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BAP1 Loss Predicts Therapeutic Vulnerability in Malignant Peritoneal Mesothelioma

BackgroundMalignant Peritoneal Mesothelioma (PeM) is a rare but frequently fatal cancer that originates from the peritoneal lining of the abdomen. Standard treatment of PeM is limited to cytoreductive surgery and/or chemotherapy, and no effective targeted therapies for PeM yet exist. In the search for novel therapeutic target candidates in PeM, we performed a comprehensive integrative multi-omics analysis of 19 treatment-naive PeM tumors.\n\nResultsThe analysis identified PeM tumors with BAP1 loss to form a distinct molecular subtype characterized by distinct expression patterns of genes involved in chromatin remodeling, DNA repair pathway, and immune checkpoint receptor activation. This PeM subtype could potentially benefit from immune checkpoint, PARP, or HDAC inhibition therapies.\n\nConclusionsOur findings uncover BAP1 as a trackable prognostic and predictive biomarker, and refine PeM disease classification. This integrated molecular characterization provides a comprehensive foundation for developing PeM precision medicine.

cancer biology

Breast cancer brain metastases show increased levels of genomic aberration based homologous recombination deficiency scores relative to their corresponding primary tumors

Due to its mechanism of action, PARP inhibitor therapy is expected to benefit mainly tumor cases with homologous recombination deficiency (HRD). Various measures of genomic scarring based HRD scores were developed as a companion diagnostic in order to correlate it with PARP inhibitor sensitivity. We compared a variety of HRD scores in primary tumors and their corresponding brain metastases and found a significant increase in this measure in brain metastases for all measures of HRD that were tested. This discrepancy warrants further investigation to assess whether this observation is common to other metastatic sites, and potentially a significant adjustment of strategy in the application of HRD measures in clinical trials for the prioritization of patients for PARP inhibitor therapy.\n\nKey messageWe quantified homologous recombination deficiency (HRD) in paired primary breast cancer and brain metastases samples based on a previously published data set. We showed that HRD significantly increases in the brain metastases relative to its paired primary tumor. An independent validation was also performed on another set of primary breast cancer and brain metastasis pairs using the \"my choice\" HRD score in collaboration with Myriad Genetics.\n\nThese confirmatory results suggest that brain metastases of breast cancer tend to have significantly higher HRD scores, which would prioritize those patients for PARP inhibitor therapy with those agents that cross the blood brain barrier such as veliparib and niraparib.

cancer biology

Naa10p promotes metastasis by stabilizing matrix metalloproteinase-2 protein in human osteosarcomas

N--Acetyltransferase 10 protein (Naa10p) mediates N-terminal acetylation of nascent proteins. Oncogenic or tumor suppressive roles of Naa10p were reported in cancers. Here, we report an oncogenic role of Naa10p in promoting metastasis of osteosarcomas. Higher NAA10 transcripts were observed in metastatic osteosarcoma tissues compared to non-metastatic tissues and were also correlated with a worse prognosis of patients. Knockdown and overexpression of Naa10p in osteosarcoma cells respectively led to decreased and increased cell migratory/invasive abilities. Re-expression of Naa10p, but not an enzymatically inactive mutant, relieved suppression of the invasive ability in vitro and metastasis in vivo imposed by Naa10p-knockdown. According to protease array screening, we identified that matrix metalloproteinase (MMP)-2 was responsible for the Naa10p-induced invasive phenotype. Naa10p was directly associated with MMP-2 protein through its acetyltransferase domain and maintained MMP-2 protein stability via NatA complex activity. MMP-2 expression levels were also significantly correlated with Naa10p levels in osteosarcoma tissues. These results reveal a novel function of Naa10p in the regulation of cell invasiveness by preventing MMP-2 protein degradation that is crucial during osteosarcoma metastasis.

