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Journal articles on the topic 'Organotropisme'

Author: Grafiati
Published: 30 June 2023

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1

Wei, Shi, and Gene P. Siegal. "Metastatic Organotropism." Advances In Anatomic Pathology 24, no. 2 (March 2017): 78–81. http://dx.doi.org/10.1097/pap.0000000000000140.

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2

Yuzhalin, Arseniy E., and Dihua Yu. "Brain Metastasis Organotropism." Cold Spring Harbor Perspectives in Medicine 10, no. 5 (September 23, 2019): a037242. http://dx.doi.org/10.1101/cshperspect.a037242.

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3

Lu, Xin, and Yibin Kang. "Organotropism of Breast Cancer Metastasis." Journal of Mammary Gland Biology and Neoplasia 12, no. 2-3 (June 14, 2007): 153–62. http://dx.doi.org/10.1007/s10911-007-9047-3.

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4

Fu, Hongmei, Eleanor Jayne Ward, and Federica M. Marelli-Berg. "Mechanisms of T cell organotropism." Cellular and Molecular Life Sciences 73, no. 16 (April 1, 2016): 3009–33. http://dx.doi.org/10.1007/s00018-016-2211-4.

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5

Gao, Yang, Igor Bado, Hai Wang, Weijie Zhang, Jeffrey M. Rosen, and Xiang H. F. Zhang. "Metastasis Organotropism: Redefining the Congenial Soil." Developmental Cell 49, no. 3 (May 2019): 375–91. http://dx.doi.org/10.1016/j.devcel.2019.04.012.

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6

Keller, Georg v. "Chelidonium und die Organotropie." Allgemeine Homöopathische Zeitung 224, no. 06 (April 10, 2007): 217–27. http://dx.doi.org/10.1055/s-2006-935880.

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7

Schmeer, Ernst H. "Rademacher und die Organotropie." Allgemeine Homöopathische Zeitung 225, no. 03 (April 10, 2007): 115–19. http://dx.doi.org/10.1055/s-2006-935894.

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8

Tang, Kai, Ying Xin, Keming Li, Xi Chen, and Youhua Tan. "Cell Cytoskeleton and Stiffness Are Mechanical Indicators of Organotropism in Breast Cancer." Biology 10, no. 4 (March 25, 2021): 259. http://dx.doi.org/10.3390/biology10040259.

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Tumor metastasis involves the dissemination of tumor cells from the primary lesion to other organs and the subsequent formation of secondary tumors, which leads to the majority of cancer-related deaths. Clinical findings show that cancer cell dissemination is not random but exhibits organ preference or organotropism. While intrinsic biochemical factors of cancer cells have been extensively studied in organotropism, much less is known about the role of cell cytoskeleton and mechanics. Herein, we demonstrate that cell cytoskeleton and mechanics are correlated with organotropism. The result of cell stiffness measurements shows that breast cancer cells with bone tropism are much stiffer with enhanced F-actin, while tumor cells with brain tropism are softer with lower F-actin than their parental cells. The difference in cellular stiffness matches the difference in the rigidity of their metastasized organs. Further, disrupting the cytoskeleton of breast cancer cells with bone tropism not only elevates the expressions of brain metastasis-related genes but also increases cell spreading and proliferation on soft substrates mimicking the stiffness of brain tissue. Stabilizing the cytoskeleton of cancer cells with brain tropism upregulates bone metastasis-related genes while reduces the mechanoadaptation ability on soft substrates. Taken together, these findings demonstrate that cell cytoskeleton and biophysical properties of breast cancer subpopulations correlate with their metastatic preference in terms of gene expression pattern and mechanoadaptation ability, implying the potential role of cell cytoskeleton in organotropism.
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9

Eng, Jennifer, Jason Link, Carl Pelz, and Rosalie Sears. "Abstract PR010: Multiplex imaging reveals features of organotropism in pancreatic ductal adenocarcinoma." Cancer Research 83, no. 2_Supplement_2 (January 15, 2023): PR010. http://dx.doi.org/10.1158/1538-7445.metastasis22-pr010.

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Abstract PDAC patients have a dismal prognosis with an 11% 5-year survival rate, driven in part by the fact that 90% of patients are diagnosed with metastatic disease. In a cohort of 300 PDAC patients, we observed that patients who had lung-only metastasis had longer overall survival than the majority of patients with metastasis to the liver. We used gene expression data to develop a signature based on gene expression in primary tumors of liver versus lung organotropism, which we called pORG. Our pORG signature predicts long term survival in PDAC patients and reveals unique features of the primary tumor, including increased interferon and immune activity in lung tropic tumors and increased proliferation and replication stress in liver-tropic tumors. To validate our findings, we generated cyclic immunofluorescence multiplex imaging data for a subset of 34 patients. Single cell image analysis revealed B and T cell infiltration and spatial clustering in low pORG/ lung tropic tumors, and markers of replication stress in high pORG patients. Our work suggests unique targetable tumor and microenvironment features linked to organotropism in PDAC. Citation Format: Jennifer Eng, Jason Link, Carl Pelz, Rosalie Sears. Multiplex imaging reveals features of organotropism in pancreatic ductal adenocarcinoma [abstract]. In: Proceedings of the AACR Special Conference: Cancer Metastasis; 2022 Nov 14-17; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_2):Abstract nr PR010.
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10

Wong, Grace L., Sara Abu Jalboush, and Hui-Wen Lo. "Exosomal MicroRNAs and Organotropism in Breast Cancer Metastasis." Cancers 12, no. 7 (July 7, 2020): 1827. http://dx.doi.org/10.3390/cancers12071827.

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Breast cancer is the most frequent malignancy for women in which one in eight women will be diagnosed with the disease in their lifetime. Despite advances made in treating primary breast cancer, there is still no effective treatment for metastatic breast cancer. Consequently, metastatic breast cancer is responsible for 90% of breast cancer-related deaths while only accounting for approximately one third of all breast cancer cases. To help develop effective treatments for metastatic breast cancer, it is important to gain a deeper understanding of the mechanisms by which breast cancer metastasizes, particularly, those underlying organotropism towards brain, bone, and lungs. In this review, we will primarily focus on the roles that circulating exosomal microRNAs (miRNAs) play in organotropism of breast cancer metastasis. Exosomes are extracellular vesicles that play critical roles in intercellular communication. MicroRNAs can be encapsulated in exosomes; cargo-loaded exosomes can be secreted by tumor cells into the tumor microenvironment to facilitate tumor–stroma interactions or released to circulation to prime distant organs for subsequent metastasis. Here, we will summarize our current knowledge on the biogenesis of exosomes and miRNAs, mechanisms of cargo sorting into exosomes, the exosomal miRNAs implicated in breast cancer metastasis, and therapeutic exosomal miRNAs.
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11

Rezaie, Jafar, Mahdi Ahmadi, Reyhaneh Ravanbakhsh, Behnam Mojarad, Shadi Mahbubfam, Shadi Abdolrahman Shaban, Kosar Shadi, Nesa Janamo Berenjabad, and Tahereh Etemadi. "Tumor-derived extracellular vesicles: The metastatic organotropism drivers." Life Sciences 289 (January 2022): 120216. http://dx.doi.org/10.1016/j.lfs.2021.120216.

