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Find video protocols related to scientific articles indexed in Pubmed.
Clinical and radiologic features of pheochromocytoma/ganglioneuroma composite tumors: a case series with comparative analysis.
Endocr Pract
PUBLISHED: 03-20-2014
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To describe and compare the clinical, biochemical, radiologic, and pathologic features of adrenal pheochromocytoma-ganglioneuroma (PC-GN) composites with the features of isolated pheochromocytomas (PCs) and adrenal ganglioneuromas (AGNs).
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Kidney cancer, version 2.2014.
J Natl Compr Canc Netw
PUBLISHED: 03-04-2014
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These NCCN Guidelines Insights highlight treatment recommendations and updates specific to the management of patients with advanced non-clear cell carcinoma included in the 2014 version of the NCCN Clinical Practice Guidelines in Oncology for Kidney Cancer.
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Enhancer of zeste homolog 2 expression is associated with metastasis and adverse clinical outcome in clear cell renal cell carcinoma: a comparative study and review of the literature.
Arch. Pathol. Lab. Med.
PUBLISHED: 10-02-2013
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Enhancer of zeste homolog 2 (EZH2), a histone methyltransferase mediating chromatin condensation and epigenetic modulation, is overexpressed in various human carcinomas and is associated with adverse clinicopathologic characteristics and biologic behavior. The expression of EZH2 in renal cell carcinomas (RCCs) has not been fully characterized yet.
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Aldehyde dehydrogenase 1 expression in primary and metastatic renal cell carcinoma: an immunohistochemistry study.
World J Surg Oncol
PUBLISHED: 05-23-2013
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ALDH1 has been shown to be a cancer stem cell marker, and its expression correlates with prognosis in a number of malignancies. We aimed to evaluate to the expression of ALDH1 in a cohort of primary and metastatic RCC specimens, and to correlate expression with pathological outcomes such as tumor stage and grade, and clinical outcomes such as progression free survival.
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Adrenocortical carcinoma: clinical outcomes and prognosis of 330 patients at a tertiary care center.
Eur. J. Endocrinol.
PUBLISHED: 01-01-2013
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Adrenocortical carcinoma (ACC) is a rare malignancy with a poor prognosis. Herein, we describe the clinical features and outcomes for a large series of ACC patients.
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Modeling a lethal prostate cancer variant with small-cell carcinoma features.
Clin. Cancer Res.
PUBLISHED: 12-12-2011
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Small-cell prostate carcinoma (SCPC) morphology predicts for a distinct clinical behavior, resistance to androgen ablation, and frequent but short responses to chemotherapy. We sought to develop model systems that reflect human SCPC and can improve our understanding of its biology.
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Banking of fresh-frozen prostate tissue using the alternate mirror image protocol: methods, validation, and impact on the pathological prognostic parameters in radical prostatectomy.
Cell Tissue Bank
PUBLISHED: 10-11-2011
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We evaluated the value of the alternative slices mirror image method used in prostate tissue banking in terms of predicting the sampling of cancerous tissue while preserving the pathological prognostic information. The concordance of diagnosis between banked sections and their mirror image paraffin- sections was studied using 50 cases corresponding to 400 H&E sections taken from 400 banked frozen blocks (two presumed benign and two presumed cancer for each case). The mean number of paraffin blocks in each case was 21. On average 29% of the prostate gland was banked and banked tissue contained cancer in 47 cases (94%). There was no difference between the concordant and discordant groups in terms of the final Gleason score, pathological stage, prostate size, number of banked blocks and the percentage of the prostate submitted for banking. However, concordant cases had larger foci of cancer in the mirror image paraffin block (P = 0.0088). In addition, the surgical margins sections which are not banked using this method provided important information about the pathological stage, surgical margins status and the final Gleason score in 2.6, 2.6, and 1.3% of cases, respectively. The alternative slices mirror image method is a straightforward method that is highly efficient in banking prostatic cancerous tissue. Overall, tumor volume and especially size of tumor foci in the image paraffin block are the most important factors in dictating the success rate of banking frozen cancerous tissue. Including surgical margins sections for histology provides additional important prognostic information in a minority of cases.
