bioRxiv Science⌕ Search

Biology subjects

Ananda, G.

Publications and source records attributed to Ananda, G..

8 recordsLinked to original sources

Targeting FGFR signaling overcomes therapeutic resistance and immune evasion in oncogenic PIK3CA-driven serous-like endometrial cancer

Serous endometrial cancer (SEC) is an aggressive subtype of endometrial cancer (EC) with poor prognosis and limited treatment options. Here, we developed a clinically relevant, immunocompetent serous-like mouse model incorporating oncogenic PIK3CA mutation, Trp53 loss, and MYC overexpression. Using this model together with human EC cell lines, patient-derived organoids (PDOs), xenografts, and patient datasets, we investigated mechanisms underlying resistance to PI3K-targeted therapy. Single-cell profiling reveals that FGFR1/2 upregulation associates with intrinsic resistance, whereas FGFR3 characterizes acquired resistance. Dual FGFR and PI3K inhibition produced superior tumor control compared with either agent alone. Mechanistically, FGFR signaling promotes immune evasion by downregulating MHC-I/HLA-mediated antigen presentation and enriching M2-type tumor-associated macrophages. FGFR inhibition reversed these changes and synergized with anti-PD-1 therapy to enhance antitumor immune responses and establish durable immune memory. Collectively, these findings identify FGFR signaling as a key driver of therapeutic resistance and immune escape in SEC and support FGFR-targeted combination strategies.

cancer biology↗

Transcriptomic Stratification of Late-Onset Alzheimer’s Cases Reveals Novel Genetic Modifiers of Disease Pathology

Late-Onset Alzheimers disease (LOAD) is a common, complex genetic disorder well-known for its heterogeneous pathology. The genetic heterogeneity underlying common complex diseases poses a major challenge for targeted therapies and the identification of novel disease-associated variants. Case-control approaches are often limited to examining a specific outcome in a group of heterogenous patients with different clinical characteristics. Here, we developed a novel approach to define relevant transcriptomic endophenotypes and stratify decedents based on molecular profiles in three independent human LOAD cohorts. By integrating post-mortem brain gene co-expression data from 2114 human samples with LOAD, we developed a novel quantitative, composite phenotype that can better account for the heterogeneity in genetic architecture underlying the disease. We used iterative weighted gene co-expression network analysis (WGCNA) analysis to reduce data dimensionality and to isolate gene sets that are highly co-expressed within disease subtypes and represent specific molecular pathways. We then performed single variant association testing using whole genome-sequencing data for the novel composite phenotype in order to identify genetic loci that contribute to disease heterogeneity. Distinct LOAD subtypes were identified for all three study cohorts (two in ROSMAP, three in Mayo Clinic, two in Mount Sinai Brain Bank). Single variant association analysis identified a genome-wide significant variant in TMEM106B (p-value < 5x10-8, rs1990620G) in the ROSMAP cohort that confers protection from the inflammatory LOAD subtype. Taken together, our novel approach can be used to stratify LOAD into distinct molecular subtypes based on affected disease pathways.

systems biology↗

HELLS and PRDM9 form a Pioneer Complex to Open Chromatin at Meiotic Recombination Hotspots

Chromatin barriers prevent spurious interactions between regulatory elements and DNA-binding proteins. One such barrier, whose mechanism for overcoming is poorly understood, is access to recombination hotspots during meiosis. Here we show that the chromatin remodeler HELLS and DNA-binding protein PRDM9 function together to open chromatin at hotspots and provide access for the DNA double-strand break (DSB) machinery. Recombination hotspots are decorated by a unique combination of histone modifications, not found at other regulatory elements. HELLS is recruited to hotspots by PRDM9, and is necessary for both histone modifications and DNA accessibility at hotspots. In male mice lacking HELLS, DSBs are retargeted to other sites of open chromatin, leading to germ cell death and sterility. Together, these data provide a model for hotspot activation where HELLS and PRDM9 function as a pioneer complex to create a unique epigenomic environment of open chromatin, permitting correct placement and repair of DSBs.

genetics↗

The genome of C57BL/6J \"Eve\", the mother of the laboratory mouse genome reference strain

