Introduction

Pancreatic cancer (PC) is one of the most lethal tumors worldwide, and in 2030 it will become the second leading cause of cancer related death (1–3). Computed tomography (CT) and magnetic resonance imaging (MRI) are the gold standards to stage the disease (4). Nevertheless, these imaging modalities are unable to provide real-time information on biological characteristics of tumors, such as vascularity, which is proportional to angiogenesis, growth rate, and necrosis (5,6). Dynamic contrast-enhanced ultrasound (D-CEUS) allows qualitative and quantitative microvascular perfusion assessment in real-time (7).

Aims & Methods

This study aimed to evaluate the role of D-CEUS in the characterization of PC. Thirty-eight patients with suspected PC were prospectively enrolled between October 2022 and March 2023. All patients underwent endoscopic ultrasound guided biopsy for histological diagnosis and CT or MRI for staging. According to these modalities, patients were divided into three categories: resectable PC (R-PC), locally advanced PC (LA-PC), and metastatic PC (M-PC). D-CEUS was performed the same day of lesion biopsy and time-intensity parameters were compared among tumor categories. The diagnostic performances of selected parameters was evaluated by receiver operating characteristic (ROC) analysis.

Results

PC was diagnosed in 36 (94.7%) patients and classified as R-PC, LA-PC and M-PC in 5 (13.9%), 13 (36.1%) and 18 (50%) patients, respectively. Among perfusion parameters, time to peak (TTP) showed a trend to increase in LA-PC patients (median 18.03 sec, interquartile range [IQR] 14) compared to R-PC group (median 12.9 sec, IQR 3.05) (p = 0.05) and it was significantly higher in LA-PC group compared to M-PC group (median 12.35 sec, IQR 4.08) (p = 0.03). A cut-off value < 11.6 sec showed a good accuracy to distinguish LA-PC from M-PC (area under the ROC curve = 0.74) with maximal specificity (100%) but low sensitivity (50%).

Conclusion

Quantitative perfusion parameters extracted from D-CEUS seem to be useful in distinguishing the invasiveness of PC. In particular TTP, a parameter related to blood flow was higher in LA-PC compared to M-PC, suggesting different microvascular characteristics of the tumors. Further studies on larger population are needed to confirm these findings and to explore the biological basis for this phenomenon.

References

1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2020. CA A Cancer J Clin 2020; 70: 7–30.
2. Rahib L, Smith BD, Aizenberg R, et al. Projecting Cancer Incidence and Deaths to 2030: The Unexpected Burden of Thyroid, Liver, and Pancreas Cancers in the United States. Cancer Res 2014; 74: 2913–2921.
3. Bray F, Ferlay J, Soerjomataram I, et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA: A Cancer Journal for Clinicians 2018; 68: 394–424.
4. Ducreux M, Cuhna AS, Caramella C, et al. Cancer of the pancreas: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol 2015; 26 Suppl 5: v56-68.
5. Zhang Z, Ji S, Zhang B, et al. Role of angiogenesis in pancreatic cancer biology and therapy. Biomedicine & Pharmacotherapy 2018; 108: 1135–1140.
6. Li S, Xu H-X, Wu C-T, et al. Angiogenesis in pancreatic cancer: current research status and clinical implications. Angiogenesis 2019; 22: 15–36.
7. Dietrich C, Averkiou M, Correas J-M, et al. An EFSUMB Introduction into Dynamic Contrast-Enhanced Ultrasound (DCE-US) for Quantification of Tumour Perfusion. Ultraschall in Med 2012; 33: 344–351.

Introduction

Sarcopenia or visceral fat has been reported to be related to pancreatic cancer prognosis. However, clinical relevance of the comprehensive analysis of body compositions and their longitudinal changes is lacking. Therefore, this study analyzed the association between body composition changes after chemotherapy and survival in patients with metastatic pancreatic cancer.

Aims & Methods

We retrospectively included 456 patients (mean age±standard deviation, 61.2±10.0 years; 272 males and 184 females) with metastatic pancreatic cancer who received palliative chemotherapy from May 2011 to December 2019. Using deep learning-based, fully automated segmentation of initial computed tomography (CT), areas of muscle, subcutaneous fat, and visceral fat were extracted from a single axial image of the portal phase at the inferior endplate level of the L3 vertebra. Skeletal muscle index (SMI), visceral adipose tissue index (VATI), subcutaneous adipose tissue index (SATI), and mean muscle attenuation (MA) at the inferior endplate level of L3 vertebra were calculated, and their effect on overall survival (OS) was analyzed. Longitudinal changes in body composition and prognostic values were also analyzed in a subgroup of patients with 2-month and 6-month follow-up CT (n=349).