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Systemic therapy for sarcomatoid renal cell carcinoma.
Expert Rev Anticancer Ther
PUBLISHED: 06-29-2011
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Renal cell carcinoma (RCC) is the most common malignant neoplasm of the kidney, and sarcomatoid RCC is an aggressive and lethal variant. Sarcomatoid features can be seen in all types of RCC and do not constitute a separate histologic type. No cellular or genetic biomarker for the sarcomatoid variant has yet been discovered. Most systemic therapies developed for metastatic RCC are less effective in sarcomatoid RCC, although some of the cytotoxic drugs may actually be more effective for sarcomatoid RCC because of its rapid rate of proliferation. Several ongoing prospective clinical trials are investigating new drug combinations for this disease.
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PTEN genomic deletions that characterize aggressive prostate cancer originate close to segmental duplications.
Genes Chromosomes Cancer
PUBLISHED: 05-04-2011
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Deletion of PTEN at 10q23.3 occurs in ?40% of human prostate cancers and is associated with aggressive metastatic potential, poor prognosis, and androgen-independence. This high frequency of recurrent PTEN deletions in prostate cancer suggests there may be unusual genomic features close to this locus that facilitate DNA alteration at 10q23.3. To explore possible mechanisms for deletions in the PTEN region, a meta-analysis of 311 published human genome array datasets was conducted and determined that the minimal prostate cancer-associated deletion at 10q23.3 corresponds to ?2.06 MB region flanked by BMPR1A and FAS. On a separate cohort comprising an additional 330 tumors, four-color fluorescence in situ hybridization analysis using probes for BMPR1A, FAS, cen(10), and PTEN showed that 132 of 330 (40%) tumors had PTEN loss, 50 (15%) of which were homozygous losses (comprising in total 100 deletion events). Breakpoints between PTEN and BMPR1A or FAS were subsequently mapped in 100 homozygous and 82 hemizygous PTEN losses, revealing that 125/182 PTEN microdeletions occurred within the 940 kB interval between BMPR1A and PTEN. Furthermore, this breakpoint interval coincides with a repeat-rich region of 414 kB containing the SD17 and SD18 segmental duplications, which contain at least 13 homologous inverted repeat sequences. Together, these data suggest that a strong selective growth advantage for loss of PTEN and upregulation of PI3K/AKT, combined with the close proximity of PTEN to a large unstable segment of repeated DNA comprising SD17 and SD18, can lead to recurrent microdeletions of the PTEN gene in prostate cancer. © 2011 Wiley Periodicals, Inc.
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ERG cooperates with androgen receptor in regulating trefoil factor 3 in prostate cancer disease progression.
Neoplasia
PUBLISHED: 06-18-2010
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To elucidate the role of ETS gene fusions in castration-resistant prostate cancer (CRPC), we characterized the transcriptome of 54 CRPC tumor samples from men with locally advanced or metastatic disease. Trefoil factor 3 (TFF3) emerged as the most highly differentially regulated gene with respect to ERG rearrangement status and resistance to hormone ablation therapy. Conventional chromatin immunoprecipitation (ChIP)-polymerase chain reaction and ChIP followed by DNA sequencing (ChIP-seq) revealed direct binding of ERG to ETS binding sites in the TFF3 promoter in ERG-rearranged prostate cancer cell lines. These results were confirmed in ERG-rearranged hormone-naive prostate cancer (HNPC) and CRPC tissue samples. Functional studies demonstrated that ERG has an inhibitory effect on TFF3 expression in hormone-naive cancer but not in the castration-resistant state. In addition, we provide evidence suggesting an effect of androgen receptor signaling on ERG-regulated TFF3 expression. Furthermore, TFF3 overexpression enhances ERG-mediated cell invasion in CRPC prostate cancer cells. Taken together, our findings reveal a novel mechanism for enhanced tumor cell aggressiveness resulting from ERG rearrangement in the castration-resistant setting through TFF3 gene expression.