cancer biology

A new look at multi-stage models of cancer incidence

Multi-stage models have long been used in combination with SEER data to make inferences about the mechanisms underlying cancer initiation. The main method for studying these models mathematically has been the computation of generating functions by solving hyperbolic partial differential equations. Here, we analyze these models using a probabilistic approach similar to the one Durrett and Moseley [7] used to study branching process models of cancer. This more intuitive approach leads to simpler formulas and new insights into the behavior of these models. Unfortunately, the examples we consider suggest that fitting multi-stage models has very little power to make inferences about the number of stages unless parameters are constrained to take on realistic values.

cancer biology

Genealogies in Growing Solid Tumors

Over the past two decades, the theory of tumor evolution has largely focused on the selective sweeps model. According to this theory, tumors evolve by a succession of clonal expansions that are initiated by driver mutations that have a fitness advantage over the resident types. A 2015 study of colon cancer [44] has suggested an alternative theory of tumor evolution, the so-called Big Bang model, in which all of the necessary driver mutations are acquired before expansion began, and the evolutionary dynamics within the expanding population are predominantly neutral. In this paper, we will describe a simple mathematical model inspired by work of Hallatschek and Nelson [25] that makes quantitative predictions about spatial patterns of genetic variability. While this model has some success in matching observed patterns in two dimensions, it fails miserably in three dimensions. Despite this failure, we think the model analyzed here will be a useful first step in building an accurate model.

cancer biology

Control and the Analysis of Cancer Growth Models

In this note, we analyze two cancer dynamical models from a system-theoretic point of view. The first model is based upon stochastic controlled versions of the classical Lotka-Volterra equations. Here we consider from a controls point of view the utility of employing ultrahigh dose flashes in radiotherapy. The second is based on work of Norton-Simon-Massague growth model that takes into account the heterogeneity of a tumor cell population. We indicate an optimal strategy based on linear quadratic control applied to a linear transformed model.

cancer biology

HOTAIR primes the Ewing sarcoma family of tumors for tumorigenesis via epigenetic dysregulation involving LSD1

The EWS-FLI1 fusion protein drives oncogenesis in the Ewing sarcoma family of tumors (ESFT) in humans, but its toxicity in normal cells requires additional cellular events for oncogenesis. We show that the lncRNA HOTAIR maintains cell viability in the presence of EWS-FLI1 and redirects epigenetic regulation in ESFT. HOTAIR is consistently overexpressed in ESFTs and is not driven by EWS-FLI1. Repression of HOTAIR in ESFT cell lines significantly reduces anchorage-independent colony formation in vitro and impairs tumor xenograft growth in vivo. Overexpression of HOTAIR in human mesenchymal stem cells (hMSCs), a putative cell of origin of ESFT, and IMR90 cells induces colony formation. Critically, HOTAIR-expressing hMSCs and IMR90 cells remain viable with subsequent EWS-FLI1 expression. HOTAIR induces histone modifications and gene repression through interaction with the epigenetic modifier LSD1 in ESFT cell lines and hTERT-hMSCs. Our findings suggest that HOTAIR maintains ESFT viability through epigenetic dysregulation.\n\nSignificanceWhile the EWS-FLI1 fusion gene was determined to be the oncogenic driver in the overwhelming majority of ESFT, it is toxic to cell physiology and requires one or more additional molecular events to maintain cell viability. As these tumors have surprisingly few genetic mutations at diagnosis, epigenetic changes have been considered to be such an event, but the mechanism by which these changes are driven remains unclear. Our work shows that HOTAIR is consistently expressed among ESFT and induces epigenetic and gene expression changes that cooperate in tumorigenesis. Furthermore, expression of HOTAIR allows for cell viability in the setting of subsequent EWS-FLI1 expression. Our findings elucidate new steps of malignant transformation in this cancer and identify novel therapeutic targets.

cancer biology

Oncogenic role of sFRP2 in P53-mutant osteosarcoma development via autocrine and paracrine mechanism

