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At least 235 records · Page 13Linked to original sources

Single-cell profiling of mitochondrial phenotyping-coupled mtDNA genotyping.

Simultaneously profiling mitochondrial DNA (mtDNA) heteroplasmy and phenotypic variability at the single-cell level remains a challenge due to the absence of integrated methods that map mitochondrial genotypes alongside their functional states. We introduce human single-cell mitochondrial phenotype-coupled mtDNA sequencing (scMPCDS), a platform that quantifies mtDNA mutations and heteroplasmy together with mitochondrial membrane potential and reactive oxygen species within individual cells. Unlike bulk sequencing or separate single-omics techniques, scMPCDS directly correlates mitochondrial genomic instability with functional outcomes. Using this approach, we demonstrate that DdCBE-mediated mtDNA editing induces cell-specific off-target mutations in the mitochondrial genome, which coincide with diverse phenotypic changes. Applying scMPCDS to HeLa cells and clear cell renal cell carcinoma tissues, we identify single-cell subpopulations exhibiting distinct mtDNA mutation burdens and altered bioenergetic profiles, implicating potential mitochondrial heterogeneity-driven tumor evolution. Overall, scMPCDS serves as a versatile tool to unravel mitochondrial genotype-phenotype relationships at the single-cell level in both normal and disease states, thereby advancing precise mitochondrial diagnostics and therapeutics.

Humans↗

Prostate-specific antigen (PSA) in the management of 500 prostatic patients.

Blood samples from 500 patients with clinical prostatic symptoms were radioimmunoassayed with prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) kits. On the basis of histological data, directed by PSA results and other investigations, 200 prostatic cancers (adenocarcinomas), 276 benign prostatic hypertrophy (BPH), 16 cases of prostatitis, 5 cancers of the bladder, and 3 prostatodynias were diagnosed. All of the serum samples from prostatic cancer patients showed elevated PSA levels at diagnosis, whereas about 70% of these showed normal PAP values. The sensitivity of the PSA assay is 100% when 2.5 ng/ml is taken as the upper limit of normal. However, the specificity and the positive predictive value are better at 10 ng/ml: 99 and 79%, respectively. High PSA values alerted the clinician when diagnosing a cancer without symptoms on rectal or ultrasonographic examination (3%). In BPH, when the PSA level is between 2.5 and 10 ng/ml, a PSA control must be performed within 2 months. If PSA increases above 10 ng/ml, the risk of cancer has to be considered. In the follow-up, PSA is a better marker than PAP to detect disease progression and seems to constitute an evolutive tumor mass index. PSA is the most sensitive, the earliest, and the most prognostically reliable marker for diagnosis and follow-up of prostate cancer patients.

Acid Phosphatase↗

Epstein-Barr virus (EBV) induced polyclonal and monoclonal B-cell lymphoproliferative diseases occurring after renal transplantation. Clinical, pathologic, and virologic findings and implications for therapy.

Nineteen renal allograft recipients developed B-cell lymphoproliferative diseases. Clinically there were two groups: a) young patients (mean age, 23 years) who presented soon (mean, 9 months) after transplantation or antirejection therapy with fever, pharyngitis, and lymphadenopathy resembling infectious mononucleosis, and b) older patients (mean age, 48 years) who presented later (mean, 6 years) after transplantation with localized tumor masses. Histologically, the diseases were classified as polymorphic diffuse B-cell hyperplasia (PDBH) or polymorphic B-cell lymphoma (PBL). Immunologic cell typing revealed either polyclonal or monoclonal B-cell proliferations. Malignant transformation of polyclonal proliferations in two patients was suggested by the finding of clonal cytogenetic abnormalities. Epstein-Barr virus (EBV) specific serology, staining of biopsy specimens for the Epstein-Barr nuclear antigen, and EBV DNA molecular hybridization studies implicated EBV as the cause of both PDBH and PBL. Acyclovir, an antiviral agent that blocks EBV replication in vitro, inhibited oropharyngeal shedding of EBV and caused complete remission in four patients with polyclonal B-cell proliferations. The monoclonal tumors were acyclovir resistant. We suggest that surgical treatment, radiotherapy, or chemotherapy may be more appropriate therapy in selected patients with acyclovir resistant tumors. Therapeutic decisions require not only documentation of the viral etiology of these tumors, but also immunologic and cytogenetic analysis to determine the stage of tumor evolution in individual patients.

