A case of bronchocentric granulomatosis associated with Aspergillus that was difficult to differentiate from lung cancer]

We encountered a case of suspected bronchocentric granulomatosis (BCG) occurring in a COPD patient. Chest CT on admission showed a nodular shadow with indentation and a notch-like opacity in right S(3)a. Based on these findings, lung cancer was suspected. As we could not establish a definitive diagnosis, video-assisted thoracic surgery was performed. The histological findings of the resected specimen demonstrated BCG with clustering of fungal hyphae in the bronchioles. As the lesion was resected completely, we did not give additional treatment with an antifungal agent. It is difficult to differentiate BCG from lung cancer preoperatively. However, considering the homogeniecity of the nodule, it may be able to differentiate this type of lesion from lung cancer based on the feature. We report a rare case of a solitary nodule caused by BCG with Aspergillosis.     

Value of ultrasound examination in differential diagnosis of pancreatic lymphoma and pancreatic cancer

AIM： To investigate the value of clinical manifestations and ultrasound examination in the differential diagnosis of pancreatic lymphoma and pancreatic cancer. METHODS： The clinical and ultrasonic characteristics of 12 cases of pancreatic lymphoma and 30 cases of pancreatic cancer were retrospectively analyzed. RESULTS： Statistically significant differences were found in the course of disease, back pain, jaundice, carcino-embryonic antigen （CEA） and CA19-9 increase, palpable abdominal lump, superficial lymph node enlargement, fever and night sweats, lesion size, bile duct expansion, pancreatic duct expansion, vascular involvement, retroperitoneal （below the renal vein level） lymph node enlargement, and intrahepatic metastasis between pancreatic lymphoma and pancreatic cancer. There were no significant differences in age of onset, gender ratio, weight loss, nausea and vomiting, lesion position, the echo of the lesion, and the blood flow of the lesion. CONCLUSION： Pancreatic lymphoma should be considered for patients with long lasting symptoms, superficial lymph node enlargement, palpable abdominal lump, fever and night sweats, relatively large lesions, and retroperitoneal （below the level of the renal vein） lymph node enlargement. A diagnosis of pancreatic cancer should be considered more likely in the patients with relatively short disease course, jaundice, back pain, CEA and CA19-9 increase, relatively small lesions, bile duct expansion, obvious pancreatic duct expansion, peripheral vascular wrapping and involvement, or intrahepatic metastases.     

Complete disappearance of metastatic abdominal tumors from gastric cancer after treatment with irsogladine maleate

Summary A 60-year-old woman with gastric cancer had undergone partial gastrectomy in September 1989. Pathological examination revealed a poorly differentiated adenocarcinoma of pT3pN3pM0 (not resected for cure), stage IV. Postoperative adjuvant therapy comprised 1-(tetrahydro-2-furanyl)-5-fluorouracil plus uracil and OK-432. On 11 August 1990, two forefinger-tip-sized tumors were palpated beneath the operation scar. They increase in size, the superior tumor reaching 4×3 cm, the inferior tumor 5×3 cm on 5 September. Then, on 17 September, the inferior tumor was resected but the superior tumor remained; the histological type was poorly differentiated adenocarcinoma. After the operation, from 20 September, she was given 4 mg irsogladine maleate orally every day. On 8 October, there was no increase in the size of the superior tumor. By 29 October, the superior tumor had disappeared and no further tumor appeared thereafter; the patient showed no sign of relapse.Abbreviations FT 1-(tetrahydro-2-furanyl)-5-fluorouracil     

Nab-paclitaxel and gemcitabine for the treatment of patients with metastatic pancreatic cancer

Adenocarcinoma of the pancreas or pancreatic cancer as we will refer to it here, is a cancer of poor prognosis with a high mortality, particularly in the advanced or metastatic setting. Until 2011 and the Phase III results of FOLFIRINOX, standard treatment options were limited to gemcitabine. Combination therapy had shown either a lack of or very limited improvement versus monotherapy with gemcitabine. With the positive results of the MPACT study in 2013 showing improved survival with nab-paclitaxel plus gemcitabine combination therapy, there are now more options for oncologists to treat patients with advanced pancreatic cancer. This paper will highlight the Phase I/II and Phase III trials of nab-paclitaxel plus gemcitabine along with discussing their biology and further possible development in treating patients with pancreatic cancer.     

