Project description:Lung tumors, as well as normal tumor-adjacent (NTA) tissue of non-small cell lung cancer (NSCLC) patients, were collected and subjected label-free quantitation shotgun proteomics in data-independent mode to identify differences between the tumors and adjacent tissue. By employing in-depth proteomics, we identified several pathways that are up- or downregulated in the tumors of non-small cell lung cancer patients.
Project description:Tumor tissue of lung carcinoid tumors (pulmonary neuroendocrine tumors) and adjacent normal lung tissue was profiled using scRNA-seq
Project description:Transgenic mice (Scgb1a1-rtTA/[tetO]-KRAS.G12D/Nkx2-1+/-) develop mucinous lung tumors. Gene expression analysis was performed using mRNAs from the whole lungs of the mice compared to that of the control mice. We used microarrays to detail the global program of gene expression underlying development of mucinous lung tumors and identified distinct classes of up-regulated genes during this process. mRNAs were isolated from the whole lungs of the transgenic mice (Scgb1a1-rtTA/[tetO]-KRAS.G12D/Nkx2-1+/-) after 2 months doxycycline administration and hybridized on Affymetrix microarrays. We sought to identify genes induced in mucinous lung tumors.
Project description:To identify altered signal transduction pathways involved in the progression and metastases of Lkb1 deficient lung tumors, we have performed an unbiased microarray analysis of primary and metastatic mouse lung tumors We used microarrays to detail the global programme of gene expression underlying metastatic progression We compared RNA expression profiles from 9 Kras and 9 Kras/Lkb1 primary tumors as well as 17 Kras/Lkb1 metastases (lymph node and distant sites)
Project description:We have previously found that tobacco carcinogen exposed Gprc5a-/- develop lung tumors including adenocarcinoma. We sought to understand the molecular pathology of these lung tumors by whole-transcriptome sequence (RNA-Seq) analysis.
Project description:To identify altered signal transduction pathways involved in the progression and metastases of Lkb1 deficient lung tumors, we have performed an unbiased microarray analysis of primary and metastatic mouse lung tumors We used microarrays to detail the global programme of gene expression underlying metastatic progression
Project description:Metastasis accounts for most cancer-associated deaths; yet, this complex process remains poorly understood, particularly the relationship between distant metastasis and primary site-derived cells. Here, we modified the classical MMTV-PyMT breast carcinoma model to trace the fate of mammary-derived carcinoma cells. We show that within the lung, when the metastatic breast carcinoma cells are conditionally depleted, transformed lung epithelial cells generate new metastases. Metastatic breast carcinoma cells transmit H19 long non-coding (lnc) RNA to lung epithelial cells through exosomes. SF3B1 bearing mutations at arginine-625 alternatively splices H19 lncRNA in lung epithelial cells, which selectively acts like a molecular sponge to sequester let-7a and induces Myc up-regulation. Under the conditional elimination of primary site-derived breast carcinoma cells, lung malignant cells expressing the mutated SF3B1 splice variant dominate the newly created tumors. Our study suggests that these new carcinoma cells originating from within the colonized organ can replace the primary site-derived malignant cells whenever their expansion is abrogated using an inducible diphtheria toxin receptor in our designed system. These findings should call for a better understanding of metastatic tumors with the specific origin during cancer metastasis.