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12

Uhlenbruck, G., H. J. Beuth, K. Oette, T. Schotten, H. L. Ko, K. Roszkowski, W. Roszkowski, R. Lütticken, and G. Pulverer. "Lektine und die Organotropie der Metastasierung." DMW - Deutsche Medizinische Wochenschrift 111, no. 25 (March 25, 2008): 991–95. http://dx.doi.org/10.1055/s-2008-1068572.

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13

Carlson, John H., Stephen F. Porcella, Grant McClarty, and Harlan D. Caldwell. "Comparative Genomic Analysis of Chlamydia trachomatis Oculotropic and Genitotropic Strains." Infection and Immunity 73, no. 10 (October 2005): 6407–18. http://dx.doi.org/10.1128/iai.73.10.6407-6418.2005.

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ABSTRACT Chlamydia trachomatis infection is an important cause of preventable blindness and sexually transmitted disease (STD) in humans. C. trachomatis exists as multiple serovariants that exhibit distinct organotropism for the eye or urogenital tract. We previously reported tissue-tropic correlations with the presence or absence of a functional tryptophan synthase and a putative GTPase-inactivating domain of the chlamydial toxin gene. This suggested that these genes may be the primary factors responsible for chlamydial disease organotropism. To test this hypothesis, the genome of an oculotropic trachoma isolate (A/HAR-13) was sequenced and compared to the genome of a genitotropic (D/UW-3) isolate. Remarkably, the genomes share 99.6% identity, supporting the conclusion that a functional tryptophan synthase enzyme and toxin might be the principal virulence factors underlying disease organotropism. Tarp (translocated actin-recruiting phosphoprotein) was identified to have variable numbers of repeat units within the N and C portions of the protein. A correlation exists between lymphogranuloma venereum serovars and the number of N-terminal repeats. Single-nucleotide polymorphism (SNP) analysis between the two genomes highlighted the minimal genetic variation. A disproportionate number of SNPs were observed within some members of the polymorphic membrane protein (pmp) autotransporter gene family that corresponded to predicted T-cell epitopes that bind HLA class I and II alleles. These results implicate Pmps as novel immune targets, which could advance future chlamydial vaccine strategies. Lastly, a novel target for PCR diagnostics was discovered that can discriminate between ocular and genital strains. This discovery will enhance epidemiological investigations in nations where both trachoma and chlamydial STD are endemic.
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14

Xie, Xiaodong, Shu Lian, Yu Zhou, Bifei Li, Yusheng Lu, Iwin Yeung, and Lee Jia. "Tumor-derived exosomes can specifically prevent cancer metastatic organotropism." Journal of Controlled Release 331 (March 2021): 404–15. http://dx.doi.org/10.1016/j.jconrel.2021.01.030.

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15

Sağnak Yılmaz, Zeynep. "Molecular Mechanism of Metastasis in Colorectal Cancer and Organotropism." Kocaeli Medical Journal 11, no. 1 (2022): 15–25. http://dx.doi.org/10.5505/ktd.2022.64624.

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16

Mieiro, Cláudia Leopoldina, Mário Pacheco, Maria Eduarda Pereira, and Armando Costa Duarte. "Mercury Organotropism in Feral European Sea Bass (Dicentrarchus labrax)." Archives of Environmental Contamination and Toxicology 61, no. 1 (August 22, 2010): 135–43. http://dx.doi.org/10.1007/s00244-010-9591-5.

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17

Adamska, Aleksandra, and Marco Falasca. "Epithelial plasticity is crucial for pancreatic cancer metastatic organotropism." Annals of Translational Medicine 6, S1 (November 2018): S53. http://dx.doi.org/10.21037/atm.2018.10.16.

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18

Coppi, F., E. Patelli, M. Seveso, G. L. Taverna, and M. Pastorello. "Round Table: “Therapy of urological tumour metastases” - Biology of metastases." Urologia Journal 59, no. 5 (October 1992): 62–65. http://dx.doi.org/10.1177/039156039205900512.

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— The Authors show the sequential events of the metastasization process based on the most recent theories. They especially underline the importance of angiogenesis and organotropism of the neoplastic cells in “metastatic fall”. The deeper knowledge of all the biological and genetic mechanisms means new diagnostic and therapeutical approaches can be applied.
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19

Singla, Nirmish, Oreoluwa Onabolu, Layton Woolford, Christina Stevens, Vanina Tcheuyap, Tiffani McKenzie, Qurratulain Yousuf, et al. "Unraveling the molecular profile underpinning pancreatic tropisms in metastatic clear cell renal cell carcinoma." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e16096-e16096. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e16096.

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e16096 Background: The tropism of cancer metastases is poorly understood yet holds prognostic value. Clear cell renal cell carcinoma (ccRCC) exhibits a broad pattern of metastases, making it an optimal model to study organotropism. Notably, when ccRCC metastasizes to the pancreas (PM) independently of other sites, it is associated with favorable outcomes in patients for unclear reasons. Here, we comprehensively analyzed the clinical and molecular profile of patients with PM. Methods: RCC patients with PM from UTSW and Cleveland Clinic were identified. Clinicopathologic data and oncologic outcomes were analyzed. Whole exome sequencing (WES), RNAseq, and histologic assessment of primary and metastatic tumors from PM patients were conducted. Results: 31 RCC patients with PM were identified. We observed remarkably favorable outcomes in our PM cohort, with a median overall survival (OS) of 10.7 years from metastatic diagnosis and a long latency between initial diagnosis and development of metastasis (median 69 months in patients who were non-metastatic at diagnosis). OS was independent of both metastatic tumor burden and known IMDC prognostic factors. We discovered that tumors from PM patients were markedly uniform and clustered together by gene expression analysis. WES and DNA copy number analyses revealed a high frequency of VHL and PBRM1 mutations, 3p loss, and 5q amplification, along with a lower frequency of 9p, 14q and 4q losses and BAP1 mutations, characteristic of indolent ccRCC. Furthermore, the genomic and histologic features of tumors from patients with PM can be recapitulated in patient-derived xenograft models. Conclusions: To our knowledge, this is the first report to unravel molecular determinants of organotropism, and we highlight that organotropism can be an independent prognostic factor. Understanding tumor heterogeneity may help refine prognostic models for metastatic RCC and hold implications for improved personalization of therapy.
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20

Yu, Tao, Cenzhu Wang, Mengyan Xie, Chengjun Zhu, Yongqian Shu, Jinhai Tang, and Xiaoxiang Guan. "Heterogeneity of CTC contributes to the organotropism of breast cancer." Biomedicine & Pharmacotherapy 137 (May 2021): 111314. http://dx.doi.org/10.1016/j.biopha.2021.111314.