Adolescent↗

HER-2/neu protein expression and gene alteration in stage I-IIIA non-small-cell lung cancer: a study of 140 cases using a combination of high throughput tissue microarray, immunohistochemistry, and fluorescent in situ hybridization.

Regarding HER-2/neu expression (gene or protein level) in lung cancer, several studies with inconsistent results have been recently reported, partially due to variable techniques used and/or heterogeneous populations examined. The objective of this study was to examine HER-2/neu expression in a well-defined cohort of non-small-cell lung cancers (NSCLC) and in nonneoplastic lung tissue utilizing a combination of high-density tissue microarray, immunohistochemistry (IHC), and fluorescent in situ hybridization (FISH) under uniform test conditions. One hundred forty stage I-IIIA primary NSCLCs and 38 non-neoplastic lung samples were examined. IHC, using an FDA-approved Hercept monoclonal antibody kit, was performed and HER-2/neu gene alteration was assessed by FISH. The association of expression of HER-2/neu with clinicopathologic parameters was analyzed. Ninety-four percent of tumor samples (131/140) were fully interpretable after tissue processing. Twenty-five of them (19%) overexpressed (2+, 3+) HER-2/neu, while 106 (81%) had no or weak expression. All thirty-four interpretable non-neoplastic lung samples were negative for HER-2/neu alteration at protein and gene level. HER-2/neu protein overexpression correlated well with HER-2/neu gene amplification (r =.83, P < 0.001). HER-2/neu overexpression was significantly associated with histologic subtype: 19 adenocarcinomas (19/82, 23%) versus 4 squamous cell carcinomas (4/44, 9%) overexpressed Her-2/neu (P = 0.04). Statistical significance was observed between HER-2/neu expression and tumor differentiation, with strong positive (3+) expression observed more frequently in poorly differentiated tumors (P = 0.01). Patients with HER-2/neu abnormalities, particularly HER-2/neu gene amplification, exhibited a shorter survival (P = 0.043). The statistically significant difference (P < 0.005) between HER-2/neu alteration in tumor samples(25/131, 19%) and in the nonneoplastic tissue (0/34, 0%) implies that HER-2/neu may have a role in the carcinogenesis of NSCLC. The findings provide evidence supporting the hypothesis that the HER-2/neu receptor may represent a useful molecular target in the treatment of NSCLC. The significant association of HER-2/neu expression and gene amplification with poorly differentiated carcinoma compared with well differentiated carcinoma suggests that HER-2/neu may be involved in NSCLC tumor evolution. Patients with HER-2/neu gene amplification and strong positive expression of HER-2/neu protein showed a strong tendency toward shorter survival.

Adult↗

Enhancer activation from transposable elements in extrachromosomal DNA.

Extrachromosomal DNA (ecDNA) drives oncogene amplification and intratumoral heterogeneity in aggressive cancers. While transposable element (TE) reactivation is common in cancer, its role on ecDNA remains unexplored. Here, we map the 3D architecture of MYC-amplified ecDNA in colorectal cancer cells and identify 68 ecDNA-interacting elements (EIEs)-genomic loci enriched for TEs that are frequently integrated onto ecDNA. We focus on an L1M4a1#LINE/L1 fragment co-amplified with MYC, which functions only in the ecDNA amplified context. Using CRISPR-CATCH, CRISPR interference, and reporter assays, we confirm its presence on ecDNA, enhancer activity, and essentiality for cancer cell fitness. These findings reveal that repetitive elements can be reactivated and co-opted as functional rather than inactive sequences on ecDNA, potentially driving oncogene expression and tumor evolution. Our study uncovers a mechanism by which ecDNA harnesses repetitive elements to shape cancer phenotypes, with implications for diagnosis and therapy.

Journal Article↗

Long-read sequencing of single cell-derived melanoma subclones reveals divergent and parallel genomic and epigenomic evolutionary trajectories.

