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Expression data from 4T1 subclones derived from mammary fat pad tumors (MFP), axillary lymph node tumors (AxLN), and axillary lymph node-derived lung metastases (AxLN-LuM)

ABSTRACT: Expression data from 4T1 subclones derived from mammary fat pad tumors (MFP), axillary lymph node tumors (AxLN), and axillary lymph node-derived lung metastases (AxLN-LuM)

PROVIDER: PRJNA560974 | ENA |

REPOSITORIES: ENA

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Expression data from 4T1 subclones derived from mammary fat pad tumors (MFP), axillary lymph node tumors (AxLN), and axillary lymph node-derived lung metastases (AxLN-LuM)

Project description:Expression data from 4T1 subclones derived from mammary fat pad tumors (MFP), axillary lymph node tumors (AxLN), and axillary lymph node-derived lung metastases (AxLN-LuM). In parallel, expression data, in the same subclones, of tail vein-derived (TV) lung metastases. The mechanism of how lymph node metastases seed distant metastases is unknown. We used the 4T1 breast cancer cell line, which is an immune competent model of triple negative breast cancer and spontaneously metastasizes in balb/c mice. 4T1-GFP/fLuc cells were injected into MFP to form tumors and 4T1-mCherry/rLuc cells were injected into axillary lymph nodes to form tumors and then allowed to metastasize to lung. TV cells were allowed to metastasize in the lung. Cells were harvested at different time intervals after the injection. Tumors were extracted, dissociated, and then expanded in vitro to obtain MFP, AxLN, AxLN-LuM and TV-LuM subclones isolated after different time lags with respect to the injection.

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Lymph Node Metastases in Colon Cancer are Polyclonal

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Transcription profiling of mouse model of estrogen receptor positive breast cancer lymph node metastasis.

Project description:The lymphatic system is a common avenue for the spread of breast cancer cells and dissemination through it occurs at least as frequently as hematogenous metastasis. Approximately 75% of primary breast cancers are estrogen receptor (ER) positive and the majority of these maintain receptor expression as lymph node (LN) metastases. However, it is unknown if ER function is equivalent in cancer cells growing in the breast and in the LNs. We have developed a model to assess estrogen responsiveness in ER(+) breast tumors and LN metastases. Fluorescent ER(+) MCF-7 tumors were grown in ovariectomized nude mice supplemented with estradiol. Once axillary LN metastasis arose, estradiol was withdrawn (EWD), for 1 or 4 weeks, or continued, to assess estradiol responsiveness. On EWD, proliferation rates fell similarly in tumors and LN metastases. However, estradiol-dependent ER down-regulation and progesterone receptor induction were deficient in LN metastases, indicating that ER-dependent transcriptional function was altered in the LN. Cancer cells from estradiol-treated and EWD primary tumors and matched LN metastases were isolated by laser capture microdissection. Global gene expression profiling identified transcripts that were regulated by the tissue microenvironment, by hormones, or by both. Interestingly, numerous genes that were estradiol regulated in tumors lost estradiol sensitivity or were regulated in the opposite direction by estradiol in LN metastases. We propose that the LN microenvironment alters estradiol signaling and may contribute to local antiestrogen resistance. Experiment Overall Design: 10 samples, including 3 each of estrogen and estrogen withdrawn axillary lymph nodes and 2 each of estrogen and estrogen withdrawn primary mammary gland tumors.

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Project description:In order to clarify the gene expression and identify genes involved in tumor progression, gene expression profiling was performed on tumor specimens. Samples comprised 18 primary tumors, 17 lymph node (LN) metastases and 7 liver metastases. Patients were grouped according to clinical data and histopathology into indolent or progressive course. RNA was subjected to a spotted oligo microarray and B-statistics were performed. Differentially expressed genes were verified using quantitative RT-PCR. Self-organising maps demonstrated three clusters. Eleven primary tumors separated in one cluster, 5 LN metastases in another whereas all liver metastases, 7 primary and 12 LN metastases, formed a third cluster. There was no correlation between indolent and progressive behaviour. The primary tumors with Ki67 > 5%, with low frequency of the carcinoid syndrome and a tendency towards shorter survival grouped together. Primary tumors differed in expression profile from their associated LN metastases. ACTG2, GREM2, REG3A, TUSC2, RUNX1, TPH1, TGFBR2 and CDH6 were differentially expressed between clusters and subgroups of tumors. The expression profile that assembles tumors as being genetically similar on the RNA expression level may not be concordant with the clinical disease course. This study reveals different gene expression profiles and novel genes not previously known to be involved in neuroendocrine tumorigenesis, and which may be of importance for tumor progression. Gene expression comparisons between 18 primary tumors, 17 lymph node metastases and 7 liver metastases.

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