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21

Rogava, Meri, Johannes C. Melms, Stephanie Davis, Clemens Hug, Bryan Ngo, Michael J. Lee, Patricia Ho, et al. "Abstract 981: A genetic-metabolic axis of metastatic liver organotropism." Cancer Research 82, no. 12_Supplement (June 15, 2022): 981. http://dx.doi.org/10.1158/1538-7445.am2022-981.

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Abstract Genomic and adaptive determinants of organ-specific metastasis are poorly understood. A model of sequential acquisition of divergent somatic mutations is insufficient to explain metastasis. Liver metastasis (LM) occurs frequently and is associated with a poor prognosis and reduced therapy response in several cancers, including in patients with melanoma and lung cancer. To identify drivers of metastatic niches, we used a syngeneic mouse melanoma model which recapitulates genomic, metastatic and therapy response patterns seen in patients. We performed a large-scale in vivo CRISPR-Cas9 knockout screen and identified perturbations that promote LM, but not primary tumor growth or metastasis to other organs (e.g. lung). The “top hit” in this screen associated with LM was loss Pip4k2c. We generated Pip4k2cKO cells and show that in otherwise isogenic melanoma cell lines, loss of Pip4k2c led to increased baseline and insulin-induced activation of the PI3K/AKT pathway, and increased invasive capacity. Rescuing Pip4k2cKO with full-length (Pip4k2cRec) or allosteric domain deficient (Pip4k2cAD) Pip4k2c ORFs, we show that hyperactivation of the PI3K/AKT pathway in is mediated by loss of the allosteric domain function, and not loss of the kinase domain of Pip4k2c. Treatment with different PI3K inhibitors effectively abrogated the pathway, but was partly bypassed in the presence of insulin in Pip4k2cKO and Pip4k2cAD, but not parental or Pip4k2cRec cells. Upon tail vein injection, Pip4k2cKO cells produced a significantly increased LM burden compared to parental cells, and this effect was rescued in Pip4k2cRec but not Pip4k2cAD, further affirming that loss of allosteric domain was required for this phenotype. We reasoned that Pip4k2cKO cells preferentially colonized the liver by co-opting the insulin-rich milieu in this organ. To test this, we used shRNA targeted against the insulin receptor (Insr) generated Pip4k2cKO/InsrshIR and showed that Insr was required but not sufficient to enhance LM burden. Given the promising in vitro activity of PI3K inhibitors, we next tested whether these could abrogate LM in vivo. Surprisingly, we found a substantial increase in LM burden in mice with Pip4k2cKO-bearing LM treated with PI3K inhibition compared to vehicle treated animals. We show that this paradoxical observation was due to host-mediated increased in glucose and insulin in response to PI3K inhibitor, which promoted a forward loop of increased liver metastasis. Breaking this loop with either ketogenic diet or treatment with a SGLT2 inhibitor in turn rescued increased these host responses and resulted in reduced LM burden in combination with PI3K inhibition. In summary, we identify a novel mechanism of metastatic liver organotropism and pharmacological and dietary combinations to reduced liver metastatic burden. Given the expanding use of PI3K inhibitors, our findings may have important clinical implications. Citation Format: Meri Rogava, Johannes C. Melms, Stephanie Davis, Clemens Hug, Bryan Ngo, Michael J. Lee, Patricia Ho, Amit Dipak Amin, Yiping Wang, Sean Chen, William Ge, David Liu, Thomas Tüting, Martin Röcken, Thomas K. Eigentler, Samuel F. Bakhoum, Andrei Molotkov, Akiva Mintz, Lewis C. Cantley, Peter K. Sorger, Benjamin Izar. A genetic-metabolic axis of metastatic liver organotropism [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 981.
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22

Nan, Xiang, Jiang Wang, Haowen Nikola Liu, Stephen T. C. Wong, and Hong Zhao. "Epithelial-Mesenchymal Plasticity in Organotropism Metastasis and Tumor Immune Escape." Journal of Clinical Medicine 8, no. 5 (May 25, 2019): 747. http://dx.doi.org/10.3390/jcm8050747.

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Most cancer deaths are due to metastasis, and almost all cancers have their preferential metastatic organs, known as “organotropism metastasis”. Epithelial-mesenchymal plasticity has been described as heterogeneous and dynamic cellular differentiation states, supported by emerging experimental evidence from both molecular and morphological levels. Many molecular factors regulating epithelial-mesenchymal plasticity have tissue-specific and non-redundant properties. Reciprocally, cellular epithelial-mesenchymal plasticity contributes to shaping organ-specific pre-metastatic niche (PMN) including distinct local immune landscapes, mainly through secreted bioactive molecular factors. Here, we summarize recent progress on the involvement of tumor epithelial-mesenchymal plasticity in driving organotropic metastasis and regulating the function of different immune cells in organ-specific metastasis.
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23

Reichert, Maximilian, Basil Bakir, Leticia Moreira, Jason R. Pitarresi, Karin Feldmann, Lauren Simon, Kensuke Suzuki, et al. "Regulation of Epithelial Plasticity Determines Metastatic Organotropism in Pancreatic Cancer." Developmental Cell 45, no. 6 (June 2018): 696–711. http://dx.doi.org/10.1016/j.devcel.2018.05.025.

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24

Azevedo, L. S., M. G. Almeida, W. R. Bastos, M. S. Suzuki, M. C. N. N. Recktenvald, M. T. S. Bastos, C. S. Vergílio, and C. M. M. de Souza. "Organotropism of methylmercury in fish of the southeastern of Brazil." Chemosphere 185 (October 2017): 746–53. http://dx.doi.org/10.1016/j.chemosphere.2017.07.081.

