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At least 19 recordsLinked to original sources
PubMed2003

Chemical-specific alterations in ras, p53, and beta-catenin genes in hemangiosarcomas from B6C3F1 mice exposed to o-nitrotoluene or riddelliine for 2 years.

The most prominent neoplastic lesions in mice in the 2-year studies of o-nitrotoluene and riddelliine were hemangiosarcomas. Fifteen o-nitrotoluene-induced hemangiosarcomas of the skeletal muscle, subcutaneous tissue, and mesentery; 12 riddelliine-induced hemangiosarcomas of the liver; and 15 spontaneous subcutaneous hemangiosarcomas were examined for genetic alterations in ras, p53, and beta-catenin genes. Mutations in at least one of these genes were identified in 13 of 15 (87%) of the o-nitrotoluene-induced hemangiosarcomas with missense mutations in p53 exons 5-8 detected in 11 of 15 (73%) of these neoplasms. Seven of 15 (47%) hemangiosarcomas from mice exposed to o-nitrotoluene had deletions at exon 2 splice sites or smaller deletions in the beta-catenin gene. K-ras mutation was detected in only 1 of the 15 (7%) o-nitrotoluene-induced hemangiosarcomas. In contrast to the o-nitrotoluene study, 7/12 (58%) riddelliine-induced hemangiosarcomas had K-ras codon 12 GTT mutations and, when screened by immunohistochemistry, 9/12 (75%) had strong staining for the p53 protein in malignant endothelial cells, the cells of origin of hemangiosarcomas. Riddelliine-induced hemangiosarcomas were negative for the beta-catenin protein. Spontaneous hemangiosarcomas from control mice lacked both p53 and beta-catenin protein expression and ras mutations. Our data indicated that p53 and beta-catenin mutations in the o-nitrotoluene-induced hemangiosarcomas and K-ras mutations and p53 protein expression in riddelliine-induced hemangiosarcomas most likely occurred as a result of the genotoxic effects of these chemicals. It also suggests that these mutations play a role in the pathogenesis of the respective hemangiosarcomas in B6C3F1(1) mice.

Animals↗
PubMed1992

A retrospective clinicopathologic study of 212 dogs with cutaneous hemangiomas and hemangiosarcomas.

The relationship between skin pigmentation and piliation and the development of hemangiomas and hemangiosarcomas in the dermis and subcutaneous tissue was studied in 212 dogs. These 212 dogs had a combined total of 306 tumors; 38 of these 212 dogs had two or more of the same tumor in a different location or a combination of hemangioma and hemangiosarcoma. The average age of the dogs at the time of excision of these tumors was greater than 10 years. There was no sex predilection for the presence or absence of tumors. Cutaneous hemangiomas (73%) were more common than cutaneous hemangiosarcomas (27%). Hemangiomas had no predilection for dermis (51%) or subcutaneous tissue (47%), but hemangiosarcomas had a marked predilection for dermis (73%) over subcutaneous tissue (7%). Dogs with short hair coats and lightly pigmented skin had more hemangiomas and hemangiosarcomas of the dermis (65%) than did dogs with variable length hair coats and pigmentation (28%). Dogs with short hair coats and lightly pigmented skin had fewer hemangiomas and hemangiosarcomas of the subcutaneous tissue (10%) than did dogs with variable length hair coats and pigmentation (22%). Dogs with short hair coats and lightly pigmented skin also had more hemangiomas and hemangiosarcomas of ventral glabrous skin (65%) than did dogs with variable length hair coats and pigmentation (22%). In addition, there was no predilection of subcutaneous hemangiosarcoma for haired (33%) versus glabrous (33%) skin, but dermal hemangiosarcoma had a marked predilection for the glabrous skin (63%) when compared with haired skin (10%). The increased incidence of dermal hemangiomas and hemangiosarcomas in ventral glabrous skin suggests an association between solar radiation and the biologic properties of glabrous skin in the genesis of these tumors.

Age Factors↗
PubMedDate not supplied

Mutations of ras protooncogenes and p53 tumor suppressor gene in cardiac hemangiosarcomas from B6C3F1 mice exposed to 1,3-butadiene for 2 years.