Osteosarcoma (OS), the most common primary bone tumor, is highly metastatic with high chemotherapeutic resistance and poor survival rates. Using induced pluripotent stem cells (iPSCs) generated from Li-Fraumeni syndrome (LFS) patients, we investigated an oncogenic role of secreted frizzled-related protein 2 (sFRP2) in P53 mutation-associated OS development. Interestingly, we found that high sFRP2 expression in OS patient samples correlates with poor survival. Systems-level analyses identified that expression of sFRP2 increases during LFS OS development and can induce angiogenesis. Ectopic sFRP2 overexpression in normal osteoblast precursors is sufficient to suppress normal osteoblast differentiation and to promote OS phenotypes through induction of oncogenic molecules such as FOXM1 and CYR61 in a {beta}-catenin independent manner. Conversely, inhibition of sFRP2, FOXM1 or CYR61 represses the tumorigenic potential. In summary, these findings demonstrate the oncogenic role of sFRP2 in P53 mutation-associated OS development and that inhibition of sFRP2 is a potential therapeutic strategy.

cancer biology

FoxN1-dependent thymic epithelial cells promote T-cell leukemia development

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes. The role of thymic microenvironmental cells and stromal factors in thymocyte malignant transformation and T-ALL development remains little explored. Here, using the TEL-JAK2 transgenic (TJ2-Tg) mouse model of T-ALL, which is driven by constitutive JAK/STAT signaling and characterized by the acquisition of Notch1 mutations, we sought to identify stromal cell alterations associated with thymic leukemogenesis. Immunofluorescence analyses showed that thymic lymphomas presented epithelial areas characterized by keratin 5 and keratin 8 expression, adjacently to keratin-negative, epithelial-free areas. Both keratin-positive and -negative areas stained conspicuously with ER-TR7 (a fibroblast marker), laminin, and CD31 (an endothelial cell marker). Besides keratin 5, keratin-positive areas were also labeled by the Ulex Europaeus agglutinin-1 medullary thymic epithelial cell (TEC) marker. To assess whether TECs are important for T-ALL development, we generated TJ2-Tg mice heterozygous for the FoxN1 transcription factor nude null mutation. In contrast to nude homozygous mice, which lack thymus and thymocytes, heterozygous mutant mice present only mild thymocyte maturation defects. In TJ2-Tg;Foxn1+/nu compound mice both emergence of malignant cells in pre-leukemic thymi and overt T-ALL onset were significantly delayed. Moreover, in transplantation assays leukemic cell expansion in the thymus of recipient Foxn1+/nu mice was reduced as compared to control littermates. These results indicate that FoxN1 insufficiency impairs specifically thymic leukemogenesis but not thymocyte development.\n\nSummaryIn a mouse model of T-ALL, several cellular alterations were detected in thymic lymphomas, including altered epithelial distribution and increased proportion of fibroblasts or endothelial cells. Reduced dosage of FoxN1, a thymic epithelial transcription factor, delayed leukemogenesis in these mice.

cancer biology

Small interfering RNAs based on huntingtin trinucleotide repeats are highly toxic to cancer cells

Trinucleotide repeat (TNR) expansions in the genome cause a number of degenerative diseases. A prominent TNR expansion involves the triplet CAG in the huntingtin (HTT) gene responsible for Huntingtons disease (HD). Pathology is caused by protein and RNA generated from the TNR regions including small siRNA-sized repeat fragments. An inverse correlation between the length of the repeats in HTT and cancer incidence has been reported for HD patients. We now show that siRNAs based on the CAG TNR are toxic to cancer cells by targeting genes that contain long reverse complimentary TNRs in their open reading frames. Of the 60 siRNAs based on the different TNRs, the 6 members in the CAG/CUG family of related TNRs are the most toxic to both human and mouse cancer cells. siCAG/CUG TNR-based siRNAs induce cell death in vitro in all tested cancer cell lines and slow down tumor growth in a preclinical mouse model of ovarian cancer with no signs of toxicity to the mice. We propose to explore TNR-based siRNAs as a novel form of anti-cancer reagents.

