of T cells, Tregs may contribute to CRC progression also through releasing IL-17, or differentiating into Tfr cells that potentially antagonize a protective Tfh response, events that were both detected in tumor-associated Tregs. Overall, our data indicate that Treg accumulation may contribute through multiple mechanisms to CRC establishment and progression.
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http://dx.doi.org/10.1080/2162402X.2016.1175800DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006916PMC
July 2016

Effect of surgery on pancreatic tumor-dependent lymphocyte asset: modulation of natural killer cell frequency and cytotoxic function.

Pancreas 2015 Apr;44(3):386-93

From the *Section of Interdisciplinary Surgery F. Durante, Department of Surgical Sciences, †Department of Molecular Medicine, ‡Istituto Italiano di Tecnologia, CLNS, and §Department of Experimental Medicine, Sapienza University of Rome, Italy.

Objectives: Tumor burden and invasiveness establish a microenvironment that surgery could alter. This study shows a comprehensive analysis of size, dynamics, and function of peripheral lymphocyte subsets in pancreatic cancer patients before and at different times after duodenopancreatectomy.

Methods: Lymphocyte frequency and natural cytotoxicity were evaluated by flow cytometry and in vitro assay on peripheral blood from initial and advanced-stage pancreatic cancer patients before (BS), at day 7 (PS7), and at day 30 (PS30) after surgery.

Results: An increase in natural killer (NK) cells and the diminution of B-cells occurred at PS30, whereas cytotoxicity decreased at PS7. The positive correlation between NK frequency and cytotoxicity at BS and PS7 revealed an altered NK behavior. The elevation of NK cell frequency at PS30, an initial defect in CD56bright NK, and the aberrant correlation between NK frequency and cytotoxicity remained significant in advanced-stage patients, whereas the diminution of NK cytotoxicity only affected initial stage patients.

Conclusions: The NK cell functional ability is altered in presurgery patients; duodenopancreatectomy is associated with short-term impairment of NK function and with a long-term NK cell augmentation and reversion of the aberrant NK behavior, which may impact on immunosurveillance against residual cancer.
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http://dx.doi.org/10.1097/MPA.0000000000000288DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4358707PMC
April 2015
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