Risk of all‐type cancer,hepatocellular carcinoma,non‐Hodgkin lymphoma and pancreatic cancer in patients infected with hepatitis B virus

The increased risk of hepatocellular carcinoma (HCC) among patients infected with hepatitis B virus (HBV) is well established; however, long‐term risk estimates are needed. Recently, it has been suggested that HBV is associated with non‐Hodgkin lymphoma (NHL) and pancreatic cancer (PC). The aim of this Danish nationwide cohort study was to evaluate the association between HBV infection and all‐type cancer, HCC, NHL and PC. A cohort of patients infected with HBV (n = 4345) and an age‐ and sex‐matched population‐based comparison cohort of individuals (n = 26 070) without a positive test for HBV were linked to The Danish Cancer Registry to compare the risk of all‐type cancer, HCC, NHL and PC among the two groups. The median observation period was 8.0 years. Overall, the incidence rate ratio (IRR) for all‐type cancer among HBV‐infected patients was 1.1 (95% confidence intervals (CI) 0.9–1.3). The IRR of HCC was 17.4 (CI 5.5–54.5), whereas the IRR of PC and NHL was 0.9 (CI 0.3–2.5) and 1.2 (CI 0.4–3.6), respectively. HBV‐infected patients had a 10‐year risk of 0.24% (Cl 0.12–0.44) for HCC, whereas the comparison cohort had a 10‐year risk of 0.03% (Cl 0.02–0.07) for HCC. The risk of all‐type cancer, NHL and PC was not higher in the HBV‐infected cohort compared to non‐HBV infected. We found a 17‐fold higher risk of HCC for HBV‐infected individuals.     

In situ surgical procedures for locally advanced pancreatic cancer: partial abdominal evisceration and intestinal autotransplantation

Background/purpose

Pancreatic cancers in which invasion to the root of the mesentery are suspected have been regarded as unresectable in general. We report the surgical techniques in two cases of locally advanced pancreatic cancer for which in situ surgical procedures including partial abdominal evisceration and intestinal autotransplantation were performed.

Methods

The patients were a woman 57 years of age and a man 64 years of age. Both cases had a locally advanced cancer that had originated in the pancreatic uncus and was found to have invaded the root of the mesentery, as well as the superior mesenteric artery (SMA) and the superior mesenteric vein (SMV). The cancers in both patients were assessed as resectable because the jejunal artery and vein were secured intact at a site peripheral from the root of the mesentery, and the origin of the SMA along with the portal and splenic veins was intact at a proximal site, so pancreatectomy and resection of the transverse and ascending colons were performed. The SMA and the SMV were ablated just below each origin at a site proximal to the root of the mesentery. At a distal site, two jejunal arteries and one jejunal vein were kept intact and all the remaining arteries and veins were ablated. The remaining small intestine had become a free autograft. As for the portal and jejunal veins, end-to-end anastomosis was performed. Reconstruction of the SMA was achieved with an end-to-end anastomosis, using the right internal iliac artery as a graft. Reconstruction of the alimentary tract was achieved using small intestine as an autograft.

Results

Both patients survived the major operative procedures. Warm ischemia time was 84 min for the SMA and 12 min for the SMV-portal system in Case 1 while it was 30 min for the SMA and 25 min for the SMV-portal system in Case 2. No ex-vivo resection technique was used. Leakage occurred in both cases at the anastomotic lesion between the small intestine and the left colon. Abdominal drainage and conservative treatment were applied in both cases. Cure was achieved within 3 months postoperatively in Case 1 and within 2.5 months in Case 2. Subsequently, the patients returned to their preoperative lives. Case 1 died 11 months and Case 2 died 12 months after the operation due to abdominal dissemination and liver metastases.

