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Article ; Online: The blood-tumour barrier in cancer biology and therapy.

Steeg, Patricia S

2021 Volume 18, Issue 11, Page(s) 696–714

Abstract: The protective blood-brain barrier has a major role in ensuring normal brain function by severely limiting and tightly controlling the ingress of substances into the brain from the circulation. In primary brain tumours, such as glioblastomas, as well as ... ...

Abstract	The protective blood-brain barrier has a major role in ensuring normal brain function by severely limiting and tightly controlling the ingress of substances into the brain from the circulation. In primary brain tumours, such as glioblastomas, as well as in brain metastases from cancers in other organs, including lung and breast cancers and melanoma, the blood-brain barrier is modified and is referred to as the blood-tumour barrier (BTB). Alterations in the BTB affect its permeability, and this structure participates in reciprocal regulatory pathways with tumour cells. Importantly, the BTB typically retains a heterogeneous capacity to restrict the penetration of many therapeutic agents into intracranial tumours, and overcoming this challenge is a key to improving the effectiveness of treatment and patient quality of life. Herein, current knowledge of BTB structure and function is reviewed from a cell and cancer biology standpoint, with a focus on findings derived from in vivo models and human tumour specimens. Additionally, how this knowledge can be translated into clinical advances for patients with cancer is discussed.
MeSH term(s)	Blood-Brain Barrier/physiopathology ; Female ; Humans ; Male ; Neoplasms/physiopathology ; Neoplasms/therapy
Language	English
Publishing date	2021-07-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/s41571-021-00529-6
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Article ; Online: A perspective on the metastasis suppressor field.

Khan, Imran / Steeg, Patricia S

Cancer metastasis reviews

2023 Volume 42, Issue 4, Page(s) 1061–1063

Abstract: Metastasis is the leading cause of cancer patient mortality. Metastasis suppressors are genes that, upon reexpression in metastatic tumor cells to levels observed in their nonmetastatic counterparts, significantly reduce metastasis without affecting the ... ...

Abstract	Metastasis is the leading cause of cancer patient mortality. Metastasis suppressors are genes that, upon reexpression in metastatic tumor cells to levels observed in their nonmetastatic counterparts, significantly reduce metastasis without affecting the growth of the primary tumor. Analysis of > 30 metastasis suppressors revealed complex mechanisms of action that include multiple signaling pathways, transcriptional patterns, posttranscriptional regulatory mechanisms, and potential contributions of genomic stability. Clinical testing of strategies to re-establish a validated metastasis suppressor pathway in tumors is best directed to the adjuvant setting, with the goal of inhibiting the outgrowth of occult micrometastases.
MeSH term(s)	Humans ; Genes, Tumor Suppressor ; Neoplasms/genetics ; Neoplasms/pathology ; Signal Transduction ; Neoplasm Metastasis ; Gene Expression Regulation, Neoplastic
Language	English
Publishing date	2023-08-15
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1007/s10555-023-10131-0
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Article ; Online: Keeping brain metastases dormant.

Khan, Imran / Steeg, Patricia S

Nature cancer

2021 Volume 3, Issue 1, Page(s) 3–5

MeSH term(s)	Brain Neoplasms/therapy ; Humans
Language	English
Publishing date	2021-12-24
Publishing country	England
Document type	Journal Article ; Comment
ISSN	2662-1347
ISSN (online)	2662-1347
DOI	10.1038/s43018-021-00321-6
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Article ; Online: Endocytosis: a pivotal pathway for regulating metastasis.

Khan, Imran / Steeg, Patricia S

British journal of cancer

2020 Volume 124, Issue 1, Page(s) 66–75

Abstract: A potentially important aspect in the regulation of tumour metastasis is endocytosis. This process consists of internalisation of cell-surface receptors via pinocytosis, phagocytosis or receptor-mediated endocytosis, the latter of which includes clathrin- ...

Abstract	A potentially important aspect in the regulation of tumour metastasis is endocytosis. This process consists of internalisation of cell-surface receptors via pinocytosis, phagocytosis or receptor-mediated endocytosis, the latter of which includes clathrin-, caveolae- and non-clathrin or caveolae-mediated mechanisms. Endocytosis then progresses through several intracellular compartments for sorting and routing of cargo, ending in lysosomal degradation, recycling back to the cell surface or secretion. Multiple endocytic proteins are dysregulated in cancer and regulate tumour metastasis, particularly migration and invasion. Importantly, four metastasis suppressor genes function in part by regulating endocytosis, namely, the NME, KAI, MTSS1 and KISS1 pathways. Data on metastasis suppressors identify a new point of dysregulation operative in tumour metastasis, alterations in signalling through endocytosis. This review will focus on the multicomponent process of endocytosis affecting different steps of metastasis and how metastatic-suppressor genes use endocytosis to suppress metastasis.
MeSH term(s)	Cell Movement/physiology ; Endocytosis/physiology ; Humans ; Neoplasm Invasiveness/pathology ; Neoplasms/metabolism ; Neoplasms/pathology
Language	English
Publishing date	2020-12-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-020-01179-8
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Article ; Online: Targeting metastasis.

