Classical form of Kaposi sarcoma localized in penis.
Ontology highlight
ABSTRACT:
SUBMITTER: Dunev VR
PROVIDER: S-EPMC6562291 | biostudies-literature | 2019 May
REPOSITORIES: biostudies-literature
Publications
Classical form of Kaposi sarcoma localized in penis.
Dunev V R VR Kolev N H NH Genov P P PP Sachdeva M M Karaivanov M P MP
Urology case reports 20190222
We present you a case of 43 year old man with classical form of Kaposi sarcoma (KS) localized to the Penis who was HIV negative. Detailed pathological and immunohistochemistry characteristic of the tumor was done. Pathology reported it as KS with nodular and polypoid form. Classical form of KS with localization in male genitalia is rare identity and serves as a diagnostic challenge. ...[more]
Similar Datasets
Project description:Kaposi sarcoma (KS) risk is affected by perturbed immunity. Herein, we compared plasma from 15 human immunodeficiency virus (HIV)-negative classic KS cases to plasma from 29 matched controls, using a multiplex panel of immunity markers. Of 70 markers, CXCL10 (IP-10), sIL-1RII, sIL-2RA, and CCL3 (MIP-1A) were strongly and significantly associated with KS, after adjustment for age and smoking status. These and previous observations are consistent with a tumor-promoting role for these cytokines, particularly CXCL10, but the small sample size and case-control design preclude firm conclusions on KS risk or pathogenesis. Larger, well-designed prospective studies are needed to better assess the association of these markers with KS.
| S-EPMC4334829 | biostudies-literature
Project description:Much has been learned since the discovery of KSHV in 1994 about its epidemiology and pathology but much of what has been learned has yet to be translated into clinical practice. In this review, we survey the current state of knowledge on KSHV epidemiology and KS pathogenesis and highlight therapeutic opportunities in both the developed and developing world.
| S-EPMC3085592 | biostudies-literature
Project description:ABSTRACT We report a case of a 35-year-old, non-HIV-infected male diagnosed simultaneously with a disseminated form of Kaposi’s sarcoma (KS; skin, stomach and colon are involved) and Hodgkin’s lymphoma. There is no sign of changes in the immune status, but three herpes viruses were detected in the patient’s blood (EBV, HHV6 and HHV8). He received ABVD chemotherapy and achieved complete metabolic remission for Hodgkin’s lymphoma. Moreover, the signs of the disseminated KS were resolved. Our observations indicate that a combination of distinct types of viruses may play an important role in triggering the development of angio- and lymphoproliferative disorders in the same person. In addition, treatment with chemotherapy cycles, which included doxorubicin and vinblastine, led to the stable remission of both diseases.
| S-EPMC7507874 | biostudies-literature
Project description:Intra-host tumor virus variants may influence the pathogenesis and treatment responses of some virally-associated cancers. However, the intra-host variability of Kaposi sarcoma-associated herpesvirus (KSHV), the etiologic agent of Kaposi sarcoma (KS), has to date been explored with sequencing technologies that possibly introduce more errors than that which occurs in the viral population, and these studies have only studied variable regions. Here, full-length KSHV genomes in tumors and/or oral swabs from 9 Ugandan adults with HIV-associated KS were characterized. Furthermore, we used deep, short-read sequencing using duplex unique molecular identifiers (dUMI)-random double-stranded oligonucleotides that barcode individual DNA molecules before library amplification. This allowed suppression of PCR and sequencing errors to ~10-9/base as well as afforded accurate determination of KSHV genome numbers sequenced in each sample. KSHV genomes were assembled de novo, and rearrangements observed were confirmed by PCR and Sanger sequencing. 131-kb KSHV genome sequences, excluding major repeat regions, were successfully obtained from 23 clinical specimens, averaging 2.3x104 reads/base. Strikingly, KSHV genomes were virtually identical within individuals at the point mutational level. The intra-host heterogeneity that was observed was confined to tumor-associated KSHV mutations and genome rearrangements, all impacting protein-coding sequences. Although it is unclear whether these changes were important to tumorigenesis or occurred as a result of genomic instability in tumors, similar changes were observed across individuals. These included inactivation of the K8.1 gene in tumors of 3 individuals and retention of a region around the first major internal repeat (IR1) in all instances of genomic deletions and rearrangements. Notably, the same breakpoint junctions were found in distinct tumors within single individuals, suggesting metastatic spread of rearranged KSHV genomes. These findings define KSHV intra-host heterogeneity in vivo with greater precision than has been possible in the past and suggest the possibility that aberrant KSHV genomes may contribute to aspects of KS tumorigenesis. Furthermore, study of KSHV with use of dUMI provides a proof of concept for utilizing this technique for detailed study of other virus populations in vivo.
| S-EPMC7845968 | biostudies-literature
Project description:We identified a novel Kaposi's sarcoma herpesvirus-related rhadinovirus (Colobine gammaherpesvirus 1) in a mantled guereza (Colobus guereza kikuyensis). The animal had multiple oral tumors characterized by proliferation of latent nuclear antigen 1-positive spindle cells and was not co-infected with immunosuppressive simian viruses, suggesting that it had Kaposi sarcoma caused by this novel rhadinovirus.