Conclusions

We were able to perform in situ procedures including partial abdominal evisceration and intestinal autotransplantation for two cases of pancreatic cancer with possible invasion to the root of the mesentery. There are few reports of such procedures. There has been one report of a case which applied an ex vivo technique. It is expected that the development of adequate adjuvant therapy will lead to further improvement in the prognosis of pancreatic cancers.     

Resection or cryosurgery relates with pancreatic tumor type: Primary pancreatic cancer with previous non-pancreatic cancer or secondary metastatic cancer within the pancreas

ObjectivesWe investigated the incidence of primary pancreatic cancer with previous non-pancreatic cancer (PPC) and secondary metastatic cancer within the pancreas (SMC) to elucidate the differential diagnosis and treatment of these lesions.MethodsThe clinical data of 2539 patients with pancreatic mass in Tianjin Cancer Hospital from January 2000 to December 2012 were retrospectively analyzed. All of the 66 patients who showed double or multiple primary cancers or metastatic pancreatic malignancies were included into the PPC group or SMC group, respectively. In addition, PPC patients were compared with 570 patients suffering from pancreatic cancer (PC) alone.ResultsFor the PPC group (n = 34), the most common previous non-pancreatic cancers were gastric cancer, breast cancer, and thyroid cancer. For the SMC group (n = 32), the most common metastatic tumors were lung cancer, renal cell carcinoma (RCC), and gastric cancer. Multivariate analysis identified age (OR = 1.099; 95% CI, 1.007–1.199), previous tumor type (OR = 1.164; 95% CI, 1.046–1.296), and time interval between two tumors (OR = 1.021; 95% CI, 1.003–1.039) as significant indicators. Significantly better survival times were observed after resection than after cryosurgery in the PPC group (p < 0.001) but not in the SMC group (p = 0.670).ConclusionsOverall, primary pancreatic cancers are as common as metastasis to the pancreas in patients with a previous cancer. A longer time interval between two tumors indicates a higher possibility that a new pancreatic cancer will occur. Some cancers (particularly RCC) are more likely to metastasize to the pancreas than other cancers. For metastatic cancers, cryosurgery is as effective as resection as a treatment option.     

NAD+ depletion by type I interferon signaling sensitizes pancreatic cancer cells to NAMPT inhibition

Emerging evidence suggests that intratumoral interferon (IFN) signaling can trigger targetable vulnerabilities. A hallmark of pancreatic ductal adenocarcinoma (PDAC) is its extensively reprogrammed metabolic network, in which nicotinamide adenine dinucleotide (NAD) and its reduced form, NADH, are critical cofactors. Here, we show that IFN signaling, present in a subset of PDAC tumors, substantially lowers NAD(H) levels through up-regulating the expression of NAD-consuming enzymes PARP9, PARP10, and PARP14. Their individual contributions to this mechanism in PDAC have not been previously delineated. Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD salvage pathway, a dominant source of NAD in cancer cells. We found that IFN-induced NAD consumption increased dependence upon NAMPT for its role in recycling NAM to salvage NAD pools, thus sensitizing PDAC cells to pharmacologic NAMPT inhibition. Their combination decreased PDAC cell proliferation and invasion in vitro and suppressed orthotopic tumor growth and liver metastases in vivo.