Isogenic laboratory mouse strains are used to enhance reproducibility as individuals within a strain are essentially genetically identical. For the most widely used isogenic strain, C57BL/6, there is also a wealth of genetic, phenotypic, and genomic data, including one of the highest quality reference genomes (GRCm38.p6). However, laboratory mouse strains are living reagents and hence genetic drift occurs and is an unavoidable source of accumulating genetic variability that can have an impact on reproducibility over time. Nearly 20 years after the first release of the mouse reference genome, individuals from the strain it represents (C57BL/6J) are at least 26 inbreeding generations removed from the individuals used to generate the mouse reference genome. Moreover, C57BL/6J is now maintained through the periodic reintroduction of mice from cryopreserved embryo stocks that are derived from a single breeder pair, aptly named C57BL/6J Adam and Eve. To more accurately represent the genome of todays C57BL/6J mice, we have generated a de novo assembly of the C57BL/6J Eve genome (B6Eve) using high coverage, long-read sequencing, optical mapping, and short-read data. Using these data, we addressed recurring variants observed in previous mouse studies. We have also identified structural variations that impact coding sequences, closed gaps in the mouse reference assembly, some of which are in genes, and we have identified previously unannotated coding sequences through long read sequencing of cDNAs. This B6Eve assembly explains discrepant observations that have been associated with GRCm38-based analyses, and has provided data towards a reference genome that is more representative of the C57BL/6J mice that are in use today.

genomics↗

The impact of sex on alternative splicing

Over 95% of human genes undergo alternative splicing (AS) in a developmental, tissue-specific, or signal transduction-dependent manner. Here, we present a large-scale survey of sex-biased differential alternative splicing (DAS) across 7027 samples of 39 tissues from 532 individuals (351 males and 181 females) from the Genotype-Tissue Expression project. We detected a total of 1278 statistically significant DAS events affecting 888 different genes and 4417 significant differential gene expression (DGE) events in 3221 genes. Only 267 (29.3%) of the differentially spliced genes were also differentially expressed. Genes that displayed sex-biased DGE or DAS across multiple tissues were enriched in functions related to signaling including histone demethylation. The probability of a gene showing significant differential AS varies by chromosome and is highest for the X chromosome, with differentially spliced X chromosomal genes additionally being more likely to escape X chromosomal inactivation. A small but significant association was found between sex-biased AS and transcripts that undergo physiological nonsense-mediated decay (NMD). We show a significant overlap of differential splicing and genes that display estrogen-induced alternative splicing, that are involved in estrogen response pathway. Further, we show overlap of the involved exons with estrogen-receptor bindings sites. Our results provide a comprehensive survey of sex-biased AS and its characteristics across a large collection of human tissues.

genomics↗

Bioinformatics workflows for genomic analysis of tumors from Patient Derived Xenografts (PDX): challenges and guidelines

Bioinformatics workflows for analyzing genomic data obtained from xenografted tumor (e.g., human tumors engrafted in a mouse host) must address several challenges, including separating mouse and human sequence reads and accurate identification of somatic mutations and copy number aberrations when paired normal DNA from the patient is not available. We report here data analysis workflows that address these challenges and result in reliable identification of somatic mutations, copy number alterations, and transcriptomic profiles of tumors from patient derived xenograft models. We validated our analytical approaches using simulated data and by assessing concordance of the genomic properties of xenograft tumors with data from primary human tumors in The Cancer Genome Atlas (TCGA). The commands and parameters for the workflows are available at https://github.com/TheJacksonLaboratory/PDX-Analysis-Workflows.

bioinformatics↗

Tissue-specific trans regulation of the mouse epigenome

Although a variety of writers, readers, and erasers of epigenetic modifications are known, we have little information about the underlying regulatory systems controlling the establishment and maintenance of the epigenetic landscape, which varies greatly among cell types. Here, we have explored how natural genetic variation impacts the epigenome in mice. Studying levels of H3K4me3, a histone modification at sites such as promoters, enhancers, and recombination hotspots, we found tissue-specific trans-regulation of H3K4me3 levels in four highly diverse cell types: male germ cells, embryonic stem (ES) cells, hepatocytes and cardiomyocytes. To identify the genetic loci involved, we measured H3K4me3 levels in male germ cells in a mapping population of 60 BXD recombinant inbred lines, identifying extensive trans-regulation primarily controlled by six major histone quantitative trait loci (hQTL). These chromatin regulatory loci act dominantly to suppress H3K4me3, which at hotspots reduces the likelihood of subsequent DNA double-strand breaks. QTL locations do not correspond with enzyme known to metabolize chromatin features. Instead their locations match clusters of zinc finger genes, making these possible candidates that explain the dominant suppression of H3K4me3. Collectively, these data describe an extensive, tissue-specific set of chromatin regulatory loci that control functionally related chromatin sites.

genomics↗

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↗