Results

Higher MA at initial CT was significantly associated with better OS in both males and females (hazard ratio [HR]: 0.706; 95% confidence interval [CI], 0.538–0.925; P=0.012 for males, and 0.656; 95% CI, 0.475–0.906; P=0.010 for females), whereas higher SATI (HR, 0.568; 95% CI, 0.388–0.830; P=0.003) was significantly associated with better OS in female patients only. In longitudinal analysis, SMI, VATI, and SATI significantly decreased between initial and 2-month follow-up CT, whereas mean MA significantly decreased between 2-month and 6-month follow-up CT. In stratified cox regression analysis of longitudinal changes, SATI change was significantly associated with OS in male patients (HR, 0.513; 95% CI, 0.354–0.745; P<0.001), while other body composition parameters were not.

Table 4. Stratified Cox Regression Analysis of Overall survival with 2-month CT scan

Conclusion

In patients with metastatic pancreatic cancer, body composition mostly changed during the first 2 months after starting chemotherapy, and the prognostic factors associated with OS differed between males and females. Therefore, deep learning-based body composition analysis can help predict metastatic pancreatic cancer prognosis.

References

1. Sung H, Ferlay J, Siegel RL, et al. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA Cancer J Clin 2021;71(3):209-249.
2. Siegel RL, Miller KD, Fuchs HE, Jemal A. Cancer Statistics, 2021. CA Cancer J Clin 2021;71(1):7-33.
3. Prado CM, Lieffers JR, McCargar LJ, et al. Prevalence and clinical implications of sarcopenic obesity in patients with solid tumours of the respiratory and gastrointestinal tracts: a population-based study. Lancet Oncol 2008;9(7):629-635.
4. The global, regional, and national burden of pancreatic cancer and its attributable risk factors in 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol 2019;4(12):934-947.
5. Michaud DS, Giovannucci E, Willett WC, Colditz GA, Stampfer MJ, Fuchs CS. Physical activity, obesity, height, and the risk of pancreatic cancer. Jama 2001;286(8):921-929.
6. Andersen DK, Korc M, Petersen GM, et al. Diabetes, Pancreatogenic Diabetes, and Pancreatic Cancer. Diabetes 2017;66(5):1103-1110.
7. Park JH, Han K, Hong JY, et al. Changes in Metabolic Syndrome Status are Associated With Altered Risk of Pancreatic Cancer: A Nationwide Cohort Study. Gastroenterology 2022;162(2):509-520.e507.

Disclosure

We have no conflict of interest to disclose

Introduction

Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is a precursor of pancreatic cancer. While earlier research has shown a high prevalence of synchronous/metachronous extrapancreatic tumors in IPMN patients, these studies have often been small with retrospective data collection.

Aims & Methods

Through the Epidemiology Strengthened by histoPathology Reports in Sweden (ESPRESSO) cohort, consisting of computerized histopathology data from all 28 pathology departments in Sweden during the period 1965-2017, we retrieved data on IPMN.
Each index case was matched to ≤5 general population controls.
Through Cox proportional hazards regression models, we estimated hazard ratios (HRs) for future gastrointestinal (GI) cancer precursors and death. In secondary analyses, full siblings were used as comparators.
We excluded IPMN patients with high-grade dysplasia (HGD) to avoid the risk of misclassification.
Outcome topography included esophagus, stomach, colon and rectum and outcome morphology included Barrett’s esophagus, gastric metaplasia, mucosa type 1-3, tubulous adenoma, sessile serrated polyp, tubulovillous adenoma and villous adenoma.

