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Article: Improving patient stratification and selection for curative-intent treatment in localized pancreatic cancer.

Martos, Mary P / Amirian, Haleh / Dickey, Erin M / Box, Edmond W / Merchant, Nipun B / Hosein, Peter J / Hester, Caitlin A / Datta, Jashodeep

Hepatobiliary surgery and nutrition

2024 Volume 13, Issue 2, Page(s) 325–328

Language	English
Publishing date	2024-03-29
Publishing country	China (Republic : 1949- )
Document type	Editorial ; Comment
ZDB-ID	2812398-0
ISSN	2304-389X ; 2304-3881
ISSN (online)	2304-389X
ISSN	2304-3881
DOI	10.21037/hbsn-23-668
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Article ; Online: Transmembrane TNF-TNFR2 signaling as a critical immunoregulatory node in pancreatic cancer.

Dickey, Erin M / Bianchi, Anna / Amirian, Haleh / Hosein, Peter J / Faustman, Denise / Brambilla, Roberta / Datta, Jashodeep

Oncoimmunology

2024 Volume 13, Issue 1, Page(s) 2326694

Abstract: Pancreatic cancer is characterized by extreme therapeutic resistance. In pancreatic cancers harboring high-risk genomes, we describe that cancer cell-neutrophil signaling circuitry provokes neutrophil-derived transmembrane (tm)TNF-TNFR2 interactions that ...

Abstract	Pancreatic cancer is characterized by extreme therapeutic resistance. In pancreatic cancers harboring high-risk genomes, we describe that cancer cell-neutrophil signaling circuitry provokes neutrophil-derived transmembrane (tm)TNF-TNFR2 interactions that dictate inflammatory polarization in cancer-associated fibroblasts and T-cell dysfunction - two hallmarks of therapeutic resistance. Targeting tmTNF-TNFR2 signaling may sensitize pancreatic cancer to chemo±immunotherapy.
MeSH term(s)	Humans ; Receptors, Tumor Necrosis Factor, Type II/genetics ; Tumor Necrosis Factor-alpha ; Signal Transduction ; Pancreatic Neoplasms
Chemical Substances	Receptors, Tumor Necrosis Factor, Type II ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2024-03-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2645309-5
ISSN	2162-402X ; 2162-402X
ISSN (online)	2162-402X
ISSN	2162-402X
DOI	10.1080/2162402X.2024.2326694
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Article ; Online: Racial Disparity in 30-Day Outcomes of Metabolic and Bariatric Surgery.

Amirian, Haleh / Torquati, Alfonso / Omotosho, Philip

Obesity surgery

2019 Volume 30, Issue 3, Page(s) 1011–1020

Abstract: Background: There is evidence of racial disparity in the long-term weight loss outcomes of bariatric surgery. However, there has been a more limited evaluation of the impact of race on immediate perioperative outcomes. The aim of this study was to ... ...

Abstract	Background: There is evidence of racial disparity in the long-term weight loss outcomes of bariatric surgery. However, there has been a more limited evaluation of the impact of race on immediate perioperative outcomes. The aim of this study was to compare 30-day postoperative outcomes among different races. Study design: The 2016 Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program (MBSAQIP) database was queried to identify patients aged ≥ 18 and body mass index ≥ 35 who underwent primary laparoscopic Roux-en-Y gastric bypass (LRYGB) or laparoscopic sleeve gastrectomy (LSG) with known information on race. We then evaluated the effect of five different races on four different 30-day outcomes. Results: Of the total 106,932 patients (79.5% White, 19.3% African American (AA), 0.5% Asian, 0.4% American Indian or Alaska Native, 0.3% Native Hawaiian or other Pacific Islander), 30-day rates of postoperative complication, readmission, re-intervention, and reoperation were 6, 3.8, 1.3, and 1.2%, respectively. After controlling for other covariates in multivariate logistic regression and selecting White as reference, AA was the only race associated with a higher risk of postoperative complications (odds ratio [OR] 1.13; confidence interval [CI] 1.06-1.2) and readmissions (OR 1.47; CI 1.3-1.6). AA and American Indian or Alaska Native were also associated with higher re-interventions (OR 1.31; CI 1.15-1.51 and OR 2.11; CI 1.03-4.34). Furthermore, AA was associated with lower 30-day reoperations (OR 0.83; CI 0.7-0.9). Conclusion: This study found significant racial differences in short-term outcomes following bariatric surgery. Factors underlying these disparities are unclear and warrant further investigation.
MeSH term(s)	Adolescent ; Adult ; African Americans/statistics & numerical data ; Aged ; Bariatric Surgery/adverse effects ; Bariatric Surgery/statistics & numerical data ; Databases, Factual ; Female ; Health Status Disparities ; Humans ; Laparoscopy/adverse effects ; Laparoscopy/statistics & numerical data ; Male ; Middle Aged ; Obesity, Morbid/diagnosis ; Obesity, Morbid/ethnology ; Obesity, Morbid/surgery ; Patient Readmission/statistics & numerical data ; Postoperative Complications/ethnology ; Postoperative Complications/etiology ; Postoperative Complications/therapy ; Prognosis ; Racial Groups/statistics & numerical data ; Reoperation/adverse effects ; Reoperation/statistics & numerical data ; Treatment Outcome ; United States/epidemiology ; Weight Loss/physiology ; Young Adult
Keywords	covid19
Language	English
Publishing date	2019-11-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1070827-3
ISSN	1708-0428 ; 0960-8923
ISSN (online)	1708-0428
ISSN	0960-8923
DOI	10.1007/s11695-019-04282-9
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Article ; Online: Racial Disparity Between Whites and African Americans in Incidence and Outcome of Pancreatic Cancer: Have We Made a Difference?