cancer biology

Cancer exosomes induce tumor neo-neurogenesis potentiating tumor growth

Patients with densely innervated tumors do worse than those with less innervated cancers. We hypothesize that neural elements are acquired by a tumor-induced process, called neo-neurogenesis. Here, we use PC12 cells in a simple system to test this hypothesis. PC12 cells extend processes, called neurites, only when appropriately stimulated. Using this system, we show that patient tumors release vesicles (exosomes) which induce PC12 neurite outgrowth. Using a cancer mouse model, we show that tumor cells compromised in exosome release grow slower and are less innervated than controls indicating a contribution of innervation to disease progression. We find that neo-neurogenesis is mediated in part by the axonal guidance molecule, EphrinB1, contained in exosomes. These findings support testing EphrinB1 blockers to inhibit tumor innervation and improve survival.\n\nOne Sentence SummaryTumors release exosomes which not only promote their own innervation but also potentiate their growth.

cancer biology

Integration and analysis of CPTAC proteomics data in the context of cancer genomics in the cBioPortal

The Clinical Proteomic Tumor Analysis Consortium (CPTAC) has produced extensive mass spectrometry based proteomics data for selected breast, colon and ovarian tumors from The Cancer Genome Atlas (TCGA). We have incorporated the CPTAC proteomics data into the cBioPotal to support easy exploration and integrative analysis of these proteomic datasets in the context of the clinical and genomics data from the same tumors. cBioPortal is an open source platform for exploring, visualizing, and analyzing multi-dimensional cancer genomics and clinical data. The public instance of the cBioPortal (http://cbioportal.org/) hosts more than 100 cancer genomics studies including all of the data from TCGA. Its biologist-friendly interface provides many rich analysis features, including a graphical summary of gene-level data across multiple platforms, correlation analysis between genes or other data types, survival analysis, and network visualization. Here, we present the integration of the CPTAC mass spectrometry based proteomics data into the cBioPortal, consisting of 77 breast, 95 colorectal, and 174 ovarian tumors that already have been profiled by TCGA for mutations, copy number alterations, gene expression, and DNA methylation. As a result, the CPTAC data can now be easily explored and analyzed in the cBioPortal in the context of clinical and genomics data. By integrating CPTAC data into cBioPortal, limitations of TCGA proteomics array data can be overcome while also providing a user-friendly web interface, a web API and an R client to query the mass spectrometry data together with genomic, epigenomic, and clinical data.

cancer biology

USP7 cooperates with NOTCH1 to drive the oncogenic transcriptionalprogram in T cell leukemia

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease, affecting children and adults. Treatments1-6 show high response rates but have debilitating effects and carry risk of relapse5,7,8. Previous work implicated NOTCH1 and other oncogenes1,2,9-20. However, direct inhibition of these pathways affects healthy tissues and cancer alike. Here, we demonstrate that ubiquitin-specific protease 7 (USP7)21-32 controls leukemia growth by stabilizing the levels of the NOTCH1 and JMJD3 demethylase. USP7 is overexpressed T-ALL and is transcriptionally regulated by NOTCH1. In turn, USP7 controls NOTCH1 through deubiquitination. USP7 is bound to oncogenic targets and controls gene expression through H2B ubiquitination and H3K27me3 changes via stabilization of NOTCH1 and JMJD3. We also show that USP7 and NOTCH1 bind T-ALL superenhancers, and USP7 inhibition alters associated gene activity. These results provide a new model for deubiquitinase activity through recruitment to oncogenic chromatin loci and regulation of both oncogenic transcription factors and chromatin marks to promote leukemia. USP7 inhibition33 significantly blocked T-ALL cell growth in vitro and in vivo. Our studies also show that USP7 is upregulated in the aggressive high-risk cases of T-ALL and suggest that USP7 expression might be a prognostic marker in ALL and its inhibition could be a therapeutic tool against aggressive leukemia.

cancer biology

Recapitulation of human germline coding variation in an ultra-mutated infant leukemia