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Macroscopic sessile tumor architecture is a pathologic feature of biologically aggressive upper tract urothelial carcinoma.
Urol. Oncol.
PUBLISHED: 05-14-2010
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Macroscopic sessile tumor architecture was associated with adverse outcomes after radical nephroureterectomy (RNU) for upper tract urothelial carcinoma (UTUC). Before inclusion in daily clinical decision-making, the prognostic value of tumor architecture needs to be validated in an independent, external dataset. We tested whether macroscopic tumor architecture improves outcome prediction in an international cohort of patients.
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Prioritizing genes associated with prostate cancer development.
BMC Cancer
PUBLISHED: 03-25-2010
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The genetic control of prostate cancer development is poorly understood. Large numbers of gene-expression datasets on different aspects of prostate tumorigenesis are available. We used these data to identify and prioritize candidate genes associated with the development of prostate cancer and bone metastases. Our working hypothesis was that combining meta-analyses on different but overlapping steps of prostate tumorigenesis will improve identification of genes associated with prostate cancer development.
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The mammalian target of rapamycin pathway is widely activated without PTEN deletion in renal cell carcinoma metastases.
Cancer
PUBLISHED: 02-19-2010
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Inhibitors of the mammalian target of rapamycin (mTOR) are emerging as promising therapies for metastatic renal cell carcinoma (RCC). Because rational treatment strategies require understanding the activation status of the underlying signaling pathway being targeted at the desired stage of disease, the authors examined the activation status of different components of the mTOR pathway in RCC metastases and matched primary tumors.
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PTEN genomic deletion is associated with p-Akt and AR signalling in poorer outcome, hormone refractory prostate cancer.
J. Pathol.
PUBLISHED: 04-30-2009
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PTEN haploinsufficiency is common in hormone-sensitive prostate cancer, though the incidence of genomic deletion and its downstream effects have not been elucidated in clinical samples of hormone refractory prostate cancer (HRPC). Progression to androgen independence is pivotal in prostate cancer and mediated largely by the androgen receptor (AR). Since this process is distinct from metastatic progression, we examined alterations of the PTEN gene in locally advanced recurrent, non-metastatic human HRPC tissues. Retrospective analyses of PTEN deletion status were correlated with activated downstream phospho-Akt (p-Akt) pathway proteins and with the androgen receptor. The prevalence of PTEN genomic deletions in transurethral resection samples of 59 HRPC patients with known clinical outcome was assessed by four-colour FISH analyses. FISH was performed using six BAC clones spanning both flanking PTEN genomic regions and the PTEN gene locus, and a chromosome 10 centromeric probe. PTEN copy number was also evaluated in a subset of cases using single nucleotide polymorphism (SNP) arrays. In addition, the samples were immunostained with antibodies against p-Akt, p-mTOR, p-70S6, and AR. The PTEN gene was deleted in 77% of cases, with 25% showing homozygous deletions, 18% homozygous and hemizygous deletions, and 34% hemizygous deletions only. In a subset of the study group, SNP array analysis confirmed the FISH findings. PTEN genomic deletion was significantly correlated to the expression of downstream p-Akt (p < 0.0001), AR (p = 0.025), and to cancer-specific mortality (p = 0.039). PTEN deletion is common in HRPC, with bi-allelic loss correlating to disease-specific mortality and associated with Akt and AR deregulation.
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Renal cell carcinoma with inferior vena caval extention: impact of tumour extent on surgical outcome.
BJU Int.
PUBLISHED: 04-17-2009
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To evaluate our experience with surgical resection of renal cell carcinoma (RCC) with inferior vena cava (IVC) involvement and examine the relationship between prognosis and tumour extent.
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Fascin regulates prostate cancer cell invasion and is associated with metastasis and biochemical failure in prostate cancer.
Clin. Cancer Res.
PUBLISHED: 02-21-2009
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Prostate cancer metastasis to secondary organs is considered an initial event in the development of hormone refractory disease and remains the major cause of death among prostate cancer patients. In this study, we investigated the role of fascin, a cytoskeleton actin-bundling protein involved in the formation of filopodia and cell migration, in prostate cancer progression.