Amirian, Haleh / Kwon, Deukwoo / Vickers, Selwyn M / Livingstone, Alan / Jayaweera, Dushyantha / Saluja, Ashok K

Gastroenterology

2021 Volume 162, Issue 4, Page(s) 1346–1348.e3

MeSH term(s)	Black or African American ; Humans ; Incidence ; Pancreatic Neoplasms/epidemiology ; Racial Groups ; United States/epidemiology ; White People ; Pancreatic Neoplasms
Language	English
Publishing date	2021-12-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2021.12.256
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Article ; Online: Tumor Cell-Intrinsic p38 MAPK Signaling Promotes IL1α-Mediated Stromal Inflammation and Therapeutic Resistance in Pancreatic Cancer.

Singh, Samara P / Dosch, Austin R / Mehra, Siddharth / De Castro Silva, Iago / Bianchi, Anna / Garrido, Vanessa T / Zhou, Zhiqun / Adams, Andrew / Amirian, Haleh / Box, Edmond W / Sun, Xiaodian / Ban, Yuguang / Datta, Jashodeep / Nagathihalli, Nagaraj S / Merchant, Nipun B

Cancer research

2024 Volume 84, Issue 8, Page(s) 1320–1332

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is characterized by a KRAS-driven inflammatory program and a desmoplastic stroma, which contribute to the profoundly chemoresistant phenotype. The tumor stroma contains an abundance of cancer-associated fibroblasts ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is characterized by a KRAS-driven inflammatory program and a desmoplastic stroma, which contribute to the profoundly chemoresistant phenotype. The tumor stroma contains an abundance of cancer-associated fibroblasts (CAF), which engage in extensive paracrine cross-talk with tumor cells to perpetuate protumorigenic inflammation. IL1α, a pleiotropic, tumor cell-derived cytokine, plays a critical role in shaping the stromal landscape. To provide insights into the molecular mechanisms regulating IL1A expression in PDAC, we performed transcriptional profiling of The Cancer Genome Atlas datasets and pharmacologic screening in PDAC cells and identified p38α MAPK as a key positive regulator of IL1A expression. Both genetic and pharmacologic inhibition of p38 MAPK significantly diminished IL1α production in vitro. Chromatin- and coimmunoprecipitation analyses revealed that p38 MAPK coordinates the transcription factors Sp1 and the p65 subunit of NFκB to drive IL1A overexpression. Single-cell RNA sequencing of a highly desmoplastic murine PDAC model, Ptf1aCre/+; LSL-KrasG12D/+; Tgfbr2flox/flox (PKT), confirmed that p38 MAPK inhibition significantly decreases tumor cell-derived Il1a and attenuates the inflammatory CAF phenotype in a paracrine IL1α-dependent manner. Furthermore, p38 MAPK inhibition favorably modulated intratumoral immunosuppressive myeloid populations and augmented chemotherapeutic efficacy to substantially reduce tumor burden and improve overall survival in PKT mice. These findings illustrate a cellular mechanism of tumor cell-intrinsic p38-p65/Sp1-IL1α signaling that is responsible for sustaining stromal inflammation and CAF activation, offering an attractive therapeutic approach to enhance chemosensitivity in PDAC. Significance: Inhibition of p38 MAPK suppresses tumor cell-derived IL1α and attenuates the inflammatory stroma and immunosuppressive tumor microenvironment to overcome chemotherapeutic resistance in pancreatic cancer.
MeSH term(s)	Mice ; Animals ; Drug Resistance, Neoplasm/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Cancer-Associated Fibroblasts/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism ; Inflammation/pathology ; Tumor Microenvironment
Chemical Substances	p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2024-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-23-1200
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Article: ALCAM: A Novel Surface Marker on EpCAM