BackgroundMixed lineage leukemia/Histone-lysine N-methyltransferase 2A gene rearrangements occur in 80% of infant acute lymphoblastic leukemia, but the role of cooperating events is unknown. While infant leukemias typically carry few somatic lesions, we identified a case with over 100 somatic point mutations per megabase and here report unique genomic-features of this case.\n\nResultsThe patient presented at 82 days of age, one of the earliest manifestations of cancer hypermutation recorded. The transcriptional profile showed global similarities to canonical cases. Coding lesions were predominantly clonal and almost entirely targeting alleles reported in human genetic variation databases with a notable exception in the mismatch repair gene, MSH2. There were no rare germline alleles or somatic mutations affecting proof-reading polymerase genes POLE or POLD1, however there was a predicted damaging mutation in the error prone replicative polymerase, POLK. The patients diagnostic leukemia transcriptome was depleted of rare and low-frequency germline alleles due to loss-of-heterozygosity, while somatic point mutations targeted low-frequency and common human alleles in proportions that offset this discrepancy. Somatic signatures of ultra-mutations were highly correlated with germline single nucleotide polymorphic sites indicating a common role for 5-methylcytosine deamination, DNA mismatch repair and DNA adducts.\n\nConclusionsThese data suggest similar molecular processes shaping population-scale human genome variation also underlies the rapid evolution of an infant ultra-mutated leukemia.

cancer biology

Interfering with MIF-CD74 signalling on macrophages and dendritic cells with a peptide-based approach restores the immune response against metastatic melanoma.

Mounting an effective immune response against cancer requires the activation of innate and adaptive immune cells. Metastatic melanoma is the most aggressive form of skin cancer. Immunotherapies that boost the activity of effector T cells have shown a remarkable success in melanoma treatment. Patients, however, can develop resistance to such therapies by mechanisms that include the establishment of an immune suppressive tumour microenvironment. Understanding how metastatic melanoma cells suppress the immune system is vital to develop effective immunotherapies against this disease. In this study, we find that the innate immune cells, macrophages and dendritic cells are suppressed in metastatic melanoma. The Ig-CDR-based peptide C36L1 is able to restore macrophages and dendritic cells immunogenic functions and to inhibit metastatic growth in vivo. Mechanistically, we found that C36L1 interferes with the MIF-CD74 tumour-innate immune cells immunosuppressive signalling pathway and thereby restores an effective anti-tumour immune response. C36L1 directly binds to CD74 on macrophages and dendritic cells, disturbing CD74 structural dynamics and inhibiting MIF signalling through CD74. Our findings suggest that interfering with MIF-CD74 immunosuppressive signalling in macrophages and dendritic cells using peptide-based immunotherapy can restore the anti-tumour immune response in metastatic melanoma. Our study provides the rationale for further development of peptide-based therapies to restore the anti-tumour immune response.

cancer biology

MicroRNA-92a negatively regulates neurofibromin 2 and inhibits its tumor suppressive function

Inactivation of the tumor suppressor Merlin leads to the development of benign nervous system tumors of neurofibromatosis type 2. Merlin deficiency is also observed in human malignancies including colorectal and lung cancers. Causes of Merlin inactivation include deleterious mutations in the encoding neurofibromin 2 gene (NF2) and aberrant Merlin proteasomal degradation. Here, we show that NF2 is also regulated by microRNAs (miRNAs) through interaction with evolutionarily conserved miRNA response elements (MREs) within its 3-untranslated region (3 UTR). Dual luciferase assays in HCT116 and A549 show downregulation of wild type NF2 by miR-92a via its 3UTR but not NF2-3UTR with mutated MRE. HCT116 cells transfected with miR-92a show significant downregulation of endogenous NF2 mRNA and protein levels, which were rescued by co-transfection of a target protector oligonucelotide specific for the miR-92a binding site within NF2-3UTR. MiR-92a overexpression in HCT116 and A549 resulted in increased migration and proliferation, apoptosis resistance, and altered F-actin organization compared to controls. This study provides functional proof of the unappreciated role of miRNAs in NF2 regulation and tumor progression.

cancer biology

Detection and benchmarking of somatic mutations in cancer genomes using RNA-seq data