Results

A total of 117 patients with IPMN, 539 age- and sex-matched controls, and 122 siblings were included. Among patients with IPMN, the mean age at diagnosis was 68.3 years and 48% were female.
Compared to IPMN patients, sibling controls were slightly younger (mean 65.5 years).
Patients with IPMN were also more likely to have prior diabetes, chronic obstructive pulmonary disease, obesity, dyslipidemia, and alcohol-related disease.
Almost all IPMN cases (97%) had ≥3 healthcare visits within the last year before diagnosis.
A Charlson Comorbidity Index score of ≥3 was seen in 28% of IPMN cases, compared to in 11% of controls and 9% of siblings.
IPMN cases were at increased risk of earlier GI cancer precursors compared to controls from the general population (OR=6.67; 95%CI=3.45-14.29), but the association failed to reach statistical significance when we compared with siblings (OR=2.00; 95%CI=0.92-4.35).
Over a median of 2.1 years of follow up, we confirmed two (1.7%) incident GI cancer precursors in IPMN vs. four (0.7%) in controls, corresponding to an HR of 1.89 (95%CI=0.34-10.55).
By contrast, IPMN patients were at increased risk of death (HR 3.61 (95%CI=1.79-7.27)).
The most common cause of death in IPMN was pancreatic cancer (n=14; 45.2% of all deaths).
Pancreatic cancer was the cause of death in only two (2.7%) controls and one (7.7%) sibling.
Extrapancreatic cancers were found in eight (6.8%) IPMN patients, 21 (3.9%) controls and four (3.3%) siblings.

Conclusion

We found no association between IPMN and other GI cancer precursors. This argues against comprehensive routine surveillance for other GI cancer precursors in IPMN patients.
Mortality was increased in IPMN with pancreatic cancer being the most common cause of death, indicating the need for lifelong follow up in all resected and non-resected patients with IPMN.

Disclosure

Dr Ludvigsson is coordinating a study on behalf of the Swedish IBD quality register (SWIBREG). This study has received funding from the Janssen corporation. Dr Ludvigsson has also received financial support from MSD to develop a paper reviewing national healthcare registers in China. Dr Vujasinovic and Dr Löhr have received lecture fees from Abbott and Viatris. Dr Vujasinovic and Dr Löhr have also received financial support for writing a scientific book from Viatris. All other authors declare that they have no conflicts of interest and nothing to declare.

Introduction

​​​​​The high heterogeneity characterizing both the neoplastic epithelium and its microenvironment (TME) contributes to poor prognosis and treatment outcomes in pancreatic ductal adenocarcinoma (PDAC) which remains one of the deadliest solid malignancies. The dynamic bidirectional tumor-stroma dialog established in PDAC involved several cancer-associated fibroblast (CAF) subpopulations that either restrain or promote disease progression and contribute to global TME rewiring. Although our understanding of the tumor-stroma interface is continuously growing, the impact of specific gene mutations in the tumor epithelium on the programming of distinct oncogenic TME patterning remains largely uncharted. Homologous recombination deficiency (HRD), caused by mutations in genes such as ATM, not only promotes PDAC aggressiveness with the accumulation of genomic instability and the emergence of invasive tumor cells but also favors a strong desmoplastic reaction suggesting specific TME reprogramming.

Aims & Methods

To investigate whether and how HRDness impacts TME biology, we examined murine ATM- and/or P53-knockout PDACs, as well as human counterpart tissues. Specifically, we generated Atm^fl/fl; LSL-Kras^G12D/+; Ptf1a^Cre/+; Trp53^fl/fl mice and used a cohort of 21 clinically annotated ATM and/or TP53-mutated human PDACs. Murine tumor cell lines were isolated and cultured in vitro and ex vivo with pancreatic-stellate cells, used as CAF progenitors, to characterize their ability to mediate specific fibroblastic reprograming. Additional transcriptomics, proteomics, and secretome analyses allowed us to capture the molecular routes associated with the ATM-loss-dependent ability to rewire CAFs. Finally, computational and histological investigations were conducted to validate our findings in human PDACs.

Results

Both human and murine systems revealed that ATM status significantly affects the TME composition, with an imbalanced myCAF/iCAF ratio in favor of an αSMA+ myofibroblastic CAF enrichment in ATM-depleted tumors. Specifically, secretomics and proteomics investigations demonstrated a greater TGFβ release capacity in ATM-deficient PDAC cells and further in vivo and in vitro analyses a downstream activation of canonical TGFβ signaling in CAFs, supporting their myofibroblastic differentiation. Transcriptomic and in vitro analysis also revealed a reactive oxygen species (ROS)-mediated phenomenon modulating tumor cell contractility and secretome, further affecting the molecular dialog established with CAFs. Strikingly, the ATM loss-mediated CAF rewiring correlated with chemoresistance, and invasive features reverted upon TGFβ interference. Consistently, we demonstrate in several ex vivo and in vivo models that combinatorial therapy with a TGFβRI inhibitor reverses cancer-promoting TME remodeling and exacerbates FOLFIRINOX cytotoxic effects in ATM-deficient HRD PDAC.