1,3-Butadiene is a multisite carcinogen in rodents. Incidences of cardiac hemangiosarcomas were significantly increased in male and female B6C3F1 mice that inhaled 1,3-butadiene (BD) for 2 years. Eleven BD-induced cardiac hemangiosarcomas were examined for genetic alterations in ras protooncogenes and in the p53 tumor suppressor gene. Nine of 11 (82%) BD-induced hemangiosarcomas had K-ras mutations and 5 of 11 (46%) had H-ras mutations. All of the K-ras mutations were G-->C transversions (GGC-->CGC) at codon 13; this pattern is consistent with reported results in BD-induced lung neoplasms and lymphomas. Both K-ras codon 13 CGC mutations and H-ras codon 61 CGA mutations were detected in 5 of 9 (56%) hemangiosarcomas. The 11 hemangiosarcomas stained positive for p53 protein by immunohistochemistry and were analyzed for p53 mutations using cycle sequencing of polymerase chain reaction (PCR) amplified DNA isolated from paraffin-embedded sections. Mutations in exons 5 to 8 of the p53 gene were identified in 5 of 11 (46%) hemangiosarcomas, and all of these were from the 200- or 625-ppm exposure groups that also had K-ras codon 13 CGC mutations. Our data indicate that K-ras, H-ras, and p53 mutations in these hemangiosarcomas most likely occurred as a result of the genotoxic effects of BD and that these mutations may play a role in the pathogenesis of BD-induced cardiac hemangiosarcomas in the B6C3F1 mouse.

Animals↗
PubMed2004

A retrospective study of visceral and nonvisceral hemangiosarcoma and hemangiomas in domestic animals.

Cases of hemangiosarcoma submitted to the Colorado State University Veterinary Diagnostic Laboratory during a 6-year period were reviewed. Visceral hemangiosarcomas represent less than 2% of canine specimens submitted for histologic examination and nonvisceral hemangiosarcoma less than 1%. Most nonvisceral hemangiosarcomas of dogs occur in skin. Hemangiosarcomas are less common in cats and usually occur in skin. They are also rare in other animal species. Animals with nonvisceral hemangiosarcomas are usually mature; dogs and cats average 10 years of age. The tumors develop in many different locations, and there is no sex predilection. A wide variety of dog breeds are affected, but Italian greyhounds, greyhounds, and whippets are overrepresented. Clinical outcomes of 76 cases of nonvisceral hemangiosarcomas in dogs and cats were obtained from submitting veterinarians. Completeness of excision of a tumor is the most important factor that can be used in predicting clinical outcome for an affected dog or cat. In all cases in which the animals were clinically normal for at least 1 year after surgical removal of a nonvisceral hemangiosarcoma, the margins were reported to be free of neoplastic cells. Degree of differentiation, mitotic rate, size of tumor, and presence or absence of epidermal ulceration, mast cells, or solar elastosis did not correlate with clinical outcome.

Animals↗
PubMed1981

Electron microscopic observations of hepatic and subcutaneous hemangiosarcomas induced in mice exposed to vinyl chloride monomer.

Both subcutaneous and hepatic hemangiosarcomas were induced in mice exposed to vinyl chloride monomer, and for the first time, the ultrastructure of hemangiosarcomas related to vinyl chloride exposure has been described. The subcutaneous hemangiosarcoma developed in a mouse's ear 29 weeks after exposure to 10 ppm vinyl chloride for 4 weeks, and the hepatic hemangiosarcoma was found in a mouse's liver at necropsy 56 weeks after exposure to 600 ppm vinyl chloride for 4 weeks. Both tumors showed a localized, cystic nodular appearance with a dark red tone. Histologically, an angiomatous architecture, the presence of neoplastic mesenchymal cell aggregates, focal necrosis, and hemorrhagic foci were common. Ultrastructurally, two neoplastic cell types, a mesenchymal and a well-differentiated endothelial cell type, were identified in both tumors. In addition, in the hepatic tumor, a pericyte-like neoplastic cell was also present. The incidence of hemangiosarcoma was much lower than that of lung tumors (alveologenic tumor) in mice exposed to vinyl chloride at the same concentrations for the same duration. This study suggests that there is no basic difference in ultrastructure between the vinyl chloride-induced hemangiosarcomas and hemangiosarcomas not related to this chemical exposure.

Animals↗
PubMedDate not supplied

Association of liver hemangiosarcoma and secondary iron overload in B6C3F1 mice--the National Toxicology Program experience.