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25

Rolle, M. "Organotropismus der Brucellen bei nicht immunen und immunisierten Meerßchweinchen*." Zentralblatt für Veterinärmedizin 6, no. 8 (May 13, 2010): 714–22. http://dx.doi.org/10.1111/j.1439-0442.1959.tb00615.x.

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26

Hu, G., Y. Kang, and X. F. Wang. "From Breast to the Brain: Unraveling the Puzzle of Metastasis Organotropism." Journal of Molecular Cell Biology 1, no. 1 (July 24, 2009): 3–5. http://dx.doi.org/10.1093/jmcb/mjp005.

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27

Wei, Shi, and Gene P. Siegal. "Surviving at a distant site: The organotropism of metastatic breast cancer." Seminars in Diagnostic Pathology 35, no. 2 (March 2018): 108–11. http://dx.doi.org/10.1053/j.semdp.2017.11.008.

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28

Rogava, Meri, Tyler Joseph Aprati, Wei-Yu Chen, Johannes Melms, Clemens Hug, Amit Dipak Amin, Bryan Ngo, et al. "Abstract 3514: A genetic-metabolic circuit of liver-specific metastatic organotropism." Cancer Research 83, no. 7_Supplement (April 4, 2023): 3514. http://dx.doi.org/10.1158/1538-7445.am2023-3514.

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Abstract Liver metastasis (LM) occurs frequently in patients with melanoma and is associated with a poor prognosis and reduced therapy response. To identify drivers of metastatic niches, we used a syngeneic mouse melanoma model which recapitulates genomic, metastatic and therapy response patterns seen in patients, and performed a large-scale in vivo CRISPR-Cas9 knockout screen, which identified perturbations that strongly promoted liver but not lung metastasis. The “top hit” in this screen associated with LM was loss Pip4k2c. Mechanistically, loss of Pip4k2c sensitized both mouse and human melanoma to insulin-mediated PI3K/AKT pathway activation. Interestingly, this observation was dependent on the allosteric but not kinase domain activity. Treatment with different PI3K inhibitors abrogated the pathway in vitro, but was partly bypassed in the presence of insulin. As expected, loss of Pip4k2c was associated with significant increase in LM but not lung-metastatic burden in both syngeneic and patient-derived xenograft models, and this phenotype was rescued by reconstitution of full-length, but not allosteric domain deficient Pip4k2c constructs. We reasoned that Pip4k2cKO cells preferentially colonized the liver by co-opting the insulin-rich milieu in this organ. To test this, we generated Pip4k2c-/-/InsrshIR-KD and showed that Insr was required but not sufficient to enhance LM burden. Surprisingly, treatment with PI3K inhibition in vivo resulted in increased and not decreased LM burden as we had expected. PET-CT imaging of animals treated with PI3K revealed increased glucose uptake in LM in the presence of PI3K inhibition. We therefore reasoned that paradoxical activation due to host-mediated increase in glucose and insulin in response to PI3K inhibitor, may results in increased homing and metastasis to the liver. In further in vivo experiments, we showed that breaking this loop with either SGLT2 inhibitor or ketogenic diet circumvented host responses and resulted in reduced LM burden, while having no effect on lung metastasis burden. To further substantiate these findings, we performed single cell RNA-seq of concurrent liver and lung metastasis bearing mice which revealed strong tumor-intrinsic enrichment of central carbon metabolism. Lastly, analysis of 243 human liver vs extra-hepatic metastases across 75 cancers and addition of newly generated RNA-seq data of additional melanoma LM, revealed concordant pathways enrichment of glycolysis and oxidative phosphorylation LM. Together, we identify an axis of liver-metastatic organotropism that can be abrogated with a combination of PI3K inhibition and SGLT2-inhibition or concurrent ketogenic diet. Citation Format: Meri Rogava, Tyler Joseph Aprati, Wei-Yu Chen, Johannes Melms, Clemens Hug, Amit Dipak Amin, Bryan Ngo, Michae l Lee, Patricia Ho, Yiping Wang, Stephen Tang, Ethan Earlie, Sean Chen, Thomas Tüting, Martin Röcken, Thomas K. Eigentler, Samuel F. Bakhoum, Andrei Molotkov, Akiva Mintz, Dirk Schadendorf, Lewis C. Cantley, Peter K. Sorger, Ashley Laughney, David Liu, Benjamin Izar. A genetic-metabolic circuit of liver-specific metastatic organotropism [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3514.
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Cardone, Rosa Angela, Maria Raffaella Greco, Mattia Capulli, Edward J. Weinman, Giovanni Busco, Antonia Bellizzi, Valeria Casavola, et al. "NHERF1 acts as a molecular switch to program metastatic behavior and organotropism via its PDZ domains." Molecular Biology of the Cell 23, no. 11 (June 2012): 2028–40. http://dx.doi.org/10.1091/mbc.e11-11-0911.

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Metastatic cells are highly plastic for differential expression of tumor phenotype hallmarks and metastatic organotropism. The signaling proteins orchestrating the shift of one cell phenotype and organ pattern to another are little known. Na+/H+ exchanger regulatory factor (NHERF1) is a molecular pathway organizer, PDZ-domain protein that recruits membrane, cytoplasmic, and cytoskeletal signaling proteins into functional complexes. To gain insight into the role of NHERF1 in metastatic progression, we stably transfected a metastatic breast cell line, MDA-MB-231, with an empty vector, with wild-type NHERF1, or with NHERF1 mutated in either the PDZ1- or PDZ2-binding domains to block their binding activities. We observed that NHERF1 differentially regulates the expression of two phenotypic programs through its PDZ domains, and these programs form the mechanistic basis for metastatic organotropism. The PDZ2 domain promotes visceral metastases via increased invadopodia-dependent invasion and anchorage-independent growth, as well as by inhibition of apoptosis, whereas the PDZ1 domain promotes bone metastases by stimulating podosome nucleation, motility, neoangiogenesis, vasculogenic mimicry, and osteoclastogenesis in the absence of increased growth or invasion. Collectively, these findings identify NHERF1 as an important signaling nexus for coordinating cell structure with metastatic behavior and identifies the “mesenchymal-to-vasculogenic” phenotypic transition as an essential step in metastatic progression.
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30

Yao, Xiao-Hong, Tao Luo, Yu Shi, Zhi-Cheng He, Rui Tang, Pei-Pei Zhang, Jun Cai, et al. "A cohort autopsy study defines COVID-19 systemic pathogenesis." Cell Research 31, no. 8 (June 16, 2021): 836–46. http://dx.doi.org/10.1038/s41422-021-00523-8.