Tumor evolution is driven by various mutational processes, ranging from single-nucleotide variants (SNVs) to large structural variants (SVs) to dynamic shifts in DNA methylation. Current short-read sequencing methods struggle to accurately capture the full spectrum of these genomic and epigenomic alterations due to inherent technical limitations. To overcome that, here we introduce an approach for long-read sequencing of single-cell derived subclones, and use it to profile 23 subclones of a mouse melanoma cell line, characterized with distinct growth phenotypes and treatment responses. We develop a computational framework for harmonization and joint analysis of different variant types in the evolutionary context. Uniquely, our framework enables detection of recurrent amplifications of putative driver genes, generated by independent SVs across different lineages, suggesting parallel evolution. In addition, our approach revealed gradual and lineage-specific methylation changes associated with aggressive clonal phenotypes. We also show our set of phylogeny-constrained variant calls along with openly released sequencing data can be a valuable resource for the development of new computational methods.

Journal Article↗

Characterization of replication-competent retroviruses from nonhuman primates with virus-induced T-cell lymphomas and observations regarding the mechanism of oncogenesis.

Rapidly progressive T-cell lymphomas were observed in 3 of 10 rhesus monkeys several months after autologous transplantation of enriched bone marrow stem cells that had been transduced with a retroviral vector preparation containing replication-competent virus (R. E. Donahue, S. W. Kessler, D. Bodice, K. McDonagh, C. Dunbar, S. Goodman, B. Agricola, E. Byrne, M. Raffeld, R. Moen, J. Bacher, K. M. Zsebo, and A. W. Nienhuis, J. Exp. Med. 176:1124-1135, 1992). The animals with lymphoma appeared to be tolerant to retroviral antigens in that their sera lacked antibodies reactive with viral proteins and contained 10(4) to 10(5) infectious virus particles per ml. By molecular cloning and DNA sequencing, we have now demonstrated that the serum from one of the monkeys contained a replication-competent retrovirus that arose by recombination between vector and packaging encoding sequences (vector/helper [V/H] recombinant) in the producer clone used for transduction of bone marrow stem cells. Southern blot analysis demonstrated 14 or 25 copies of this genome per cell where present in two animals. The genome of a second replication-competent virus was also recovered by molecular cloning; it arose by recombination involving the genome of the V/H recombinant and endogenous murine retroviral genomes in the producer clone. Twelve copies of this amphotropic virus/mink cell focus-forming virus genome were present in tumor DNA of one animal, but it was not found in tumor DNA of the other two animals with lymphoma. Southern blot analysis of DNA from various tissues demonstrated common insertion site bands in several samples of tumor DNA from one animal, suggesting clonal origin of the lymphoma. Our data are most consistent with a pathogenic mechanism in which chronic productive retroviral infection allowed insertional mutagenesis of critical growth control genes, leading to cell transformation and clonal tumor evolution.

Animals↗

Effects of proton beam irradiation on uveal melanomas: a comparative study of Ki-67 expression in irradiated versus non-irradiated melanomas.

AIMS: To assess the cellular proliferation using the monoclonal antibody Ki-67, in paraffin embedded uveal melanomas irradiated by proton beam, as well as in non-irradiated uveal melanomas. METHODS: 30 enucleated eyes were included for histopathological study and Ki-67 immunostaining. Patients were enucleated between 1991 and 1996 for uveal melanoma, 14 after proton beam irradiation and 16 without treatment (control group). The mean follow up period was 2.5 years after diagnosis and 1 year after enucleation. RESULTS: A significant relation was found between Ki-67 score and mitotic index (r = 0.56, p = 0.001), histological largest tumour diameter (r = 0.38, p = 0. 03), fibrosis (r = -0.35, p = 0.05), absence of tumoral pigmentation (p = 0.05), and presence of vascular thrombosis (p = 0.03). The Ki-67 score was significantly higher in the non-irradiated group (p = 0.01) and in the group of patients whose cause of enucleation was tumoral evolution (p = 0.005) compared with the group of patients enucleated after neovascular glaucoma. The Ki-67 score was very high in a case of orbital recurrence of uveal melanoma and metastatic death. 70% of metastasised tumours showed a Ki-67 score higher than the median value. CONCLUSION: Ki-67 labelling is a reliable method of estimating the proliferative activity in uveal melanomas after proton beam irradiation. The Ki-67 score is significantly correlated with prognostic variables (mitotic index and histological largest tumour diameter), and with radiation effects after proton beam irradiation.