Conclusion

These findings reveal that ATM-deficient HRD malignant cells mediate a TGFβ-dependent myofibroblastic CAF fate switch, in turn promoting tumor cell invasion and chemoresistance. Overall, our study conceptualizes how genotype-specific tumor-stroma feedback and -forward signaling axes redraft TME towards a cancer-promoting outcome and introduces exploiting genotype-specific vulnerabilities via multiple tumor-stroma interference strategies.

Introduction

Metastatic pancreatic adenocarcinoma (mPDAC) has poor prognosis with a 5-year survival rate of 3%. In non-metastatic, unresectable locally advanced pancreatic cancer (LAPC) patients, endoscopic-ultrasound (EUS)-guided intra-tumoral ³²P-microparticles implantation resulted in 90.5% local disease control rate [LDCR], defined as Stable Disease [SD] or better, at 16 weeks¹. This is the first study to examine the outcome of ³²P-microparticles (OncoSil™; OncoSil Medical) implantation, in combination with chemotherapy, for treatment of patients with mPDAC.

Aims & Methods

Outcome data of mPDAC patients treated with combination of chemotherapy and intra-tumoral ³²P microparticles (8% of tumour volume, delivering ~100Gy to the tumour) from 5 centres in Australia and UK were retrospectively reviewed. In all cases, ³²P implantation was performed after at least 2 cycles of chemotherapy, which were either FOLFIRINOX or gemcitabine/nab-paclitaxel (Gen-Nab). Data were expressed as median value and P<0.05 was considered as significant.

Results

14 patients (7F:7M; age: 64.5 years; ECOG 0/1/2: 21.4%/57.1%/21.4%) were treated with Gem-Nab (n=10) and FOLFIRINOX (n=4) prior to ³²P-microparticles implantation. Patients had a median of 3 metastases (range, 1-7) in liver (42.9%), lung (35.7%), liver/lung (7.1%), liver/peritoneum (7.1%) or lung/peritoneum (7.1%), with median primary tumour longest diameter [LD] and volume of 40.5mm and 21.8cm³, respectively. ³²P microparticles were implanted with a 100% technical success, at a median 3.1 months from the initial chemotherapy. Prior to OncoSil^TM implantation, only 50% (n=7) had evidence of either stable disease (n=5) or partial response (n=2) based on RECIST criteria. After OncoSil^TM implantation, local disease control rate was 100% at 3 months (stable disease:10 patients; partial response: 4 patients). There was a median 25% reduction in primary tumour LD, with 1 (7%) patient having a marked response and underwent resection (R0 on histology). Median CA19-9 declined from 856.5U/mL to 72U/mL. After a median follow-up of 35.3 months, site of progression after Oncosil implantation were: distant (n=8), local/distant (n=4), local (n=1) and no progression (n=1). Median progression-free survival (PFS) after ³²P implantation was 5.6 months (95% CI: 4.3-non-calculable [nc]), and the overall median survival was 13.9 months (95% CI: 12.2-nc). No Grade 4/5 acute toxicities were observed; 3 (21.4%) patients had device- or procedure-related Grade 1/2 AEs (abdominal pain; nausea; fatigue; dyspepsia) that were also attributed to chemotherapy.

Conclusion

The addition of EUS-guided ³²P-microparticles implantation to standard chemotherapy is feasible and safe for mPDAC patients, with 100% local disease control rate at 3 months post-implantation. This promising data suggests the role of combined intra-tumoral ³²P-microparticles and chemotherapy in the treatment of mPDAC and warrants further evaluation in a large prospective trial.

References

1. Ross, P.J., et al., PanCO: An open-label, single-arm pilot study of phosphorus-32 (P-32; Oncosil) microparticles in patients with unresectable locally advanced pancreatic adenocarcinoma (LAPC) in combination with FOLFIRINOX or gemcitabine + nab-paclitaxel (GNP) chemotherapies. Journal of Clinical Oncology, 2019. 37(15_suppl): p. 4125-4125.