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AbstractSevere COVID-19 disease caused by SARS-CoV-2 is frequently accompanied by dysfunction of the lungs and extrapulmonary organs. However, the organotropism of SARS-CoV-2 and the port of virus entry for systemic dissemination remain largely unknown. We profiled 26 COVID-19 autopsy cases from four cohorts in Wuhan, China, and determined the systemic distribution of SARS-CoV-2. SARS-CoV-2 was detected in the lungs and multiple extrapulmonary organs of critically ill COVID-19 patients up to 67 days after symptom onset. Based on organotropism and pathological features of the patients, COVID-19 was divided into viral intrapulmonary and systemic subtypes. In patients with systemic viral distribution, SARS-CoV-2 was detected in monocytes, macrophages, and vascular endothelia at blood–air barrier, blood–testis barrier, and filtration barrier. Critically ill patients with long disease duration showed decreased pulmonary cell proliferation, reduced viral RNA, and marked fibrosis in the lungs. Permanent SARS-CoV-2 presence and tissue injuries in the lungs and extrapulmonary organs suggest direct viral invasion as a mechanism of pathogenicity in critically ill patients. SARS-CoV-2 may hijack monocytes, macrophages, and vascular endothelia at physiological barriers as the ports of entry for systemic dissemination. Our study thus delineates systemic pathological features of SARS-CoV-2 infection, which sheds light on the development of novel COVID-19 treatment.
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31

Sellner, Franz, Sabine Thalhammer, and Martin Klimpfinger. "Isolated Pancreatic Metastases of Renal Cell Carcinoma—Clinical Particularities and Seed and Soil Hypothesis." Cancers 15, no. 2 (January 4, 2023): 339. http://dx.doi.org/10.3390/cancers15020339.

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A meta-analysis of 1470 isolated pancreatic metastases of renal cell carcinoma revealed, that, in addition to the unusual exclusive occurrence of pancreatic metastases and the favourable treatment results, the isPMRCC is characterised by further peculiarities of the clinical course: The lack of prognostic significance of volume and growth rate dependent risk factors and the independence of treatment results from standard or local resections. As an explanation for all these peculiarities, according to today’s knowledge, a strong acting seed and soil mechanism can serve, which allows embolized tumour cells to grow to metastases only in the pancreas, and prevents them definitively or for years in all other organs. The good prognosis affects not only isolated PM, but also multi-organ metastases of the RCC, in which the additional occurrence of PM is also associated with a better prognosis. Genetic studies revealed specific changes in cases of PM of RCC: Lack of loss of 9p21.3 and 14q31.2, which are otherwise specific gene mutations at the onset of generalization, a low weight genome instability index, i.e., high genetic stability, and a low rate of PAB1 and a high rate of BPRM1 alterations, which signal a more favourable course. The cause of pancreatic organotropism in isPMRCC is still unclear, so only those factors that have been identified as promoting organotropism in other, more frequent tumour entities can be presented: Formation of the pre-metastatic niche, chemokine receptor–ligand mechanism, ability to metabolic adaptation, and immune surveillance.
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Zielinski, Rafal J., Krzysztof Grela Grela, Roberto Cardenas-Zuniga, Stanislaw Skora, Izabela Fokt, Edward Felix, Damian Grybowski, and Waldemar Priebe. "Abstract 4048: New approach to target metastatic colorectal cancer organotropism with L-Annamycin." Cancer Research 82, no. 12_Supplement (June 15, 2022): 4048. http://dx.doi.org/10.1158/1538-7445.am2022-4048.

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Abstract Colorectal cancer (CRC) is a frequently occurring disease and the second most common cause of cancer deaths when men and women are combined. CRC metastasis is strongly associated with mortality. The liver and lungs are the most frequent sites of distant disease, accounting for ~70% and ~12% of cases, respectively. We hypothesize that anticancer agents that mimic the organotropism of metastatic CRC will be highly effective in treating CRC patients. Our studies have identified that Annamycin (ANN), a potent topoisomerase II poison that displays organotropism imitating that of metastatic CRC. ANN is an analog of doxorubicin (Dox) that shows unique properties. Notably, ANN is active against multidrug-resistant tumors and undergoes efficient uptake by lungs and liver. ANN is easily formulated in multilamellar liposomes (L-ANN), which further increases ANN levels in lungs and liver. Objective. The objective of this study was to assess the efficacy of L-ANN in experimental CRC liver and lung metastasis models. Methods. The efficacy of L-ANN was tested in syngeneic models of metastatic CRC established in lungs or liver. For lung metastasis model, CT26-Luc cells were injected intravenously (IV) into Balb/c mice, followed by weekly IV treatment of L-ANN (4 and 6 mg/kg). The liver metastatic model was established using intrasplenic injection protocol. Mice received six weekly IV injections of 4 mg/kg of L-ANN or vehicle. Bioluminescent imaging (BLI), Magnetic Resonance Imaging (MRI) or Computer Tomography (CT) were used to track tumor progression. Results. L-ANN exhibited robust antitumor activity in both models. In the lung metastasis model, a dose-dependent delay in the tumor progression was visualized by both BLI and CT scan in the L-ANN treated group. The delay correlated with 272% extension of survival in the group receiving 6 mg/kg L-ANN [median survival (MS) 79d for treated vs 29d vehicle, p<0.0001] and 234% for the animals dosed with L-ANN at 4 mg/kg [MS 68d, p=0.0012]. In the liver metastasis model, all vehicle-treated mice showed massive tumors in the liver and peritoneal cavity as monitored by BLI and MRI. In the vehicle group, 13/14 died or were euthanized by 35d (median survival was 34.5d). Yet, no tumors were detected by BLI or MRI in L-ANN treated mice as of 44d and 0/14 mice died (100% survival). This indicates a highly significant (P< 0.0001) extension of survival (ongoing experiment). Conclusion. In summary, the strategy to develop anticancer agents that imitate metastatic CRC organotropism appears to be highly promising and is supported by these results. Our previous in vivo studies of L-ANN in sarcoma lung metastasis models already led to initiation of multicenter clinical studies (NCT04887298). This study demonstrating L-ANN efficacy in CRC models provides convincing evidence for further preclinical development aimed at initiation of clinical studies in CRC metastatic patients. Citation Format: Rafal J. Zielinski, Krzysztof Grela Grela, Roberto Cardenas-Zuniga, Stanislaw Skora, Izabela Fokt, Edward Felix, Damian Grybowski, Waldemar Priebe. New approach to target metastatic colorectal cancer organotropism with L-Annamycin [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 4048.
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Antimisiaris, Sophia, Spyridon Mourtas, and Antonia Marazioti. "Exosomes and Exosome-Inspired Vesicles for Targeted Drug Delivery." Pharmaceutics 10, no. 4 (November 6, 2018): 218. http://dx.doi.org/10.3390/pharmaceutics10040218.