Pancreatic ductal adenocarcinoma (PDAC) is the major type of pancreatic cancer, with a median overall survival of less than 1 y (1). In addition to an aggressive tumor biology and late stage at diagnosis, the poor prognosis of PDAC is due to its resistance to current therapies. In recent years, studies have profiled its extensively reprogrammed metabolic network and characterized its extreme tumor microenvironment (2–5). These studies have identified PDAC cells’ dependence on glycolysis (2, 6), lipogenesis (2, 7), glutamine metabolism (8, 9), alanine metabolism, and tricarboxylic acid cycle/oxidative phosphorylation (10, 11). Strategies targeting each of these specific metabolic pathways have been attempted but have not been successfully translated into clinical therapeutics. However, all of these rewired metabolic pathways rely on nicotinamide adenine dinucleotide (NAD) or its reduced form, NADH, as cofactors.NAD is central to cellular bioenergetic and metabolic functions. NAD is synthesized via three major pathways: the de novo biosynthesis kynurenine pathway, the Preiss–Handler pathway, and the salvage pathway (12). The kynurenine pathway starts with the catabolism of the amino acid tryptophan that is then converted via two steps to the intermediate kynurenine, which can generate NAD, kynurenic acid, or xanthurenic acid. The Preiss–Handler pathway and the salvage pathway synthesize NAD from pyridine bases. The Preiss–Handler pathway synthesizes NAD from nicotinic acid (NA) in three steps via the intermediate NA adenine dinucleotide. The NAD salvage pathway starts from the recycling of nicotinamide (NAM) to nicotinamide mononucleotide (NMN) by intracellular nicotinamide phosphoribosyltransferase (NAMPT), followed by the conversion of NMN into NAD via the NMN adenylyltransferases (NMNATs) (12). A recent quantitative analysis revealed that liver cells actively synthesize NAD de novo from tryptophan, releasing NAM into the blood, thereby supporting NAD biosynthesis in the rest of the body, whereas both tumor cells and most other tissues use NAM as the main NAD source (13). NAMPT is the rate-limiting step by which tumor cells utilize NAM in the synthesis of NAD. It is also important to note that, while there are many metabolic enzymes that use NAD or NADH as cofactors and affect the NAD/NADH ratio, NAD(H) is consumed and broken down into NAM by the poly(ADP ribose) polymerase (PARP) family proteins, the sirtuin (SIRT) family proteins, and CD38 (14).NAMPT inhibitors (NAMPTis) showed promising potency in a variety of preclinical tumor models, including pancreatic cancer (15–18). Two NAMPTis, FK866 (19) and CHS-828 (20, 21), have been tested in clinical trials, where lack of objective responses and dose-limiting toxicity suggest it is necessary to identify subsets of tumors with high sensitivity to NAMPT inhibition. Multiple studies have examined intracellular factors that affect cancer cell sensitivity to NAMPT inhibition, such as NAMPT levels (22), NA phosphoribosyltransferase levels (23), PPM1D mutations (15), and CD38 levels (24). We hypothesized that, in addition to intracellular factors, the tumor microenvironment also impacts PDAC cell NAD(H) levels and thus the sensitivity to NAMPTis.In this study, we found that type I interferons (IFNs) lower PDAC cell NAD(H) levels through the up-regulation of NAD(H)-consuming enzymes PARP9, PARP10, and PARP14 (PARP9/10/14). Unlike their better studied relatives, PARP1 and PARP2, which catalyze poly-ADP ribosylation, PARP9/10/14 catalyze the transfer of a single unit of ADP ribose to their targets, a process referred to as monoADP ribosylation (25). The roles of PARP9/10/14 in mediating NAD depletion in PDAC cells have not been previously explored to the authors’ knowledge. We further hypothesized that IFN-mediated NAD depletion caused by the up-regulation of PARP9/10/14 sensitizes PDAC cells to NAMPTis, which we confirmed in both in vitro and in vivo PDAC models.     

Hepatobiliary and Pancreatic: Rapid growing cystic ovarian metastasis from pancreatic cancer

Pancreatic cancer rarely develops cystic ovarian metastasis. We present a 63‐year‐old female patient with unresectable pancreas head cancer. Seven months after the introduction of the chemoradiotherapy, a giant intrapelvic cystic tumor with rapid growth was found. The tumor was resected because the patient complained of severe bloating and no other new metastatic sites could be identified. Postoperative pathological examination diagnosed it as an ovarian metastasis from the pancreas cancer.     

Micrometastases from HBP malignancies and metastatic cancer

Despite advances in early diagnosis and surgical treatment, the prognosis for patients with primary malignant tumors of the hepatobiliary tract and pancreas has not changed markedly over the last decades. Early metastatic relapse after complete resection indicates the presence of disseminated tumor cells undetectable by current tumor staging methods. Sensitive immunohistocytochemical and nucleic acid‐based assays have been developed to detect single tumor cells present in lymph nodes, bone marrow, or blood. Standardization of the current occult tumor cell detection protocols are needed before “micrometastatic” tumor staging can be used in clinical practice. We present an overview of recent studies on the frequency and prognostic value of occult disseminated tumor cells in the lymph nodes, bone marrow, and blood of patients with hepatopancreatobiliary malignancies and metastatic colorectal cancer identified by immunohistocytochemistry or nucleic acid‐based assays.     