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Plasmacytoid urothelial carcinoma of the bladder: a case report.
Cases J
PUBLISHED: 01-14-2009
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Plasmacytoid bladder cancer is a rare variant of transitional cell carcinoma. A 57-year-old man was referred to our institution for management of invasive transitional cell carcinoma diagnosed at a peripheral hospital. His complaints were of vague lower abdominal pain with associated urgency and frequency requiring oxybutynin. Metastatic workup was negative and was subsequently scheduled for a radical cystectomy. Routine colonoscopy 3 weeks prior to surgery was negative. Intraoperatively, he was found to have metastatic urothelial cancer involving the cecum and multiple metastatic deposits within the mesentery of the small intestines. He underwent a palliative cystectomy with ileal conduit formation. Final pathology revealed metastatic plasmacytoid variant of urothelial cancer. Histology and immunohistochemistry were compatible with plasmacytoid variant of urothelial cancer. Here we present our case of this rare variant of urothelial cancer with a review of its characteristics.
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The 16p13.3 (PDPK1) Genomic Gain in Prostate Cancer: A Potential Role in Disease Progression.
Transl Oncol
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Prostate cancer (PCa) is a leading cause of cancer death, and distinguishing aggressive from indolent tumors is a major challenge. Identification and characterization of genomic alterations associated with advanced disease can provide new markers of progression and better therapeutic approaches.
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Contemporary approach to diagnosis and classification of renal cell carcinoma with mixed histologic features.
Chin J Cancer
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Renal cell carcinoma (RCC) is an important contributor to cancer-specific mortality worldwide. Targeted agents that inhibit key subtype-specific signaling pathways have improved survival times and have recently become part of the standard of care for this disease. Accurately diagnosing and classifying RCC on the basis of tumor histology is thus critical. RCC has been traditionally divided into clear-cell and non-clear-cell categories, with papillary RCC forming the most common subtype of non-clear-cell RCC. Renal neoplasms with overlapping histologies, such as tumors with mixed clear-cell and papillary features and hybrid renal oncocytic tumors, are increasingly seen in contemporary practice and present a diagnostic challenge with important therapeutic implications. In this review, we discuss the histologic, immunohisto-chemical, cytogenetic, and clinicopathologic aspects of these differential diagnoses and illustrate how the classification of RCC has evolved to integrate both the tumors microscopic appearance and its molecular fingerprint.
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Plasmacytoid urothelial carcinoma, a chemosensitive cancer with poor prognosis, and peritoneal carcinomatosis.
J. Urol.
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Plasmacytoid urothelial carcinoma is a rare variant histology with poorly defined clinical behavior. We report clinical outcome information on patients with predominant plasmacytoid urothelial carcinoma.
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Retrospective analysis of survival outcomes and the role of cisplatin-based chemotherapy in patients with urethral carcinomas referred to medical oncologists.
Urol. Oncol.
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Primary carcinomas of the urethra (PCU) are rare and often advanced when diagnosed. Treatment standards are lacking. We studied treatment response and survival in a cohort of patients with PCU, with emphasis on modern platinum-containing chemotherapy regimens plus surgery for advanced disease.
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Mitosis phase enrichment with identification of mitotic centromere-associated kinesin as a therapeutic target in castration-resistant prostate cancer.
PLoS ONE
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The recently described transcriptomic switch to a mitosis program in castration-resistant prostate cancer (CRPC) suggests that mitotic proteins may be rationally targeted at this lethal stage of the disease. In this study, we showed upregulation of the mitosis-phase at the protein level in our cohort of 51 clinical CRPC cases and found centrosomal aberrations to also occur preferentially in CRPC compared with untreated, high Gleason-grade hormone-sensitive prostate cancer (P<0.0001). Expression profiling of chemotherapy-resistant CRPC samples (n?=?25) was performed, and the results were compared with data from primary chemotherapy-naïve CRPC (n?=?10) and hormone-sensitive prostate cancer cases (n?=?108). Our results showed enrichment of mitosis-phase genes and pathways, with progression to both castration-resistant and chemotherapy-resistant disease. The mitotic centromere-associated kinesin (MCAK) was identified as a novel mitosis-phase target in prostate cancer that was overexpressed in multiple CRPC gene-expression datasets. We found concordant gene expression of MCAK between our parent and murine CRPC xenograft pairs and increased MCAK protein expression with clinical progression of prostate cancer to a castration-resistant disease stage. Knockdown of MCAK arrested the growth of prostate cancer cells suggesting its utility as a potential therapeutic target.