| S-EPMC6649314 | biostudies-literature
Project description:Kaposi's sarcoma (KS) is a heterogeneous angioproliferative tumor that generally arises in the skin. At least four forms of this disease have been described, with the 'HIV'-related form being the most aggressive and can involve mucosae or visceral organs. Three quarters of KS cases occur in sub-Saharan Africa (SSA) as geographic variation is explained by the disparate prevalence of KS-associated herpes virus (KSHV), which is the underlying cause of this disease. It can infect endothelial and/or mesenchymal cells that consequently transdifferentiate to an intermediate state. KSHV establishes a latent phase in host cells in which latency proteins and various non-coding RNAs (ncRNAs) play a complex role in proliferation and angiogenesis. It also undergoes periods of sporadic lytic reactivation triggered by various biological signals in which lytic stage proteins modulate host cell signaling pathways and are key in KS progression. Complex interactions with the microenvironment with production of inflammatory cytokines with paracrine signaling is a standout feature of KS development and maintenance. KSHV impairs the immune response by various mechanisms such as the degradation of a variety of proteins involved in immune response or binding to cellular chemokines. Treatment options include classical chemotherapy, but other novel therapies are being investigated.
| S-EPMC9030761 | biostudies-literature
Project description:Kaposi sarcoma (KS) is the most common neoplasm of people living with HIV today. In Sub-Saharan Africa, KS is among the most common cancers in men, overall. Not only HIV-positive individuals present with KS; any immune compromised person infected with KS-associated herpesvirus (KSHV) or human herpesvirus 8 is at risk: the elderly, children in KSHV-endemic areas, and transplant recipients. KS diagnosis is based on detection of the viral protein latency-associated nuclear antigen (LANA) in the biopsy, but not all cases of KS are the same or will respond to the same therapy. Standard KS therapy has not changed in 20 years, but newer modalities are on the horizon and will be discussed.
| S-EPMC5509489 | biostudies-literature
Project description:BackgroundEwing sarcoma is a malignancy that commonly affects the skeletal system and primary extraskeletal involvement is rare. Extraskeletal Ewing sarcoma (EES) arises in soft tissue anywhere in the body. These are very rarely seen aggressive tumours. There have been only 7 reported cases of EES of penis.Case presentationWe report a 22-year-young patient who presented to our hospital with a ulcero-proliferative growth in the shaft of penis. There were no other complaints indicating any metastasis. Incisional biopsy was suggestive of invasive malignancy. He was scheduled for a partial penectomy. Final HPE and IHC were suggestive of EES.ConclusionEES as a subtype of Ewing sarcoma is rare and it can occur in any soft tissue site. Hence, clinicians need to differentiate this entity from other soft tissue sarcomas. Early diagnosis and timely treatment of EES are pivotal for a favourable prognosis due to its aggressive nature.Supplementary informationThe online version contains supplementary material available at 10.1007/s13193-023-01793-x.
| S-EPMC10611654 | biostudies-literature
Project description:Kaposi sarcoma is the most common cancer in human immunodeficiency virus-positive individuals and is caused by Kaposi sarcoma-associated herpesvirus (KSHV). It is believed that a small number of latently infected Kaposi sarcoma tumor cells undergo spontaneous lytic reactivation to produce viral progeny for infection of new cells. Here, we use matched donor-derived human dermal blood and lymphatic endothelial cells (BEC and LEC, respectively) to show that KSHV-infected BECs progressively lose viral genome as they proliferate. In sharp contrast, KSHV-infected LECs predominantly entered lytic replication, underwent cell lysis, and released new virus. Continuous lytic cell lysis and de novo infection allowed LEC culture to remain infected for a prolonged time. Because of the strong propensity of LECs toward lytic replication, LECs maintained virus as a population, despite the death of individual host cells from lytic lysis. The master regulator of lymphatic development, Prox1, bound the promoter of the RTA gene to upregulate its expression and physically interacted with RTA protein to coregulate lytic genes. Thus, LECs may serve as a proficient viral reservoir that provides viral progeny for continuous de novo infection of tumor origin cells, and potentially BECs and mesenchymal stem cells, which give rise to Kaposi sarcoma tumors. Our study reveals drastically different host cell behaviors between BEC and LEC and defines the underlying mechanisms of the lymphatic cell environment supporting persistent infection in Kaposi sarcoma tumors. SIGNIFICANCE: This study defines the mechanism by which Kaposi's sarcoma could be maintained by virus constantly produced by lymphatic cells in HIV-positive individuals.
| S-EPMC7759148 | biostudies-literature
Project description:: The search for the etiologic agent for Kaposi sarcoma led to the discovery of Kaposi sarcoma-associated herpesvirus (KSHV) in 1994. KSHV, also called human herpesvirus-8, has since been shown to be the etiologic agent for several other tumors and diseases, including primary effusion lymphoma (PEL), an extracavitary variant of PEL, KSHV-associated diffuse large B-cell lymphoma, a form of multicentric Castleman disease, and KSHV inflammatory cytokine syndrome. KSHV encodes several genes that interfere with innate and specific immunity, thwart apoptosis, enhance cell proliferation and cytokine production, and promote angiogenesis, and these play important roles in disease pathogenesis. HIV is an important cofactor in Kaposi sarcoma pathogenesis, and widespread use of antiretroviral therapy has reduced Kaposi sarcoma incidence. However, Kaposi sarcoma remains the second most frequent tumor arising in HIV-infected patients in the United States and is particularly common in sub-Saharan Africa. KSHV prevalence varies substantially in different populations. KSHV is secreted in saliva, and public health measures to reduce its spread may help reduce the incidence of KSHV-associated diseases. Although there have been advances in the treatment of Kaposi sarcoma, KSHV-multicentric Castleman disease, and PEL, improved therapies are needed, especially those that are appropriate for Kaposi sarcoma in resource-poor regions.
| S-EPMC6310482 | biostudies-literature