Familial pancreatic cancer: from genes to improved patient care

Pancreatic cancer is essentially a disease caused by inherited and acquired mutations in cancer-causing genes. A number of the genes responsible for the aggregation of pancreatic cancer in families have been discovered, including BRCA2, p16/CDKN2A, STK11 and PRSS1. Individuals can be tested for germline mutations in these genes; however, until recently, little could be done about the risk of pancreatic cancer if a patient was found to carry a mutation. Currently, new approaches are being developed to screen at-risk individuals for curable precancerous pancreatic lesions and laboratory studies have led to novel therapies that specifically target some of these genetic defects. This review focuses on the genetic basis for the familial aggregation of pancreatic cancer, with emphasis placed on the implications of the genetic alterations on clinical patient care.     

Ultrasound-guided percutaneous pancreatic tumor biopsy in pancreatic cancer: a comparison with metastatic liver tumor biopsy, including sensitivity, specificity, and complications

Background The aims of this study were to investigate the diagnostic value and safety of ultrasound-guided percutaneous pancreatic tumor biopsy (pancreatic biopsy) in patients with suspected unresectable pancreatic cancer, and to compare the data with those obtained by metastatic liver tumor biopsy (liver metastases biopsy). Methods Data were collected retrospectively from 388 patients (398 procedures) for whom a final diagnosis was available and who underwent ultrasoundguided pancreatic or liver metastases biopsy with a 21-gauge needle (core biopsy) or a 22-gauge needle (fine-needle aspiration biopsy: FNAB). The sensitivity, specificity, and accuracy of pancreatic and liver metastases biopsies were evaluated. Biopsy-related complications were collected and analyzed. Results Data from 271 pancreatic and 112 liver metastases biopsy procedures were available. For pancreatic core biopsy and FNAB, the sensitivity, specificity, and accuracy were 93%, 100%, and 93%, and 86%, 100%, and 86%, respectively, all of which were comparable to those of liver metastases biopsy. The complication rate in pancreatic biopsy was 21.4%, including a 4.4% incidence of post-biopsy ephemeral fever. The complication rate in liver metastases biopsy was 38.7%, including an 8.0% incidence of ephemeral fever. Fever and infection occurred more frequently among patients who underwent liver metastases biopsy (4.4% vs. 11%: P = 0.038). In pancreatic biopsy cases, a prebiopsy high serum total bilirubin level was a statistically significant predictor of ephemeral fever. Conclusions Ultrasound-guided percutaneous pancreatic biopsy is an effective and safe modality for confirming the pathologic diagnosis in patients with unresectable pancreatic cancer.     

The effectiveness of nab-paclitaxel plus gemcitabine and gemcitabine monotherapy in first-line metastatic pancreatic cancer treatment: A real-world evidence

Pancreatic cancer is one of the most lethal malignancies with a rise in mortality rates. FOLFIRINOX and nab-paclitaxel plus gemcitabine demonstrated a survival benefit compared to gemcitabine alone. Both protocols are now considered the standard of first-line treatment with no significant difference between them, primarily based on observational studies. Although new therapeutic options have emerged recently, the prognosis remains poor. We conducted a retrospective single-center study on 139 patients treated for metastatic pancreatic adenocarcinoma (mPDAC) with gemcitabine monotherapy (Gem) or nab-paclitaxel + gemcitabine (Nab-P/Gem) in the first line. The aim of our study was to evaluate the effectiveness in terms of overall survival (OS) and progression-free survival (PFS) as well as the influence of patient and disease characteristics on outcomes. Nab-P/Gem resulted in OS of 13.87 months compared to 8.5 months in patients receiving Gem. The same trend was achieved in PFS, 5.37 versus 2.80 months, respectively, but without reaching statistical significance. Furthermore, the 6-month survival in the Nab-P/Gem group was also higher, 78.1% versus 47.8%. In terms of survival, the group of elderly patients, patients of poorer performance, with higher metastatic burden and liver involvement, benefited the most from combination therapy. In our analysis ECOG performance status (p.s.), previous primary tumor surgery, and liver involvement were found to be independent prognostic factors. The addition of nab-paclitaxel to gemcitabine resulted in a significant improvement in the OS of patients with mPDAC. Subgroup analysis demonstrated that patients with some unfavorable prognostic factors benefited the most.     