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The similarities between exosomes and liposomes, together with the high organotropism of several types of exosomes, have recently prompted the development of engineered-exosomes or exosome-mimetics, which may be artificial (liposomal) or cell-derived vesicles, as advanced platforms for targeted drug delivery. Here, we provide the current state-of-the-art of using exosome or exosome-inspired systems for drug delivery. We review the various approaches investigated and the shortcomings of each approach. Finally the challenges which have been identified to date in this field are summarized.
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Keller, Georg v. "Stellungnahme zur Arbeit E. H. SCHMEER: RADEMACHER und die Organotropie." Allgemeine Homöopathische Zeitung 225, no. 03 (April 10, 2007): 119–20. http://dx.doi.org/10.1055/s-2006-935895.

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Xu, F., L. Yang, C. Liu, J. Ying, and Y. Wang. "P04.10 Relapsed or Metastatic Organotropism in Early Stage Lung Cancer after Radical Surgery." Journal of Thoracic Oncology 16, no. 3 (March 2021): S264—S265. http://dx.doi.org/10.1016/j.jtho.2021.01.389.

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Spoof, Lisa, Svetlana Klimova, Andrey Mikhailov, John E. Eriksson, and Jussi Meriluoto. "Synthesis and organotropism of 3H-dihydro derivatives of the cyanobacterial peptide hepatotoxin nodularin." Toxicon 41, no. 2 (February 2003): 153–62. http://dx.doi.org/10.1016/s0041-0101(02)00245-3.

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Pretzsch, E., F. Bösch, J. Neumann, P. Ganschow, A. Bazhin, M. Guba, J. Werner, and M. Angele. "Mechanisms of Metastasis in Colorectal Cancer and Metastatic Organotropism: Hematogenous versus Peritoneal Spread." Journal of Oncology 2019 (September 19, 2019): 1–13. http://dx.doi.org/10.1155/2019/7407190.

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Metastasis is the major cause of death in patients with colorectal carcinoma (CRC). The most common sites of metastasis are the liver and the peritoneum. Peritoneal carcinomatosis is often considered the end stage of the disease after the tumor has spread to the liver. However, almost half of CRC patients with peritoneal carcinomatosis do not present with liver metastasis. This brings up the question of whether peritoneal spread can still be considered as the end stage of a metastasized CRC or whether it should just be interpreted as a site of metastasis alternative to the liver. This review tries to discuss this question and summarize the current status of literature on potential characteristics in tumor biology in the primary tumor, i.e., factors (transcription factors and direct and indirect E-cadherin repressors) and pathways (WNT, TGF-β, and RAS) modulating EMT, regulation of EMT on a posttranscriptional and posttranslational level (miRNAs), and angiogenesis. In addition to tumor-specific characteristics, factors in the tumor microenvironment, immunological markers, ways of transport of tumor cells, and adhesion molecules appear to differ between hematogenous and peritoneal spread. Factors such as integrins and exosomal integrins, cancer stem cell phenotype, and miRNA expression appear to contribute in determining the metastatic route. We went through each step of the metastasis process comparing hematogenous to peritoneal spread. We identified differences with respect to organotropism, epithelial-mesenchymal transition, angiogenesis and inflammation, and tumor microenvironment which will be further elucidated in this review. A better understanding of the underlying mechanisms and contributing factors of metastasis development in CRC has huge relevance as it is the foundation to help find specific targets for treatment of CRC.
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Abdou, Melina, Beñat Zaldibar, Rebeca Medrano, Jörg Schäfer, Urtzi Izagirre, Lionel Dutruch, Alexandra Coynel, Gérard Blanc, and Manu Soto. "Organotropism and biomarker response in oyster Crassostrea gigas exposed to platinum in seawater." Environmental Science and Pollution Research 27, no. 4 (October 24, 2018): 3584–99. http://dx.doi.org/10.1007/s11356-018-3443-7.

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Zielinski, Rafal J., Krzysztof Grela, Shaohua Peng, Edd Felix, Roberto Cardenas-Zuniga, Damian Grybowski, Stanislaw Skora, Izabela Fokt, and Waldemar Priebe. "Abstract 4947: Exploration of Annamycin Organotropism to Target Primary and Metastatic Liver Cancers." Cancer Research 83, no. 7_Supplement (April 4, 2023): 4947. http://dx.doi.org/10.1158/1538-7445.am2023-4947.

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Abstract Background. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and is responsible for more than 12,000 deaths per year in the US. In addition to primary tumors, the liver is a common site for metastases of many types of cancer, including colorectal, and pancreatic cancer. The life expectancy and outlook for people with liver metastases are typically poor.Annamycin (ANN) is a novel anthracycline of our design that is clinically evaluated as a liposome formulated drug product, L-ANN. ANN and L-ANN display unique organotropism that differs from doxorubicin (DOX). In addition, ANN was shown to have increased potency against multidrug resistant cancer cell lines, and, importantly, L-ANN appeared to be non-cardiotoxic. Objective. The objective of this study was to analyze the pharmacokinetics of two formulations of ANN in the liver in comparison with DOX and to determine its tumoricidal potential in an HCC model in situ and in an experimental model of liver metastasis. Methods. The pharmacokinetics and tissue-organ distribution studies of L-ANN, free ANN, or DOX were performed in mice and rats. The levels of ANN and DOX in plasma and tissue homogenates were assessed using LC/MS. The antitumor efficacy of L-ANN was studied using HEPA 1-6 hepatocellular carcinoma models (subcutaneous, orthotopic, and experimental liver metastatic models) and compared with CT26 colon cancer liver metastasis experiments.Results. ANN exhibited dramatically higher accumulation in the liver parenchyma when compared to DOX (6-fold higher AUC values). We found that the increased liver uptake of the drug had a direct effect on activity of the drug in vivo. First, we observed clear, dose-dependent inhibition of the subcutaneous tumor growth after systemic (IV) administration of L-ANN. Next, remarkable activity of L-ANN was observed in orthotopic models. For instance, significant inhibition of the tumor growth and extension of the survival of L-ANN treated mice vs. vehicle-receiving animals was observed in HEPA 1-6 models (median survival 29.5 vs 50 days (p<0.0001) and 28 vs 59 days (p<0.0001), respectively). The significant delay in tumor progression was similar to that recorded in the CT26 experimental metastatic models, and L-ANN treatment strongly correlated with survival in this model as well (median survival 32 vs 53 days in L-ANN and vehicle groups, respectively, p<0.0001).Conclusions. Annamycin is a potent, non-cardiotoxic anthracycline with proven in vivo activity against different types of tumors. It showed increased penetration and accumulation in the liver, which correlated with high antitumor activity in HEPA 1-6 hepatocellular carcinoma and CT26 colon cancer liver metastasis models. Expanded studies to assess L-ANN activity in different tumor liver metastasis models as well as HCC models are being planned. It should be noted that L-ANN is currently undergoing clinical trials in patients with pulmonary metastasis soft tissue sarcoma and acute myeloid leukemia. Citation Format: Rafal J. Zielinski, Krzysztof Grela, Shaohua Peng, Edd Felix, Roberto Cardenas-Zuniga, Damian Grybowski, Stanislaw Skora, Izabela Fokt, Waldemar Priebe. Exploration of Annamycin Organotropism to Target Primary and Metastatic Liver Cancers. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4947.
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Aprati, Tyler J., Michael P. Manos, Will Ge, Giuseppe Tarantino, Xue Bai, Osama E. Rahma, Alexander Gusev, Genevieve Marie Boland, Kenneth L. Kehl, and David Liu. "Leveraging longitudinal clinical annotations and panel sequencing to characterize dynamics of organotropism in metastatic melanoma." Journal of Clinical Oncology 41, no. 16_suppl (June 1, 2023): 9526. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.9526.