Adult↗

Integrating molecular subtypes, genomics and functional dependencies to identify context-specific therapeutic vulnerabilities in small cell lung cancer.

Small cell lung cancer is one of the most aggressive malignancies, characterized by rapid tumor growth, early metastatic spread and extremely poor survival. Although most patients initially respond to platinum-based chemotherapy, relapse is almost inevitable and treatment options at recurrence remain limited. The recent introduction of immune checkpoint inhibitors has provided only modest clinical benefit, largely due to the fact that these tumors are immunologically cold. These limitations highlight the urgent need to better understand the molecular features of small cell lung cancer in order to identify more effective therapeutic strategies. In this review, we summarize current knowledge of the molecular landscape of small cell lung cancer, with particular emphasis on transcriptome-based classifications that have identified four major molecular subtypes defined by distinct transcriptional regulators and gene expression programs. We discuss how these classifications have improved the biological understanding of the disease and stimulated efforts to develop subtype-specific therapeutic strategies. At the same time, we highlight important limitations of this framework, including the remarkable transcriptional plasticity of tumor cells, which allows dynamic transitions between subtypes and may contribute to therapeutic resistance. To address these challenges, we examine additional molecular features that may represent more stable vulnerabilities, including recurrent genomic alterations, such as the widespread loss of tumor suppressor genes or oncogene amplifications through extrachromosomal DNA. We also discuss emerging approaches aimed at identifying novel context-specific cancer dependencies, including genome-scale functional screens in vitro and in vivo and genetic restraint analyses. Finally, we consider the growing potential of liquid biopsy strategies, which exploit the high level of circulating tumor DNA in patients with this disease to detect clinically relevant genomic alterations and monitor tumor evolution. Overall, this review highlights both the opportunities and challenges associated with molecular stratification in small cell lung cancer. The integration of transcriptional classifications with genomic and functional approaches may help identify more robust therapeutic vulnerabilities and guide the development of more effective treatments for this highly aggressive disease.

Cancer vulnerabilities↗

Gliosarcoma with features of osteoblastic osteosarcoma: a review.

CONTEXT: Gliosarcoma is a rare tumor of the central nervous system characterized by a biphasic histologic pattern, consisting of a gliomatous and a sarcomatous component, respectively. In most instances the sarcomatous component is represented by a fibrosarcoma, but other stromal malignancies have also been described. Osteosarcomatous differentiation in gliosarcoma has been rarely reported. OBJECTIVE: To review characteristic radiologic and histopathologic features of this rare neoplasm, to debate about possible differential diagnoses that should be taken into consideration, and to provide an overview of the potential histopathogenesis of gliosarcomas. DATA SOURCES: Relevant articles indexed in PubMed (National Library of Medicine) and reference medical texts. CONCLUSIONS: Recent molecular studies suggest that sarcomatous and gliomatous components of gliosarcoma might be derived from a single precursor cell clone, progressing in 2 subclones with distinct morphologic features during tumor evolution. Nonetheless, events determining splitting of the original clone into 2 histologic populations remain to be investigated.

Central Nervous System Neoplasms↗

[Brachytherapy in the treatment of vesicoprostatic rhabdomyosarcomas in children].