新发糖尿病——胰腺癌早期筛查和诊断的临床线索

胰腺癌是一种高度恶性的消化系统恶性肿瘤,因其起病隐匿、缺乏有效特异的早期筛查手段,发现时多为晚期,已失去手术时机,预后很差。糖尿病是胰腺癌发生的危险因素,新发糖尿病可能是胰腺癌的病因或早期表现之一,有助于胰腺癌的早期发现与诊断;而不同降糖药物的应用可能对胰腺癌的发生具有一定影响。在糖尿病患者中发现胰腺癌的特异性血清微小RNA(microRNA),可能成为未来胰腺癌早期筛查和预后监测的非侵入性生物标志物。     

Molecular targeting therapy for pancreatic cancer: current knowledge and perspectives from bench to bedside

Current medical interventions for pancreatic cancer are insufficient. Recent molecular investigations have elucidated complex genetic mechanisms of cancer that especially involve multiple signal transduction pathways; this enables us to develop molecular medicines targeting specific genetic molecules in the pathways. These molecular medicines seem to promise clues for curing cancers, including pancreatic cancer. This review describes current knowledge and perspectives regarding the development of molecular medicines for pancreatic cancer by focusing on growth factor receptor systems and three major signal transduction pathways: the RAS-MAPK, PI3K-AKT-mTOR, and hedgehog pathways.     

Clinical epidemiological analysis of the relationship between pancreatic cancer and diabetes mellitus: Data from a single institution in China

OBJECTIVE: To investigate the relationship between pancreatic cancer (PC) and diabetes mellitus. METHODS: All PC patients diagnosed and treated at Zhongshan hospital from January 1991 to December 2007 were retrospectively analyzed. During this period, 770 non‐digestive tract, non‐neoplastic and non‐hormone‐related patients matched for sex and age were collected as controls. The incidence of diabetes mellitus between the two groups was compared. RESULTS: Between the PC group and the control group, sex and age of the patients were well matched. The incidence of diabetes mellitus was 34.63% in the PC group and 8.83% in the control group (P < 0.001, RR = 5.19). In the PC group there was no correlation between age, sex, site of the cancer, tumor differentiation, lymph node metastasis, TNM staging and the incidence of diabetes mellitus. In this group with diabetes, 74.56% experienced onset within two years of cancer diagnosis. Of the control patients, 57.35% had had diabetes for under 2 years (P = 0.009, RR = 2.18). In the PC group with diabetes, 5.9% had had diabetes for more than 10 years while compared with 8.8% of the controls (P = 0.42). CONCLUSION: Whether diabetes mellitus is a result of or a risk factor for PC is still unclear. The incidence of diabetes mellitus is much higher in the PC patients. The onset of diabetes mellitus in adults might be an alerting factor that could lead to an early diagnosis of pancreatic cancer.     

The relationship between SPARC expression in primary tumor and metastatic lymph node of resected pancreatic cancer patients and patients' survival

BACKGROUND:Previous researches in pancreatic cancer demonstrated a negative correlation between secreted protein acidic and rich in cysteine (SPARC) expression in primary tumor and survival,but not for SPARC expression in lymph node.In the present study,we aimed to evaluate the SPARC expression in various types of tissues and its impact on patients' prognosis.METHODS:The expression of SPARC was examined by immunohistochemistry in resected pancreatic cancer specimens.Kaplan-Meier analyses and Cox proportional hazards regression were applied to assess the mortality risk.RESULTS:A total of 222 tissue samples from 73 patients were collected to evaluate the SPARC expression,which included 73 paired primary tumor and adjacent normal tissues,38 paired metastatic and normal lymph nodes.The proportion of positive SPARC expression in metastatic lymph node was high (32/38),whereas in normal lymph node it was negative (0/38).Positive SPARC expression in primary tumor cells was associated with a significantly decreased overall survival (P=0.007) and disease-free survival (P=0.003),whereas in other types of tissues it did not show a predictive role for prognosis.Univariate and multivariate analyses both confirmed this significance.CONCLUSION:SPARC can serve a dual function role as both predictor for prognosis and potentially biomarker for lymph node metastasis in resected pancreatic cancer patients.     