The literature evidencing the role of iron in promoting a range of neoplasms in humans and animals prompted us to search for a possible association between chemically induced hemosiderosis and hemangiosarcomas in the liver of mice in selected studies conducted by the National Toxicology Program (NTP). Its historical control database was examined for studies in which treatment-related liver hemangiosarcoma was noted; 130 consecutive NTP studies in B6C3F1 mice from Technical Report (TR)-340 to TR-493 were evaluated. Three compounds (2-butoxyethanol, p-nitroaniline, and para-chloroaniline) were associated with a relatively high incidence of Kupffer cell pigmentation consisting of hemosiderin in both sexes; only the male mice developed a relatively low incidence of treatment-related hemangiosarcoma. With a fourth compound (o-nitroanisole), a relatively low incidence (16/50, high-dose males) of chemical-related hemosiderosis was noted, with no associated increase of hemangiosarcoma. Two chemicals (pentachlorophenol and tetrafluoroethylene) increased the incidence of liver hemangiosarcoma in male and female mice, with no increase in Kupffer cell pigmentation. The overall association between liver hemangiosarcoma and Kupffer cell pigmentation was highly significant (p < 0.001). The cause for hemosiderosis in all cases was the erythrocytic hemolytic effect of the compounds. The reason for the sex-increased susceptibility for development of hemangiosarcoma is unknown but may be due to a hormone-related, reduced antioxidative defensive capacity through modulation of the activities of antioxidative enzymes.

Aniline Compounds↗
PubMed2001

Evaluation of recombinant interleukin-2 immunotherapy for human hemangiosarcoma in a SCID mice model (WB-SCID).

We treated the patients with cutaneous hemangiosarcoma with recombinant interleukin-2 (rIL-2) immunotherapy that showed clear therapeutic effects. This immunotherapy is popular for the treatment of hemangiosarcoma in Japan. The purpose of this study is to clarify the clinical effects in an animal experiment. After establishing a SCID mouse model of human hemangiosarcoma WB-SCID, we used this model to investigate anti-tumor effects of rIL-2 and LAK cells. We demonstrated that hemangiosarcoma cells are LAK-sensitive, and LAK cells induced by rIL-2 suppress the growth of hemangiosarcoma. Our results may assure the clinical effects of rIL-2 immunotherapy on hemangiosarcoma.

Aged↗
PubMed2001

Potent inhibition of hemangiosarcoma development in mice by cidofovir.

The acyclic nucleoside phosphonate analogue cidofovir is a broad-spectrum anti-DNA virus agent, which also possesses potent inhibitory activity against various tumors associated with papillomaviruses in animal models and patients. Moreover, we recently described the potent inhibition of polyomavirus (PyV)-induced hemangioma formation in rats by cidofovir. This activity could not be explained by an antiviral mechanism. We have now evaluated the effect of cidofovir on the growth of hemangiosarcomas originating from PyV-transformed (PV/2b/35) cells, which do not produce polyomavirus. In vitro, cidofovir proved to be cytostatic for PV/2b/35 cells at a 50% cytostatic concentration (CC(50)) of 2.3 microg/ml. At cidofovir concentrations > or =20 microg/ml, cytotoxicity due to induction of apoptosis was observed. In vivo, intratumoral therapy with cidofovir, at 100 mg/kg 3 times a week, completely inhibited the development and even caused regression of established PV/2b/35 hemangiosarcomas in nude mice. Five days after the start of treatment, few proliferating cells were noted in the cidofovir-treated tumors, whereas control tumors were characterized by high expression of proliferating cell nuclear antigen (PCNA). Moreover, cidofovir induced apoptosis in the hemangiosarcomas, as evidenced by Tunel (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) staining. Also after intraperitoneal administration, cidofovir afforded a prominent protection against the growth of intraperitoneally or intracerebrally inoculated hemangiosarcoma cells in SCID mice. In conclusion, cidofovir possesses a direct antitumor activity, which is mediated by induction of tumor cell apoptosis. Cidofovir should be further explored for its potential in the treatment of fast-growing vascular tumors, like hemangiomas and hemangiosarcomas.

Animals↗
PubMed1999

Spontaneous and thiazolidinedione-induced B6C3F1 mouse hemangiosarcomas exhibit low ras oncogene mutation frequencies.