Signorelli, Rossana / Giret, Teresa Maidana / Umland, Oliver / Hadisurya, Marco / Lavania, Shweta / Charles Richard, John Lalith / Middleton, Ashley / Boone, Melinda Minucci / Ergonul, Ayse Burcu / Tao, Weiguo Andy / Amirian, Haleh / Iliuk, Anton / Khan, Aliya / Diaz, Robert / Cortes, Daniel Bilbao / Garcia-Buitrago, Monica / Charles Jacob, Harrys Kishore

Biomedicines

2022 Volume 10, Issue 8

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2022-08-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10081983
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Article ; Online: Identification of novel early pancreatic cancer biomarkers KIF5B and SFRP2 from "first contact" interactions in the tumor microenvironment.

Charles Jacob, Harrys Kishore / Signorelli, Rossana / Charles Richard, John Lalith / Kashuv, Tyler / Lavania, Shweta / Middleton, Ashley / Gomez, Beatriz Aguilar / Ferrantella, Anthony / Amirian, Haleh / Tao, Junyi / Ergonul, Ayse Burcu / Boone, Melinda Minucci / Hadisurya, Marco / Tao, Weiguo Andy / Iliuk, Anton / Kashyap, Manoj Kumar / Garcia-Buitrago, Monica / Dawra, Rajinder / Saluja, Ashok Kumar

Journal of experimental & clinical cancer research : CR

2022 Volume 41, Issue 1, Page(s) 258

Abstract: Background: Pancreatic cancer is one of the most difficult cancers to detect early and most patients die from complications arising due to distant organ metastases. The lack of bona fide early biomarkers is one of the primary reasons for late diagnosis ... ...

Abstract	Background: Pancreatic cancer is one of the most difficult cancers to detect early and most patients die from complications arising due to distant organ metastases. The lack of bona fide early biomarkers is one of the primary reasons for late diagnosis of pancreatic cancer. It is a multifactorial disease and warrants a novel approach to identify early biomarkers. Methods: In order to characterize the proteome, Extracellular vesicles (EVs) isolated from different in vitro conditions mimicking tumor-microenvironment interactions between pancreatic cancer epithelial and stromal cells were analyzed using high throughput mass spectrometry. The biological activity of the secreted EVome was analyzed by investigating changes in distant organ metastases and associated early changes in the microbiome. Candidate biomarkers (KIF5B, SFRP2, LOXL2, and MMP3) were selected and validated on a mouse-human hybrid Tissue Microarray (TMA) that was specifically generated for this study. Additionally, a human TMA was used to analyze the expression of KIF5B and SFRP2 in progressive stages of pancreatic cancer. Results: The EVome of co-cultured epithelial and stromal cells is different from individual cells with distinct protein compositions. EVs secreted from stromal and cancer cells cultures could not induce significant changes in Pre-Metastatic Niche (PMN) modulation, which was assessed by changes in the distant organ metastases. However, they did induce significant changes in the early microbiome, as indicated by differences in α and β-diversities. KIF5B and SFRP2 show promise for early detection and investigation in progressive pancreatic cancer. These markers are expressed in all stages of pancreatic cancer such as low grade PanINs, advanced cancer, and in liver and soft tissue metastases. Conclusions: Proteomic characterization of EVs derived from mimicking conditions of epithelial and stromal cells in the tumor-microenvironment resulted in the identification of several proteins, some for the first time in EVs. These secreted EVs cannot induce changes in distant organ metastases in in vivo models of EV education, but modulate changes in the early murine microbiome. Among all the proteins that were analyzed (MMP3, KIF5B, SFRP2, and LOXL2), KIF5B and SFRP2 show promise as bona fide early pancreatic cancer biomarkers expressed in progressive stages of pancreatic cancer.
MeSH term(s)	Animals ; Biomarkers, Tumor/metabolism ; Humans ; Kinesins ; Matrix Metalloproteinase 3 ; Membrane Proteins ; Mice ; Pancreatic Neoplasms/pathology ; Proteome/metabolism ; Proteomics/methods ; Tumor Microenvironment ; Pancreatic Neoplasms
Chemical Substances	Biomarkers, Tumor ; KIF5B protein, human ; Membrane Proteins ; Proteome ; SFRP2 protein, human ; Sfrp2 protein, mouse ; Matrix Metalloproteinase 3 (EC 3.4.24.17) ; Kif5b protein, mouse (EC 3.6.1.-) ; Kinesins (EC 3.6.4.4)
Language	English
Publishing date	2022-08-24
Publishing country	England
Document type	Journal Article
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-022-02425-y
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Article ; Online: Cell-Autonomous Cxcl1 Sustains Tolerogenic Circuitries and Stromal Inflammation via Neutrophil-Derived TNF in Pancreatic Cancer.