Brachytherapy has been widely used at the Institut Gustave-Roussy since 1972 in pediatric oncology. In genitourinary rhabdomyosarcoma, because of its ballistic and physical characteristics, it represents the optimal treatment whenever irradiation is required and brachytherapy feasible. Between 1976 and 1998, 23 children with bladder or prostate rhabdomyosarcoma were treated with a protocol including brachytherapy, with five of them treated with a salvage brachytherapy. All but one brachytherapy was performed during the surgery. Among the 18 brachytherapies performed as a first-line treatment, eight presented a tumoral evolution: five presented a local evolution, one a local and nodal evolution and two a nodal evolution. Brachytherapy allowed a conservative treatment among ten out of 11 children alive with no evidence of disease. Among the five patients with salvage brachytherapy, two presented a second recurrence. Sequelae were minimal, consisting of one grade I rectitis and one asymptomatic vesical and ureteral reflux. These results are consistent with the published data using more radical treatment. Brachytherapy can represent an alternative to radical surgery, when indications are clearly defined in bladder or prostate rhabdomyosarcoma. This type of treatment can be performed only integrated with other treatments, more particularly with surgery. This approach requires a close cooperation between the different specialists: pediatricians, surgeons and brachytherapists.

Adolescent↗

[Von Recklinghausen's disease associated with pancreatic somatostatinoma].

INTRODUCTION: Pancreatic somatostatinoma is a rare entity and its association with Von Recklinghausen's disease has only been described on two occasions. We report a new observation, with clinical and evolving status differing from those described in isolated cases of somatostatinoma. OBSERVATION: A 28 year-old man presenting with familial Von Recklinghausen's disease, had suffered for 10 years from paroxysmic abdominal pain. He was hospitalized for intense pain. Imaging revealed a retroperineal tumoral formation. Following duodenopancreatectomy, somatostatinoma was diagnosed. Diffuse metastatic miliary was revealed and multiple glandular metastases. DISCUSSION: Other than the rarity of the morbid association (pancreatic somatostatinoma and Von Recklinghausen's disease) described, this case is particular in that the patient was very young, symptomatology was unapparent and tumoral evolution was minimal.

Adult↗

[Cortico-suprarenal carcinoma].

The authors show the case of a 69 years old male with a large corticosuprarenalian tumor that was detected on an random abdominal echographic examination. The patient was operated in the General Surgery Department. of Prof. Agrippa Ionescu Hospital, Bucharest. We performed ablation of the large left suprarenalian gland malign tumor with left nephrectomy, splenectomy and partial pancreatectomy. The hystopathological examination reveals a diffuse corticosuprenalian carcinoma. The case is interesting because of low incidence of this kind of malign tumor and also of the unusual tumor evolution in a long time up to its large size (12 cm in diameter).

Adrenal Cortex Neoplasms↗

Measurement of genomic instability in preleukemic P190BCR/ABL transgenic mice using inter-simple sequence repeat polymerase chain reaction.

BCR/ABL associated leukemias are characterized by a high degree of chromosomal and genomic instability. The genomic instability is usually associated with disease progression, as in chronic myelogenous leukemia or a poor prognosis as observed in hallmark Philadelphia chromosome-positive acute lymphoblastic leukemia. It is unclear whether the phenotype of genomic instability is a primary consequence of Bcr/Abl expression or if it is secondarily acquired in the multistep process of tumor evolution. To address this issue, we measured the frequency of insertions and deletions in P190(BCR/ABL) transgenic mice. These mice ubiquitously express Bcr/Abl for an average of 3 months before developing B-cell type lymphoma/leukemia. Genome scanning for insertions and deletions in samples of DNA extracted from kidney and spleen tissues taken from preleukemic animals was performed using the inter-simple sequence repeat PCR. We observed an increased frequency of insertions and deletions in the tissues of preleukemic animals, which could be partially reversed with the c-Abl specific inhibitor STI571. These results suggest that the expression of Bcr/Abl can directly induce a mutator phenotype that antedates overt neoplastic transformation, and that STI571 appears to be capable of reversing this effect.

Animals↗

[Familial adenomatous polyposis: long term follow-up of patients after surgical treatment. Prognostic factors].