Steeg, Patricia S

Nature reviews. Cancer

2016 Volume 16, Issue 4, Page(s) 201–218

Abstract: Tumour metastasis, the movement of tumour cells from a primary site to progressively colonize distant organs, is a major contributor to the deaths of cancer patients. Therapeutic goals are the prevention of an initial metastasis in high-risk patients, ... ...

Abstract	Tumour metastasis, the movement of tumour cells from a primary site to progressively colonize distant organs, is a major contributor to the deaths of cancer patients. Therapeutic goals are the prevention of an initial metastasis in high-risk patients, shrinkage of established lesions and prevention of additional metastases in patients with limited disease. Instead of being autonomous, tumour cells engage in bidirectional interactions with metastatic microenvironments to alter antitumour immunity, the extracellular milieu, genomic stability, survival signalling, chemotherapeutic resistance and proliferative cycles. Can targeting of these interactions significantly improve patient outcomes? In this Review preclinical research, combination therapies and clinical trial designs are re-examined.
MeSH term(s)	Humans ; Neoplasm Metastasis/physiopathology ; Neoplasm Metastasis/prevention & control
Language	English
Publishing date	2016-03-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/nrc.2016.25
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Zs.A 5563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The relationship of NM23 (NME) metastasis suppressor histidine phosphorylation to its nucleoside diphosphate kinase, histidine protein kinase and motility suppression activities.

Khan, Imran / Steeg, Patricia S

Oncotarget

2018 Volume 9, Issue 12, Page(s) 10185–10202

Abstract: The NM23/NME gene was identified as a metastasis suppressor. It's re-expression inhibited cancer cell motility and suppressed metastasis, without effecting primary tumor size in multiple model systems. The mechanisms of NME suppression of motility and ... ...

Abstract	The NM23/NME gene was identified as a metastasis suppressor. It's re-expression inhibited cancer cell motility and suppressed metastasis, without effecting primary tumor size in multiple model systems. The mechanisms of NME suppression of motility and metastasis are incompletely known. Of particular interest, has been NME histidine 118 phosphorylation, involved in nucleoside diphosphate kinase (NDPK) and histidine protein kinase (HPK) activities. Using recently developed monoclonal antibodies to phosphohistidine, we have addressed the correlation of NME phosphohistidine with motility suppression, and distinguished the NDPK and HPK contributions. While general levels of NME correlated with its 1-phosphohistidine form in two cell line model systems, two exceptions were noted: Tumor cells actively migrating in scratch assays, even if expressing high levels of NME1, were low in its 1-phosphohistidine form. Site-directed mutagenesis of NME1 histidine 118 and proline 96 was examined by transfection experiments and partial purification of recombinant proteins. NME1
Language	English
Publishing date	2018-02-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.23796
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Article ; Online: Distinct uptake and elimination profiles for trastuzumab, human IgG and biocytin-TMR in experimental HER2+ brain metastases of breast cancer.

Silvestri, Vanesa L / Tran, Andy D / Chung, Monika / Chung, Natalie / Gril, Brunilde / Robinson, Christina / Difilippantonio, Simone / Wei, Debbie / Kruhlak, Michael J / Peer, Cody J / Figg, W Douglas / Khan, Imran / Steeg, Patricia S

Neuro-oncology

2024

Abstract: Background: The aim of this study is an improved understanding of drug distribution in brain metastases. Rather than single point snapshots, we analyzed the time course and route of drug/probe elimination (clearance), focusing on the Intramural ... ...

Abstract	Background: The aim of this study is an improved understanding of drug distribution in brain metastases. Rather than single point snapshots, we analyzed the time course and route of drug/probe elimination (clearance), focusing on the Intramural Periarterial Drainage (IPAD) pathway. Methods: Mice with JIMT1-BR HER2+ experimental brain metastases were injected with biocytin-TMR and either trastuzumab or human IgG. Drugs/probes circulated for 5 min-48h, followed by perfusion. Brain sections were stained for human IgG, vascular basement membrane proteins laminin or collagen IV, and periarterial α-SMA. A machine learning algorithm was developed to identify metastases, metastatic microenvironment, and uninvolved brain in confocally scanned brain sections. Drug/probe intensity over time and total imaged drug exposure (iAUC) were calculated for 27,249 lesions and co-immunofluorescence with IPAD- vascular matrix analyzed in 11,668 metastases. Results: In metastases, peak trastuzumab levels were 5-fold higher than human IgG but 4-fold less than biocytin-TMR. The elimination phase constituted 85-93% of total iAUC for all drugs/probes tested. For trastuzumab, total iAUC during uptake was similar to the small molecule drug probe biocytin-TMR, but slower trastuzumab elimination resulted in a 1.7-fold higher total iAUC. During elimination trastuzumab and IgG were preferentially enriched in the α-SMA+ periarterial vascular matrix, consistent with the IPAD clearance route; biocytin-TMR showed heterogeneous elimination pathways. Conclusions: Drug/probe elimination is an important component of drug development for brain metastases. We identified a prolonged elimination pathway for systemically administered antibodies through the periarterial vascular matrix that may contribute to the sustained presence and efficacy of large antibody therapeutics.
Language	English
Publishing date	2024-02-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2028601-6
ISSN	1523-5866 ; 1522-8517
ISSN (online)	1523-5866
ISSN	1522-8517
DOI	10.1093/neuonc/noae025
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Zs.A 5307: Show issues

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Article ; Online: Metastasis suppressors: functional pathways.