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9526 Background: Although metastasis plays a major role in the mortality and morbidity of melanoma, patterns of metastasis and drivers of organotropism have not been well characterized clinically. Although previous efforts have been made to examine genomic drivers of organotropism, a longitudinal examination of metastasis dynamics has not been well characterized clinically. Methods: To address these questions, we leveraged a clinico-genomic dataset of patients with metastatic melanoma (Kehl et al. 2021). From this dataset, we assembled a cohort consisting of 26,143 artificial intelligence-annotated imaging reports from 879 patients with metastatic melanoma with an average of 2 years of followup after initial metastatic diagnosis. Annotated metastasis sites included brain, bone, adrenal, liver, lymph node, lung, and mesentery. All patients were evaluated at the Dana-Farber Cancer Institute, and each patient has at least one tumor biopsy sequenced with OncoPanel, a next-generation sequencing panel that identifies mutations in 447 cancer-related genes. Lifetime incidence of metastatic sites was defined as whether a patient ever had a report annotated with that site. Time-to-event analyses on metastatic sites used the acquisition of a metastatic site as the event of interest. For each patient index dates were defined as the date of the first scan with cancer present. We used cumulative incidence models to examine the incidence of each site in our cohort, and both cause-specific hazard models and Fine-Gray modeling to account for competing events and determine the effect of genomic covariates. Results: For lifetime metastasis status, the overall incidence varied by site, with LN being the most common, occurring in ~75% of patients, and mesentery the rarest, occurring in ~12% of patients. For lifetime metastasis status, patients with adrenal metastases were positively enriched for mutations in SETD2 (P < 0.005). Among the significant genes for all sites were many genes encoding epigenetic modifiers. In the time-to-event setting, the order of the cumulative incidence functions for each site matched the lifetime frequency of sites. Through time-to-event analysis we found genes whose mutant status were significantly associated with a change in risk and/or rate of certain metastatic sites. Among other results, we found that having a mutation in SETD2 is significantly positively associated with an increase rate and risk of adrenal metastases (cause-specific HR 2.4, P < 0.005, Fine-Gray HR 2.6, P < 0.005), and NRAS mutations were significantly associated with lower rate and risk of liver metastasis (cause-specific HR 0.59 P < 0.05, Fine-Gray HR 0.58 P < 0.01). Conclusions: By using time-to-event analysis with longitudinal metastatic annotations, we identify potential drivers of organotropism in melanoma patients.
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Coulton, Alexander, and Samra Turajlic. "Metastasis and organotropism: A look through the lens of large-scale clinical sequencing data." Cancer Cell 40, no. 2 (February 2022): 134–35. http://dx.doi.org/10.1016/j.ccell.2022.01.011.

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42

Monte, Maria J., Maria R. Ballestero, Oscar Briz, Maria J. Perez, and Jose J. G. Marin. "Proapoptotic Effect on Normal and Tumor Intestinal Cells of Cytostatic Drugs with Enterohepatic Organotropism." Journal of Pharmacology and Experimental Therapeutics 315, no. 1 (June 28, 2005): 24–35. http://dx.doi.org/10.1124/jpet.105.086165.

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43

Link, Jason M., Patrick J. Worth, Dove Keith, Sydney Owen, Alison Grossblatt-Wait, Carl Pelz, Hannah Holly, et al. "Abstract PR-007: Lung-tropic, liver-averse, primary PDAC tumors are associated with greater peripheral T cell diversity and have a unique, subtype-independent, gene-expression signature that significantly correlates with longer survival." Cancer Research 81, no. 22_Supplement (November 15, 2021): PR—007—PR—007. http://dx.doi.org/10.1158/1538-7445.panca21-pr-007.