To detect functional somatic mutations in tumor samples, whole-exome sequencing (WES) is often used for its reliability and relative low cost. RNA-seq, while generally used to measure gene expression, can potentially also be used for identification of somatic mutations. However there has been little systematic evaluation of the utility of RNA-seq for identifying somatic mutations. Here, we develop and evaluate a pipeline for processing RNA-seq data from glioblastoma multiforme (GBM) tumors in order to identify somatic mutations. The pipeline entails the use of the STAR aligner 2-pass procedure jointly with MuTect2 from GATK to detect somatic variants. Variants identified from RNA-seq data were evaluated by comparison against the COSMIC and dbSNP databases, and also compared to somatic variants identified by exome sequencing. We also estimated the putative functional impact of coding variants in the most frequently mutated genes in GBM. Interestingly, variants identified by RNA-seq alone showed better representation of GBM-related mutations cataloged by COSMIC. RNA-seq-only data substantially outperformed the ability of WES to reveal potentially new somatic mutations in known GBM-related pathways, and allowed us to build a high-quality set of somatic mutations common to exome and RNA-seq calls. Using RNA-seq data in parallel with WES data to detect somatic mutations in cancer genomes can thus broaden the scope of discoveries and lend additional support to somatic variants identified by exome sequencing alone.

cancer biology

Evolution of an intratumoral ecology susceptible to successive treatment in breast cancer xenografts

The processes by which tumors evolve are essential to the efficacy of treatment, but quantitative understanding of intratumoral dynamics has been limited. Although intratumoral heterogeneity is common, quantification of evolution is difficult from clinical samples because treatment replicates cannot be performed and because matched serial samples are infrequently available. To circumvent these problems we derived and assayed large sets of human triple-negative breast cancer xenografts and cell cultures from two patients, including 86 xenografts from cyclophosphamide, doxorubicin, cisplatin, docetaxel, or vehicle treatment cohorts as well as 45 related cell cultures. We assayed these samples via exome-seq and/or high-resolution droplet digital PCR, allowing us to distinguish complex therapy-induced selection and drift processes among endogenous cancer subclones with cellularity uncertainty <3%. For one patient, we discovered two predominant subclones that were granularly intermixed in all 48 co-derived xenograft samples. These two subclones exhibited differential chemotherapy sensitivity -- when xenografts were treated with cisplatin for 3 weeks, the post-treatment volume change was proportional to the post-treatment ratio of subclones on a xenograft-to-xenograft basis. A subsequent cohort in which xenografts were treated with cisplatin, allowed a drug holiday, then treated a second time continued to exhibit this proportionality. In contrast, xenografts from other treatment cohorts, spatially dissected xenograft fragments, and cell cultures evolved unsystematically but with substantial population bottlenecks. These results show that ecologies susceptible to successive retreatment can arise spontaneously in breast cancer in spite of a background of irregular subclonal bottlenecks, and our work provides to our knowledge the first quantification of the population genetics of such a system. Intriguingly, in such an ecology the ratio of common subclones is predictive of the state of treatment susceptibility, suggesting that this ratio can be measured to optimize dynamic treatment protocols in patients.\n\nAUTHOR SUMMARYAn overarching challenge of cancer is that patients develop resistance to treatment -- an essentially evolutionary process. However, there is currently very little understanding of how tumor evolution can be exploited to improve treatment. One reason for this is that usually only 1-2 samples can be obtained per patient, so cancer evolutionary processes are still poorly understood. To solve this problem, we created many dozens of copies of the tumors from two breast cancer patients using xenografting and cell culture methods. We then compared the evolution in these tumor copies in response to different treatments, including four of the most common breast cancer chemotherapies. These studies present the most exhaustive comparisons of treatment-induced evolution that have yet been performed for individual cancer patients. Unexpectedly, high-resolution sequencing of these samples revealed a special dynamically treatable ecology in one tumor, in which tumor growth during platinum therapy was determined by the ecological balance of two tumor cell populations. Our work shows that ecologies that can be targeted by dynamic treatment strategies arise spontaneously in breast cancers. Population heterogeneity is common within cancers, and our work suggests how tracking of intratumoral evolution can be used to optimize treatment.

cancer biology