Khan, Imran / Steeg, Patricia S

Laboratory investigation; a journal of technical methods and pathology

2017 Volume 98, Issue 2, Page(s) 198–210

Abstract: Metastasis is a complex process and a major contributor of death in cancer patients. Metastasis suppressor genes are identified by their ability to inhibit metastasis at a secondary site without affecting the growth of primary tumor. In this review, we ... ...

Abstract	Metastasis is a complex process and a major contributor of death in cancer patients. Metastasis suppressor genes are identified by their ability to inhibit metastasis at a secondary site without affecting the growth of primary tumor. In this review, we have conducted a survey of the metastasis suppressor literature to identify common downstream pathways. The metastasis suppressor genes mechanistically target MAPK, G-protein-coupled receptor, cell adhesion, cytoskeletal, transcriptional regulatory, and metastasis susceptibility pathways. The majority of the metastasis suppressor genes are functionally multifactorial, inhibiting metastasis at multiple points in the cascade, and many operate in a context-dependent fashion. A greater understanding of common pathways/molecules targeted by metastasis suppressor could improve metastasis treatment strategies.
MeSH term(s)	Animals ; Cell Movement/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Models, Genetic ; Neoplasm Metastasis/genetics ; Neoplasms/genetics ; Neoplasms/pathology ; Signal Transduction/genetics ; Tumor Suppressor Proteins/genetics
Chemical Substances	Tumor Suppressor Proteins
Language	English
Publishing date	2017-10-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
DOI	10.1038/labinvest.2017.104
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Article ; Online: Perspective: The right trials.

Steeg, Patricia S

Nature

2012 Volume 485, Issue 7400, Page(s) S58–9

MeSH term(s)	Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Breast Neoplasms/drug therapy ; Breast Neoplasms/mortality ; Breast Neoplasms/pathology ; Clinical Trials as Topic/methods ; Clinical Trials as Topic/trends ; Denosumab ; Drug Industry ; Female ; Humans ; Neoplasm Metastasis/drug therapy ; Neoplasm Metastasis/pathology ; Neoplasm Metastasis/prevention & control ; Research Design/trends ; Sentinel Lymph Node Biopsy ; United States ; United States Food and Drug Administration
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Denosumab (4EQZ6YO2HI)
Language	English
Publishing date	2012-05-30
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/485S58a
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Article ; Online: Antibody-drug conjugates for cancer.

Chau, Cindy H / Steeg, Patricia S / Figg, William D

Lancet (London, England)

2019 Volume 394, Issue 10200, Page(s) 793–804

Abstract: Antibody-drug conjugates (ADCs) are immunoconjugates comprised of a monoclonal antibody tethered to a cytotoxic drug (known as the payload) via a chemical linker. The ADC is designed to selectively deliver the ultratoxic payload directly to the target ... ...

Abstract	Antibody-drug conjugates (ADCs) are immunoconjugates comprised of a monoclonal antibody tethered to a cytotoxic drug (known as the payload) via a chemical linker. The ADC is designed to selectively deliver the ultratoxic payload directly to the target cancer cells. To date, five ADCs have received market approval and over 100 are being investigated in various stages of clinical development. In this Therapeutics paper, we review recent clinical experience with the approved ADCs and other promising late-stage candidates on the horizon, following an overview of the biology and chemistry of ADCs and how the individual components of an ADC (antibody [or target], linker and conjugation chemistry, and cytotoxic payload) influence its activity. We briefly discuss opportunities for enhancing ADC efficacy, drug resistance, and future perspectives for this novel antibody-based molecular platform, which has great potential to make a paradigm shift in cancer chemotherapy.
MeSH term(s)	Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/adverse effects ; Antibodies, Monoclonal/pharmacokinetics ; Antibodies, Monoclonal/pharmacology ; Antineoplastic Agents, Immunological/administration & dosage ; Antineoplastic Agents, Immunological/adverse effects ; Antineoplastic Agents, Immunological/pharmacokinetics ; Antineoplastic Agents, Immunological/pharmacology ; Clinical Trials as Topic ; Humans ; Immunoconjugates/administration & dosage ; Immunoconjugates/adverse effects ; Immunoconjugates/pharmacokinetics ; Immunoconjugates/pharmacology ; Neoplasms/drug therapy
Chemical Substances	Antibodies, Monoclonal ; Antineoplastic Agents, Immunological ; Immunoconjugates
Language	English
Publishing date	2019-09-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	3306-6
ISSN	1474-547X ; 0023-7507 ; 0140-6736
ISSN (online)	1474-547X
ISSN	0023-7507 ; 0140-6736
DOI	10.1016/S0140-6736(19)31774-X
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