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Abstract Pancreatic Ductal Adenocarcinoma (PDAC) is predicted to become the second leading cause of cancer-related death in the United States, and most patients who present with metastatic PDAC die within a year. However, we and others have found that patients with lung metastases in the absence of liver metastases survive significantly longer than patients who present with liver metastases. We analyzed an unpublished RNASeq dataset from ~300 tumor-enriched samples from primary and metastatic PDAC specimens. Consistent with many previous publications, we found that patients with basal/squamoid-subtype tumors had significantly worse outcomes than patients with classical/ductal-subtype tumors. Additionally, we identified that most primary tumors from patients who develop lung – but not liver – metastases are classical subtype. However, this association did not wholly account for the pro-survival effect of lung-tropic, liver-averse metastatic disease because patients with lung-tropic, liver-averse, classical-subtype, primary tumors had significantly better outcomes than patients with liver-tropic, classical-subtype tumors. To identify and parse metastatic organotropism from subtype, we used organotropism-independent and subtype-independent, primary-tumor training cohorts to generate two non-overlapping gene sets that were significantly enriched in test cohorts of either primary, basal-subtype or liver-tropic tumors over primary tumors that were classical-subtype or lung-tropic and liver-averse, respectively. When applied to all primary tumors in our dataset, both the subtype-specific and organotropism-specific gene sets significantly correlated with patient outcome. From an unpublished analysis of TCRbeta CDR3 sequences from ~250 paired blood and primary tumor samples, we identified significantly greater TCRbeta diversity in blood and primary tumors from patients with lung-tropic, liver-averse disease. Additionally, we found evidence that TCRbeta rearrangements from liver-tropic primary tumors were more likely to be found in autologous peripheral blood samples than TCRbeta rearrangements from lung-tropic, liver-averse primary tumors. We also found that TCRbeta sequences were often shared between samples from patients with liver-tropic disease but never shared between samples from patients with lung-tropic, liver-averse disease. Overall, our results point to a lung-tropic, liver-averse form of PDAC that – independent of tumor subtype – leads to positive outcomes, and that T cell diversity may have a causal relationship and/or may serve as a biomarker of long-term survival with lung-tropic, liver-averse disease. Citation Format: Jason M. Link, Patrick J. Worth, Dove Keith, Sydney Owen, Alison Grossblatt-Wait, Carl Pelz, Hannah Holly, Motoyuki Tsuda, Kevin MacPherson, Jonathan Brody, Charles Lopez, Brett C. Sheppard, Rosalie C. Sears. Lung-tropic, liver-averse, primary PDAC tumors are associated with greater peripheral T cell diversity and have a unique, subtype-independent, gene-expression signature that significantly correlates with longer survival [abstract]. In: Proceedings of the AACR Virtual Special Conference on Pancreatic Cancer; 2021 Sep 29-30. Philadelphia (PA): AACR; Cancer Res 2021;81(22 Suppl):Abstract nr PR-007.
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Vis, Daniel, Sander Palit, Marie Corradi, Martijn Lolkema, Niven Mehra, Edwin Cuppen, Lodewyk FA Wessels, et al. "Abstract 972: MMR-deficiency is the most prominent genetic feature of prostate cancer metastases organotropism." Cancer Research 82, no. 12_Supplement (June 15, 2022): 972. http://dx.doi.org/10.1158/1538-7445.am2022-972.

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Abstract Prostate cancer (PCa) is the most prevalent, non-cutaneous, cancer in men in the Western world. Disease confined to the prostate can be cured, but metastatic disease cannot. PCa metastases are found in bone, lymph-nodes, liver and other visceral organs (visceral), in decreasing order of frequency. After an initial response to androgen receptor directed therapy, metastatic disease will inevitably recur as metastatic castration resistant prostate cancer (mCRPC), which is hallmarked by high morbidity and mortality. Since it is previously established, that the site of metastasis correlates with prostate cancer survival, we need a better understanding of metastatic organotropism. Therefore, we took advantage of the largest Whole Genome Sequencing (HiSeq X Ten system using the paired-end sequencing protocol) data set of mCRPC metastases to date. Molecular profiling of 326 metastases (Bone: 105, Lymph-node: 149, Liver: 49, Visceral: 23) revealed genetic determinants associated with organ-specific metastasis. First, we assessed differential occurrence of mutations in genes associated with targetable pathways. RB1 alteration were enriched in liver (35%) and in visceral metastases (30%), while lower rates were found in bone (10%) and lymph-nodes (13%)(Fisher exact test, p: 0.012). Analysis of aggregated pathway alteration data revealed a trend for increased frequency of alterations in the DNA repair and PI3K pathways in lymph node vs. bone metastases (p: 0.066 and 0.066, respectively). Next, we explored differential tumor mutational burden (TMB) between the sites. A higher TMB was observed in liver and visceral metastases compared to bone and lymph node metastases, while there was no difference between liver and visceral. The increased TMB in liver and visceral samples was associated with an MMR-deficiency mutational signature. Alterations in MSH6, MLH1 and POLD3 characterized a significant proportion of high TMB liver metastases, whereas high TMB visceral metastases predominantly showed MSH2 and POLD1 alterations.In conclusion: Our findings implicate high TMB/MMR-deficiency is a characteristic feature of liver and visceral PCa metastases, potentially impacting disease progression. Moreover, since response to immune check-point inhibitors is associated with high TMB, our findings might direct choice of therapy. Citation Format: Daniel Vis, Sander Palit, Marie Corradi, Martijn Lolkema, Niven Mehra, Edwin Cuppen, Lodewyk FA Wessels, Rene Bernards, Wilbert Zwart, Michiel S. van der Heijden, Andries M. Bergman. MMR-deficiency is the most prominent genetic feature of prostate cancer metastases organotropism [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 972.
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Greco, Maria Raffaella, Emeline Bon, Rosa Rubino, Lorenzo Guerra, Manuel Bernabe-Garcia, Stefania Cannone, Maria-Luisa Cayuela, et al. "Phosphorylation of NHERF1 S279 and S301 differentially regulates breast cancer cell phenotype and metastatic organotropism." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1865, no. 1 (January 2019): 26–37. http://dx.doi.org/10.1016/j.bbadis.2018.10.017.

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Larena, Monica G., Maria C. Martinez-diez, Maria J. Monte, Maria F. Dominguez, Maria J. Pascual, and Jose J. G. Marin. "Liver Organotropism and Biotransformation of a Novel Platinum-Ursodeoxycholate Derivative, Bamet-UD2, with Enhanced Antitumour Activity." Journal of Drug Targeting 9, no. 3 (January 2001): 185–200. http://dx.doi.org/10.3109/10611860108997927.

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Gestin, Ophélia, Thomas Lacoue-Labarthe, Marina Coquery, Nicolas Delorme, Laura Garnero, Lysiane Dherret, Théo Ciccia, Olivier Geffard, and Christelle Lopes. "One and multi-compartments toxico-kinetic modeling to understand metals’ organotropism and fate in Gammarus fossarum." Environment International 156 (November 2021): 106625. http://dx.doi.org/10.1016/j.envint.2021.106625.

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Benke, R., and V. Schirrmacher. "Change in organotropism of mouse lymphoma variants associated with selective chemotactic responsiveness to organ-derived chemoattractants." Clinical & Experimental Metastasis 9, no. 3 (May 1991): 205–19. http://dx.doi.org/10.1007/bf01753725.

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Haaf, H., and M. Metzler. "Covalent binding of diethylstilbestrol to microsomal protein in vitro correlates with the organotropism of its carcinogenicity." Carcinogenesis 6, no. 4 (1985): 659–60. http://dx.doi.org/10.1093/carcin/6.4.659.

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Lengel, H. "MA05.09 Genomic Mapping of Metastatic Organotropism: Analysis of 2326 Primary and Organ-Specific Metastases in Lung Adenocarcinoma." Journal of Thoracic Oncology 17, no. 9 (September 2022): S62—S63. http://dx.doi.org/10.1016/j.jtho.2022.07.105.

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