The purposes of this study are: 1) to evaluate if recent progresses (knowledge of natural history, genetic diagnosis and surgical treatment) have an impact upon the long term follow up of familial adenomatous polyposis (FAP); 2) to assess the prognosis factors that are relative to recent progresses in diagnosis and treatment procedures. A retrospective study of 51 cases was carried out in July 2002 to analyse the following characteristics: phenotype, treatment, operative mortality and morbidity, late complications, especially rectal stump cancer after ileo-rectal anastomosis, duodenal adenomatosis and desmoid tumors. Twenty seven men and 24 women underwent surgery: 11 colo-rectal cancers were present at first step. Initial surgical procedures included 39 total colectomies with ileo-rectal anastomosis (IRA), 6 coloproctectomies with ileo-anal anastomosis (IAA) and 6 coloproctectomies with permanent ileostomy. Operative mortality was nil. Operative morbidity affected 11 patients. The rectum had to be secondary removed in 11 patients with convert in IAA. Duodenal adenomatosis required surgery in 10 patients: 5 surgical local excisions, 4 duodenopancreatectomies and 1 palliative by-pass. Six desmoid tumors were noted during the follow-up. On the whole 3 patients were lost of sight. Nine patients died (19.1%), 4 deaths were in relation with the disease: 1 rectal cancer, 2 duodenal cancers, 1 desmoid tumor necrosis. At the end of the follow up (mean duration: 17 years) 26 IRA and 17 IAA are present with good functional results. This study, according to already published data, suggests that today the risk of death related to colorectal cancer is becoming lower than the risk of death from duodenal cancer and desmoid tumor evolution, particularly since the introduction of the restorative proctocolectomy. The genetic diagnosis is useful in order to determine the choice of surgical procedures.

Adenomatous Polyposis Coli↗

[Cytophotometric determination of DNA concentration in the cells of experimental brain tumors. II. Primary tumors of rat cerebellum induced by 9, 10-dimethyl-1, 2-benzanthracene].

The Feulgen-DNA cytophotometry was applied for studies of 31 rat cerebellum tumors induced by 9, 10-dimetyl-1,2-bensantracene. Most of these gliomas (22) were astrocytomas of different grades of malignancy. The histological diagnosis of other tumors was: glioblastoma -- 4, oligoastrocytoma -- 2, oligodendroglioma -- 1, gliosarcoma 1. The majority cells of 26 tumors had diploid or paradiploid DNA quantity, 4 tumors (1 astrocytoma, 3 dedifferentiated astroyctomas) had triploid modal classes. The tetraploid modal class and a large number of polyploid cells were found only once for glioblastoma multiforme. A supposition was made that drastic changes of ploidy could arise for the second time during the process of tumor evolution. The authors failed to show any exact differences in the ploidy of gliomas in rats with athyreosis or hyperthyreosis, and in the ploidy of somatic cells in control animals.

9,10-Dimethyl-1,2-benzanthracene↗

Induction of increased salvage pathways of nucleotide synthesis by dosage effect due to chromosome imbalances may be fundamental in carcinogenesis: the example of colorectal carcinoma.

The cytogenetic study of colorectal carcinomas is consistent with the following sequence in the tumor evolution: rearrangement of chromosome 17 with loss of 17p and often gain of 17q, loss of chromosome 18, frequent del(5q), frequent del(1p) correlated with the gain of an early replicating X. At least one gene directly involved in nucleotide synthesis, especially in the de novo pathways for thymidine is located on each of these chromosomes or chromosomes segments. A model established on the gene dosage effect, which likely results of these chromosome imbalances, may be proposed: (1) increase of thymidine kinase activity (chromosome 17q) and thus of the salvage pathway of thymidine synthesis (2) decrease of thymidine de novo pathways by decreased of thymidylate synthase (chromosome 18) and of dihydrofolate reductase (chromosome 5q) and thus accumulation of 2'-deoxyuridine-5'-P, which saves 2'-deoxycytidine 5'-P (3) decrease of cytidylate (or uridylate) kinase (chromosome 1p) and thus accumulation of 2-deoxycytidine-5-PP and of uridine-5-P (UMP) decreasing the metabolisation of orotidine-5'-P, precursor of 2-deoxycytidine-5-PP, which (4) saves -D-5-ribosyl-PP (PRPP) or even conversion of orotidine-5'-P in PRPP. The later is the immediate precursor of nucleotides in their major salvage pathways synthesis: PRPP + base----nucleotide + PPi. This reaction which would be much activated needs hypoxanthine phosphorybosyl transferase (HPRT). Its gene is carried by chromosome X which is here duplicated in its active early replicating form.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromosome Aberrations↗