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Interactions and relationships of PTEN, ERG, SPINK1 and AR in castration-resistant prostate cancer.
Histopathology
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Recently, ETS-related gene (ERG) gene rearrangements, phosphatase tensin homologue (PTEN) deletions and serine protease inhibitor Kazal type 1 (SPINK1) overexpression were investigated as potential markers for molecularly subtyping prostate cancer (PCA). However, their incidence and co-association in castration-resistant PCA (CRPC) has not been characterized fully.
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Integrative molecular profiling reveals asparagine synthetase is a target in castration-resistant prostate cancer.
Am. J. Pathol.
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The identification of new and effective therapeutic targets for the lethal, castration-resistant stage of prostate cancer (CRPC) has been challenging because of both the paucity of adequate frozen tissues and a lack of integrated molecular analysis. Therefore, in this study, we performed a genome-wide analysis of DNA copy number alterations from 34 unique surgical CRPC specimens and 5 xenografts, with matched transcriptomic profiling of 25 specimens. An integrated analysis of these data revealed that the asparagine synthetase (ASNS) gene showed a gain in copy number and was overexpressed at the transcript level. The overexpression of ASNS was validated by analyzing other public CRPC data sets. ASNS protein expression, as detected by reverse-phase protein lysate array, was tightly correlated with gene copy number. In addition, ASNS protein expression, as determined by IHC analysis, was associated with progression to a therapy-resistant disease state in TMAs that included 77 castration-resistant and 40 untreated prostate cancer patient samples. Knockdown of ASNS by small-interfering RNAs in asparagine-deprived media led to growth inhibition in both androgen-responsive (ie, LNCaP) and castration-resistant (ie, C4-2B) prostate cancer cell lines and in cells isolated from a CRPC xenograft (ie, MDA PCa 180-30). Together, our results suggest that ASNS is up-regulated in cases of CRPC and that depletion of asparagine using ASNS inhibitors will be a novel strategy for targeting CRPC cells.
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Diagnostic and Prognostic Role of Immunohistochemical Expression of Napsin-A Aspartic Peptidase in Clear Cell and Papillary Renal Cell Carcinoma: A Study Including 233 Primary and Metastatic Cases.
Appl. Immunohistochem. Mol. Morphol.
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Napsin-A aspartic peptidase (napsin-A) is an aspartic protease that is predominantly expressed in the proximal renal tubules and type II pneumocytes of the lung. Recently, napsin-A was reported to be present in a proportion of renal cell carcinomas (RCCs). However, the utilization of napsin-A immunohistochemistry as a routine diagnostic tool for RCC, and the correlation of the level of napsin-A expression with histologic features have not yet been established. In the current study, using tissue microarrays composed of primary and metastatic RCCs, napsin-A expression was demonstrated in 86 of 222 (39%) clear cell RCCs (CRCCs) and 16 of 21 (76%) papillary RCCs (PRCCs), with a strong and diffuse staining pattern observed in PRCCs and a relatively weak and focal positivity in CRCCs. Compared with primary CRCCs, a comparable proportion of metastatic CRCCs retained napsin-A expression (45/132, 34%), suggesting the potential utility of napsin-A in the evaluation of metastatic tumors. The expression of napsin-A was also found to be inversely correlated to aggressive local tumor characteristics, such as advanced pathologic stage and high Fuhrman nuclear grade. We conclude that napsin-A may be a valuable immunohistochemical marker in the diagnosis of RCCs, particularly PRCC.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.