Disclosure

Authors include 2 members of OncoSil Medical whom have assisted in obtaining data from multiple centres however first author collated and analysed data.

Introduction

Pancreatic cancer is a challenging disease with an increasing incidence and extremely poor prognosis due to a late diagnosis, an early metastatic potential and a resistance to treatment. In addition to the traditional prognostic factors (tumor status, response to treatment), the identification of new prognostic factors seems to be essential for a better adaptation of the therapeutic management. In this context, radiological sarcopenia, a new emerging concept translating skeletal muscle loss, is a frequent situation in oncology and been identified as an independent factor of poor survival in gastrointestinal neoplasia. However, few studies have evaluated the prognostic impact of psoas muscle volume, an emerging alternative to skeletal mass index, as a marker of sarcopenia in pancreatic cancer.

Aims & Methods

This study aimed to investigate the relationship between pre-therapeutic sarcopenia evaluated by the total psoas area index (TPAI) and survival outcomes in pancreatic cancer. We conducted a retrospective, single-center study, including patients diagnosed with pancreatic adenocarcinoma between 2014 and 2022. We have excluded patients having computed tomography (CT) performed in others centers and not included in our database, patients with history of other neoplasia, cirrhosis, inflammatory bowel disease and intestinal resection. Measurement of the psoas muscle area has been applied to estimate lean muscle mass as a surrogate marker of sarcopenia. These measurements were performed CT by calculating the total psoas area at the third lumbar vertebra level. Then, TPAI was calculated using the equation: TPAI (mm2/m2) = (Left Psoas Area (mm²) + Right Psoas Area (mm²/)) / Height (m²). Sarcopenia was defined by a TPAI less than 414.5 mm²/m² for female patients and 564.2 mm²/m² for male patients.

Results

A total of 30 patients were enrolled (80 % male; mean age 61 ± 11 years). The pancreatic tumor was located in the head (66.6%), in the body (16,7%) and in the tail (16.7%). The tumor was resectable in 11 patients (36%), locally advanced in 10 patients (33%) and metastatic in 9 patients (9%). Regarding treatment, 33.3% of patients underwent surgery and 30% received palliative chemotherapy. The mean TPAI was 459,66 ± 216,47 mm²/m² (range 200 - 1120 mm²/m²). The overall incidence of sarcopenia according to TPAI was 66% (N = 20). The mean survival was 12 months. Recurrence-free survival rates at 6 months, 12 months and 36 months were 50%, 36.7% and 25% respectively. In univariate analysis, sarcopenia was significantly associted to lower albumin level (31.05 ± 5.57 vs 37.8 ± 4.84, p = 0.004). The sarcopenic patients were, on average, older than the nonsarcopenic patients, but without significant difference (62 ± 12 years vs 58 ± 11 years, p>0.05). Sarcopenia was not associated with diabetes mellitus, smoking, anemia, lymphopenia or CA 19-9 level.
In term of survival, the difference between the two Kaplan-Meier curves of sarcopenic versus non-sarcopenic patients was statistically significant (log rank test p=0.01), [HR = 2,95 (95% CI = 1 – 7)], with a mean survival period of 7.80 ± 9.57 versus 20.40 ± 4.84 months respectively (p=0.028). When analyzing the receiver operating characteristic (ROC) curve, AUC of TPAI in predicting 12 months survival was 0.871 (95% CI: 0.741–1, p=0.001).

Conclusion

The TPAI is a valuable marker of sarcopenia, easy to measure correlated with negative prognostic impact in patients with pancreatic cancer allowing better pre-therapeutic stratification.

References

Amini, N.; Spolverato, G.; Gupta, R.; Margonis, G.A.; Kim, Y.; Wagner, D. Impact Total Psoas Volume on Short- and Long-Term Outcomes in Patients Undergoing Curative Resection for Pancreatic Adenocarcinoma: A New Tool to Assess Sarcopenia. J. Gastrointest Surg. 2015, 19, 1593–1602

Introduction

The retroperitoneal location of the pancreas represents a challenge for the early identification of chronic pancreatitis (CP) and pancreas neoplasms (PN). Imaging and endoscopic ultrasound (EUS) with elastography are helpful resources with variable accuracy. EUS-guided shear wave elastography (EUS-SW) measures tissue elasticity by shear waves inside the organ through acoustic radiation force impulse. Its accuracy has not been assessed for CP and solid PN.