Neoadjuvant therapy may lead to successful surgical resection and improved survival in patients with borderline resectable pancreatic cancer

Background:

Borderline resectable pancreatic cancers are technically amenable to surgical resection, but are associated with increased risk of locoregional recurrence. Patients with these tumours may be treated with neoadjuvant therapy in an attempt to improve margin-negative resection rates.

Methods:

The University of Cincinnati Pancreatic Cancer Database was retrospectively reviewed. Borderline resectable disease was defined by the following radiographic criteria: (i) short segment occlusion of the superior mesenteric vein (SMV), portal vein (PV) or SMV/PV confluence; (ii) short segment hepatic artery encasement, or (iii) superior mesenteric artery/coeliac artery abutment of <180 degrees. Patients with resectable disease who had questionable metastatic disease or poor performance status were also included.

Results:

Twenty-nine patients met the criteria. Of these, 26 underwent a full course of neoadjuvant therapy. Twelve (46%) underwent surgical resection and 14 had tumour progression or were deemed unresectable at laparotomy. The most common neoadjuvant therapy regimen was gemcitabine-based chemotherapy alone (58%). Of those undergoing surgery, 67% had margin-negative (R0) resections and 42% required venous resection. Median survival was 15.5 months for unresected patients and 23.3 months for resected patients.

Discussion:

Borderline resectable pancreatic tumours can be treated neoadjuvantly, resulting in margin-negative resection and survival rates similar to those in initially resectable disease.     

A systemic inflammation response index (SIRI) correlates with survival and predicts oncological outcome for mFOLFIRINOX therapy in metastatic pancreatic cancer

ObjectivesSystemic inflammatory response and survival has not been evaluated as a predictive factor of chemotherapy in metastatic pancreatic cancer. The aim of this study was to evaluate the prognostic and predictive value of a baseline Systemic Inflammation Response Index (SIRI) in metastatic pancreatic cancer.MethodsRetrospective study of 164 metastatic pancreatic cancer patients. Associations between overall survival (OS), progression free survival (PFS), chemotherapy and SIRI were analyzed. SIRI is defined by neutrophil x monocyte/lymphocyte 10⁹/L.ResultsMedian age 66 years. 22 (13%) received mFOLFIRINOX, 59 (36%) gemcitabine + nab-paclitaxel, 40 (24%) gemcitabine, 13 (8%) other regimens and 30 (18%) had not received treatment. Patients with SIRI<2.3 × 10⁹/L showed a statistically significant improvement in OS compared to SIRI≥2.3 × 10⁹/L [16 months versus 4.8 months, Hazard Ratio (HR) 2.87, Confidence Interval (CI) 95% 2.02–4.07, p < 0.0001] that was confirmed in multivariate analysis. In addition, patients with SIRI<2.3 × 10⁹ showed a longer PFS (12 versus 6 months, HR 1.92, IC 95% 1.314–2.800, P = 0.001). Furthermore, we observed that patients with SIRI ≥2.3 × 10⁹/L were more likely to benefit from mFOLFIRINOX therapy. Patients with an elevated SIRI treated with mFOLFIRINOX versus gemcitabine plus nab-paclitaxel and gemcitabine showed a clinically and statistically significant difference in median OS of 17 months compared to 6 and 4 months respectively (p < 0.001). Conversely, the difference was not clinically significant in the SIRI<2.3 × 10⁹/L subgroup: 15.9 months versus 16.5 and 16, respectively.ConclusionAn elevated SIRI (≥2.3 × 10⁹/L) was an independent prognostic factor for patients with metastatic pancreatic cancer, warranting prospective evaluation.