Bianchi, Anna / De Castro Silva, Iago / Deshpande, Nilesh U / Singh, Samara / Mehra, Siddharth / Garrido, Vanessa T / Guo, Xinyu / Nivelo, Luis A / Kolonias, Despina S / Saigh, Shannon J / Wieder, Eric / Rafie, Christine I / Dosch, Austin R / Zhou, Zhiqun / Umland, Oliver / Amirian, Haleh / Ogobuiro, Ifeanyichukwu C / Zhang, Jian / Ban, Yuguang /

Shiau, Carina / Nagathihalli, Nagaraj S / Montgomery, Elizabeth A / Hwang, William L / Brambilla, Roberta / Komanduri, Krishna / Villarino, Alejandro V / Toska, Eneda / Stanger, Ben Z / Gabrilovich, Dmitry I / Merchant, Nipun B / Datta, Jashodeep

Cancer discovery

2023 Volume 13, Issue 6, Page(s) 1428–1453

Abstract: We have shown that KRAS-TP53 genomic coalteration is associated with immune-excluded microenvironments, chemoresistance, and poor survival in pancreatic ductal adenocarcinoma (PDAC) patients. By treating KRAS-TP53 cooperativity as a model for high-risk ... ...

Abstract	We have shown that KRAS-TP53 genomic coalteration is associated with immune-excluded microenvironments, chemoresistance, and poor survival in pancreatic ductal adenocarcinoma (PDAC) patients. By treating KRAS-TP53 cooperativity as a model for high-risk biology, we now identify cell-autonomous Cxcl1 as a key mediator of spatial T-cell restriction via interactions with CXCR2+ neutrophilic myeloid-derived suppressor cells in human PDAC using imaging mass cytometry. Silencing of cell-intrinsic Cxcl1 in LSL-KrasG12D/+;Trp53R172H/+;Pdx-1Cre/+(KPC) cells reprograms the trafficking and functional dynamics of neutrophils to overcome T-cell exclusion and controls tumor growth in a T cell-dependent manner. Mechanistically, neutrophil-derived TNF is a central regulator of this immunologic rewiring, instigating feed-forward Cxcl1 overproduction from tumor cells and cancer-associated fibroblasts (CAF), T-cell dysfunction, and inflammatory CAF polarization via transmembrane TNF-TNFR2 interactions. TNFR2 inhibition disrupts this circuitry and improves sensitivity to chemotherapy in vivo. Our results uncover cancer cell-neutrophil cross-talk in which context-dependent TNF signaling amplifies stromal inflammation and immune tolerance to promote therapeutic resistance in PDAC. Significance: By decoding connections between high-risk tumor genotypes, cell-autonomous inflammatory programs, and myeloid-enriched/T cell-excluded contexts, we identify a novel role for neutrophil-derived TNF in sustaining immunosuppression and stromal inflammation in pancreatic tumor microenvironments. This work offers a conceptual framework by which targeting context-dependent TNF signaling may overcome hallmarks of chemoresistance in pancreatic cancer. This article is highlighted in the In This Issue feature, p. 1275.
MeSH term(s)	Humans ; Neutrophils ; Receptors, Tumor Necrosis Factor, Type II/therapeutic use ; Proto-Oncogene Proteins p21(ras)/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Inflammation/genetics ; Tumor Microenvironment/physiology ; Chemokine CXCL1/genetics ; Pancreatic Neoplasms
Chemical Substances	Receptors, Tumor Necrosis Factor, Type II ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; CXCL1 protein, human ; Chemokine CXCL1
Language	English
Publishing date	2023-03-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-22-1046
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Article: Improving patient stratification and selection for curative-intent treatment in localized pancreatic cancer.

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Article ; Online: Transmembrane TNF-TNFR2 signaling as a critical immunoregulatory node in pancreatic cancer.

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Article ; Online: Racial Disparity in 30-Day Outcomes of Metabolic and Bariatric Surgery.

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Article ; Online: Racial Disparity Between Whites and African Americans in Incidence and Outcome of Pancreatic Cancer: Have We Made a Difference?

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Article ; Online: Tumor Cell-Intrinsic p38 MAPK Signaling Promotes IL1α-Mediated Stromal Inflammation and Therapeutic Resistance in Pancreatic Cancer.

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Article: ALCAM: A Novel Surface Marker on EpCAM

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Article ; Online: Identification of novel early pancreatic cancer biomarkers KIF5B and SFRP2 from "first contact" interactions in the tumor microenvironment.

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Article ; Online: Cell-Autonomous Cxcl1 Sustains Tolerogenic Circuitries and Stromal Inflammation via Neutrophil-Derived TNF in Pancreatic Cancer.

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