Aims & Methods

We aim to estimate the diagnostic accuracy of EUS-SW for CP and solid PN. Cases with a recently confirmed diagnosis of CP or PN who underwent EUS-SW (12/2020-11/2022) were included. Cases that required EUS for subepithelial lesion assessment comprised a third study group (controls, CG). Age, gender, body mass index (BMI), diabetes, fatty liver disease, alcohol, and tobacco consumption were recorded. An expert endoscopist (RVZ) performed EUS, assessed fatty pancreas score, strain ratio (SR), histogram (SH), and ten measurements of EUS-SW elasticity (SWE) and dispersion (SWD) per case. SWE and SWD variation were based on quotient among interquartile range (IQR) and median. In cases with <30% variation, the association of SWE and SWD was estimated with study groups, baseline and EUS data through multivariate ANOVA regression. SWE and SWD cut-off values were calculated with Youden’s index. Data was analysed in R v4.0.

Results

88 cases were enrolled (37 CG, 14 CP, 37 PN), median age of 62.5 (IQR 53-70), 47.7% female. The proportion of fatty pancreas score II and III was similar in CG (37.8% and 56.8%) and CP (57.1% and 42.9%); there was a significant difference in PN, with a score II, III, and IV of 24.3%, 40.5%, and 29.7%, respectively (p<.001). Median SR was also similar among CG (3.6; IQR 2.9 - 4.3) and CP (3.9; IQR 3.6 - 4.7) but significantly different compared with PN (7.6; IQR 5.3 - 11.1; p<.001). Median SWE and SWD were 10.5 kPa (7.3 - 16.6) and 1.9 [m/s]/kHz (1.6 - 2.4), with a <30% variation in 27 (30.7%) and 57 (64.8%), respectively (table 1). Study groups (CG/CP/PN) and diabetes were associated to a higher SWE and SWD (p<.05). Predicted SWE were significantly different among PN vs CG (-13.1; -24.4 to -1.7; p=.0242) (figure 1). An SWE ≥17.4 diagnosed PN with a sensitivity, specificity, positive and negative predictive values of 75% (19-99), 91% (72-99), 60% (27-99) and 95% (63-99); while an SWD ≥2.31 predicted PN with a diagnostic accuracy of 54% (25-81), 70% (55-83), 35% (21-66), 84% (60-91), respectively.

Conclusion

EUS-SW constitutes an objectively valuable measuring tool for CP and PN diagnostic workups. Larger multicentric diagnostic trials are needed to confirm these findings. NCT05095831.

References

1. Xia C, Yin H, Zhang K, Wang Z, Yang X, Huang H. The global research status and trends of the application of endoscopic ultrasonography in pancreatic tumors over the last decades: A bibliometric study. Front Oncol. 2022 Aug 12;12:980415.
2. Salah NY, Madkour SS, Soliman KS. Pancreatic shear wave elastography in children with type 1 diabetes: relation to diabetes duration, glycemic indices, fasting C-peptide and diabetic complications. Pediatr Radiol. 2022 Nov;52(12):2348-2358. doi: 10.1007/s00247-022-05363-1. Epub 2022 Apr 23.
3. Fujita Y, Kitago M, Abe T, et al. Evaluation of pancreatic fibrosis with acoustic radiation force impulse imaging and automated quantification of pancreatic tissue components. Pancreas. 2018;47:1277–1282.
4. Jesper D, Fiedler S, Klett D, Waldner MJ, Schellhaas B, Zundler S, Neurath MF, Pfeifer L. Shear Wave Dispersion Imaging for the Characterization of Focal Liver Lesions - A Pilot study. Ultraschall Med. 2022 Oct;43(5):507-513.
5. Korta Martiartu N, Nambiar S, Nascimento Kirchner I, Paverd C, Cester D, Frauenfelder T, Ruby L, Rominger MB. Sources of Variability in Shear Wave Speed and Dispersion Quantification with Ultrasound Elastography: A Phantom Study. Ultrasound Med Biol. 2021 Dec;47(12):3529-3542.

Disclosure

Carlos Robles-Medranda is a key opinion leader and consultant for Pentax Medical, Boston Scientific, Steris, Medtronic, Motus, Micro-tech, G-Tech Medical Supply, CREO Medical, EndoSound, and Mdconsgroup. The other authors declare no conflicts of interest.