Erratum: Corrigendum: Mechanism of early dissemination and metastasis in Her2+ mammary cancer

Harper, Kathryn; Sosa, María Soledad; Entenberg, David; Hosseini, Hedayatollah; Cheung, Julie F.; Nobre, Ana Rita; Avivar-Valderas, Álvaro; Nagi, Chandandaneep; Girnius, Nomeda; Davis, Roger J.; Farías, Eduardo; Condeelis, John S.; Aguirre‐Ghiso, Julio A.

doi:10.1038/nature24666

Cited by 12 publications

(9 citation statements)

References 1 publication

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“…Disseminated cancer cells detected in patients before the manifestation of breast-cancer metastasis contain fewer genetic abnormalities than primary tumors or than tumors of patients with metastases (Klein et al, 1999;Schmidt-Kittler et al, 2003;Schardt et al, 2005). These findings, and others documented in pancreatic cancer (Rhim et al, 2012) and melanoma (Eyles et al, 2010) models, indicate that dissemination might occur during the early stages of tumor evolution (Schardt et al, 2005;Husemann et al, 2008;Sänger et al, 2011;Harper et al, 2018). However, the mechanisms that might allow early-disseminated cancer cells to complete all steps of metastasis are unknown.…”

Section: Introductionmentioning

confidence: 68%

Stem–Mesenchymal Signature Cell Genes Detected in Heterogeneous Circulating Melanoma Cells Correlate With Disease Stage in Melanoma Patients

Rapanotti

Campione

Viguria

et al. 2020

Front. Mol. Biosci.

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During the process of metastasis, cancer cells dissociate from primary tumors, migrate to distal sites, and finally colonize, eventually leading to the formation of metastatic tumors. These cancer cells, defined circulating tumor cells (CTCs) spreading through the blood stream, may develop metastatic lesions or remain dormant. Some emerging clinical evidence supports that some tumor cells may possess metastatic properties already in the earlier stages of tumorigenesis. Because the initiation and progression of vertical growth in human melanoma is fundamental to the notion of tumor virulence and progression, we decided to immune-magnetic collect and molecularly characterize circulating melanoma cells (CMCs) from melanoma patients AJCC staged = pT1b (i.e., transition from radial to vertical phase). CMCs are phenotypically and molecularly heterogeneous, thus we performed a "home-made Liquid-Biopsy," by targeting the melanoma-associated-antigen, MCAM/MUC18/CD146, and/or the melanoma-initiating marker, ABCB5. We assessed a biomarker qualitative expression panel, contemplating the angiogenic-potential, melanoma-initiating and melanoma-differentiation drivers, cellcell adhesion molecules, matrix-metallo-proteinases, which was performed on three enriched subpopulations from a total of 61 blood-samples from 21 melanoma patients. At first, a significant differential expression of the specific transcripts was documented between and within the CMC fractions enriched with MCAM-, ABCB5-, and both MCAM/ABCB5-coated beads, when analyzing two distinct groups: early AJCC-(stage I-II) and advanced-staged patients (stage II-IV). Moreover, in the early-AJCC stagedgroup, we could distinguish "endothelial," CD45 − MCAM + enriched-, "stem" S-CMCs, CD45 − ABCB5 + enriched-and a third hybrid bi-phenotypic CD45 − MCAM + /ABCB5 + enriched-fractions, due to three distinct gene-expression profiles. In particular, the endothelial-CMCs were characterized by positive expression of genes involved in

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Section: Introductionmentioning

confidence: 68%

Stem–Mesenchymal Signature Cell Genes Detected in Heterogeneous Circulating Melanoma Cells Correlate With Disease Stage in Melanoma Patients

Rapanotti

Campione

Viguria

et al. 2020

Front. Mol. Biosci.

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“…How and when tumors become invasive in patients? Are the early or late disseminated tumor cells from the primary tumor responsible for initiating metastasis in patients (35, 36)? Do the early disseminators aid in developing pre-metastatic niche (37, 38)?…”

Section: Dissemination: Get Out Of Dodgementioning

confidence: 99%

Metastatic Latency, a Veiled Threat

2019

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Metastatic relapse is observed in cancer patients with no clinical evidence of disease for months to decades after initial diagnosis and treatment. Disseminated cancer cells that are capable of entering reversible cell cycle arrest are believed to be responsible for these late metastatic relapses. Dynamic interactions between the latent disseminated tumor cells and their surrounding microenvironment aid cancer cell survival and facilitate escape from immune surveillance. Here, we highlight findings from preclinical models that provide a conceptual framework to define and target the latent metastatic phase of tumor progression. The hope is by identifying patients harboring latent metastatic cells and providing therapeutic options to eliminate metastatic seeds prior to their emergence will result in long lasting cures.

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“…Accumulating evidence indicates that insulin resistance plays a critical role in the development of AD ( Frame and Zheleva, 2006 ; Liu et al, 2011 ; Morris and Burns, 2012 ; Son et al, 2012 ; Talbot et al, 2012 ; Chen and Zhong, 2013 ; Cai et al, 2015 ; Mullins et al, 2017 ). Insulin signaling regulates amyloid precursor protein (APP) metabolism through α-, β-, and γ-secretases.…”

Section: Insulin Resistance In Admentioning

confidence: 99%

“…Aberrant phosphorylation of the tau protein in neurons is another important hallmark of AD. Interestingly, the tau phosphorylation levels are also greatly modulated by insulin signaling ( Mullins et al, 2017 ). In rodent models of insulin resistance, abundant phosphorylation of tau has been identified.…”

Section: Insulin Resistance In Admentioning

confidence: 99%

Suppressor of Cytokine Signaling 3: Emerging Role Linking Central Insulin Resistance and Alzheimer’s Disease

2018

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Currently, the etiology of Alzheimer’s disease (AD) is still elusive. Central insulin resistance has been determined to play an important role in the progress of AD. However, the mechanism underlying the development of disrupted insulin signaling pathways in AD is unclear. Suppressor of cytokine signaling 3 (SOCS3) is a member of the SOCS protein family that acts as a negative modulator of insulin signaling in sensitive tissues, such as hepatocytes and adipocytes. However, little is known about its role in neurological diseases. Recent evidence indicates that the level of SOCS3 is increased in the brains of individuals with AD, especially in areas with amyloid beta deposition, suggesting that SOCS3 may regulate the central insulin signaling pathways in AD. Here, we discuss the potential role of SOCS3 in AD and speculate that SOCS3 may be a promising therapeutic target for the treatment of AD.

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Erratum: Corrigendum: Mechanism of early dissemination and metastasis in Her2+ mammary cancer

Cited by 12 publications

References 1 publication

Stem–Mesenchymal Signature Cell Genes Detected in Heterogeneous Circulating Melanoma Cells Correlate With Disease Stage in Melanoma Patients

Stem–Mesenchymal Signature Cell Genes Detected in Heterogeneous Circulating Melanoma Cells Correlate With Disease Stage in Melanoma Patients

Metastatic Latency, a Veiled Threat

Suppressor of Cytokine Signaling 3: Emerging Role Linking Central Insulin Resistance and Alzheimer’s Disease

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