SCC178

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Showing 1-11 of 11 results for "SCC178" within Papers

Immunoprophylactic and immunotherapeutic control of hormone receptor-positive breast cancer.

Aitziber Buqué et al.

Nature communications, 11(1), 3819-3819 (2020-08-01)

Hormone receptor (HR)+ breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR+ BC, in part reflecting the lack of preclinical models that recapitulate disease

Altered immune function during long-term host-tumor interactions can be modulated to retard autochthonous neoplastic growth.

Trina J Stewart et al.

Journal of immunology (Baltimore, Md. : 1950), 179(5), 2851-2859 (2007-08-22)

Ag-specific and generalized forms of immunosuppression have been documented in animal tumor models. However, much of our knowledge on tumor-induced immunosuppression was acquired using tumor implant models, which do not reiterate the protracted nature of host-tumor interactions. Therefore, a transgenic

Pro-inflammatory megakaryocyte gene expression in murine models of breast cancer.

Roweth, et al.

Science Advances, 8, eabo5224-eabo5224 (2023)

Progression to malignancy in the polyoma middle T oncoprotein mouse breast cancer model provides a reliable model for human diseases.

Elaine Y Lin et al.

The American journal of pathology, 163(5), 2113-2126 (2003-10-28)

Animal models are powerful tools to analyze the mechanism of the induction of human breast cancer. Here we report a detailed analysis of mammary tumor progression in one mouse model of breast cancer caused by expression of the polyoma middle

Induction of mammary tumors by expression of polyomavirus middle T oncogene: a transgenic mouse model for metastatic disease.

C T Guy et al.

Molecular and cellular biology, 12(3), 954-961 (1992-03-01)

The effect of mammary gland-specific expression of the polyomavirus middle T antigen was examined by establishing lines of transgenic mice that carry the middle T oncogene under the transcriptional control of the mouse mammary tumor virus promoter/enhancer. By contrast to

PTP1B Is an Intracellular Checkpoint that Limits T-cell and CAR T-cell Antitumor Immunity.

Florian Wiede et al.

Cancer discovery, 12(3), 752-773 (2021-11-20)

Immunotherapies aimed at alleviating the inhibitory constraints on T cells have revolutionized cancer management. To date, these have focused on the blockade of cell-surface checkpoints such as PD-1. Herein we identify protein tyrosine phosphatase 1B (PTP1B) as an intracellular checkpoint

Assessing growth and response to therapy in murine tumor models.

C Patrick Reynolds et al.

Methods in molecular medicine, 111, 335-350 (2005-05-25)

Rodent models provide an important means of assessing antitumor activity vs toxicity for new cancer therapies. Tumors are often grown subcutaneously on the flank or back of animals, allowing accurate serial determination of tumor volume with calipers by measuring the

iTAG an optimized IMiD-induced degron for targeted protein degradation in human and murine cells.

Habib Bouguenina et al.

iScience, 26(7), 107059-107059 (2023-06-26)

To address the limitation associated with degron based systems, we have developed iTAG, a synthetic tag based on IMiDs/CELMoDs mechanism of action that improves and addresses the limitations of both PROTAC and previous IMiDs/CeLMoDs based tags. Using structural and sequence

Multiphoton Microscopy of FITC-labelled Fusobacterium nucleatum in a Mouse in vivo Model of Breast Cancer.

Parhi, et al.

Bio-protocol, 13, e4635-e4635 (2023)

Breast cancer cell-derived microRNA-155 suppresses tumor progression via enhancing immune cell recruitment and antitumor function.

Junfeng Wang et al.

The Journal of clinical investigation, 132(19) (2022-08-05)

Evidence suggests that increased microRNA-155 (miR-155) expression in immune cells enhances antitumor immune responses. However, given the reported association of miR-155 with tumorigenesis in various cancers, a debate is provoked on whether miR-155 is oncogenic or tumor suppressive. We aimed

The bone microenvironment invigorates metastatic seeds for further dissemination.

Weijie Zhang et al.

Cell, 184(9), 2471-2486 (2021-04-21)

Metastasis has been considered as the terminal step of tumor progression. However, recent genomic studies suggest that many metastases are initiated by further spread of other metastases. Nevertheless, the corresponding pre-clinical models are lacking, and underlying mechanisms are elusive. Using

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