Hemangiosarcomasare uncommon malignant endothelial cell tumors in humans and experimental animal species. The mechanisms giving rise to these tumors are poorly understood even though the histotypes are comparable between humans and rodents. Activating mutations in cellular ras protooncogenes have been detected in sporadic and chemically induced human and rodent hemangiosarcomas. Ras activation significantly modulates tumor angiogenesis, suggesting that mutations in ras genes might be causally related to vascular tumorigenesis. To more clearly define the role of ras in experimental vascular tumorigenesis, mutations in the Ki- and Ha-ras genes were characterized in 63 hemangiosarcomas that arose unexpectedly in control and treated B6C3F1 mice during a two-year carcinogenicity study of the thiazolidinedione troglitazone. DNA was extracted from paraffin sections of mouse hemangiosarcomas, control liver, or positive control hepatocellular carcinomas with defined mutations in the Ki- or Ha-ras genes. Exons 1 and 2 of the Ki- and Ha-ras genes were independently amplified using primer extension preamplification/locus-specific heminested PCR, and PCR amplicons were directly sequenced to identify mutations in codons 12, 13, or 61. Activating mutations were detected in 3 of 63 hemangiosarcomas: a single G-->A transition in the second position of Ki-ras codon 13 in a tumor from a treated animal and two G-->T transversions in the second position of Ha-ras codon 13, one in a single tumor from a control animal and one in a tumor from a treated animal. These mutations are consistent with endogenous mutagenesis arising from oxidative DNA damage. The low frequency of mutation (<5%) indicates that ras mutations did not contribute significantly to hemangiosarcoma development and suggests that mutational ras activation may not be a necessary step in vascular tumorigenesis in mice.

Animals↗
PubMed2005

Distinct and opposite roles for SH2 and SH3 domains of v-src in embryo survival and hemangiosarcoma formation.

The cellular proto-oncogene c-src is thought to be involved in formation, progression, and metastasis of a variety of tumor cell types, although its exact role during tumor cell genesis is not well defined. v-src, the viral oncogene counterpart of c-src, causes metastatic sarcomas, hemorrhagic disease, and hemangiosarcomas in chicken embryos and, thus, can be used as a constitutively activated form of src for experimentally-induced tumorigenesis. Here, we used retroviral vectors to express wild-type v-src or SH2 or SH3 domain-deleted forms (DeltaSH2 or DeltaSH3) to determine if different pathogenic effects resulted. Vectors were injected into early chick embryo midbrain ventricles and embryos were sacrificed at various ages up to embryonic day (E) 18. Retroviral expression of all forms of v-src resulted in transformation of pial connective tissue cells into large, rounded abnormal-appearing cells. Surprisingly, all forms of v-src were lethal. The v-src retrovirus was lethal and killed most embryos by E15 with the development of hemangiosarcomas over the injection site between E10-E12. The DeltaSH3 retrovirus was the most deadly, killing most embryos by E12, however, it never resulted in hemangiosarcoma formation. The DeltaSH2 retrovirus injected embryos survived longer than v-src or DeltaSH3 embryos, and some of these embryos also developed large hemangiosarcomas over the injection site between E13 and E18. These results demonstrate that the src SH2 domain is required to be fully lethal, whereas the presence of the SH3 domain attenuated lethality. Furthermore, the formation of hemangiosarcomas absolutely required the presence of the src SH3 domain and to some extent required the SH2 domain. This implicates distinct and opposite roles for SH2 and SH3 domains of src and their cellular binding partners in tumorigenesis and hemorrhagic disease.

Animals↗
PubMed1985

Hemangiosarcoma in the cat: retrospective evaluation of 31 surgical cases.

Hemangiosarcoma was diagnosed in 31 cats. Diagnosis was confirmed by surgical biopsy. Locations of the primary tumors were the abdominal cavity (15 cats), sc tissue (13 cats), thoracic cavity (2 cats), and nasal cavity (1 cat). Nine (60%) of the 15 cats with abdominal hemangiosarcoma had extrathoracic evidence of metastasis: this was not found in the other cats. Of the cats with tumors located in the sc tissue, 6 of 10 (60%) evaluated on a long-term basis had local recurrence of the tumor. Eleven cats were not available for follow-up evaluation, 3 cats were euthanatized at the time of surgery, and 2 others were euthanatized within the first postoperative week subsequent to histologic diagnosis of hemangiosarcoma. Of the remaining 15 cats, 4 with abdominal hemangiosarcoma and 5 with hemangiosarcoma of the sc tissue died at means of 22 and 44 weeks, respectively.

Animals↗
PubMed1975

Hemangiosarcoma of spleen with spontaneous rupture.

A 76-year-old man with spontaneous rupture of a hemangiosarcoma of the spleen, together with a review of 49 previously reported patients with splenic hemangiosarcoma are presented. Twenty-three were women and 27 were men. All but 3 were adults. Fiften were 50-59 years of age. The symptomatology was nonspecific. Three patients developed microangiopathic hemolytic anemia. Spontaneous rupture occurred in 17 cases (34%). Metastases occurred in 42 cases; they were primarily hematogenous and most often in the liver. Lymph node involvement, however, was present in 13 cases. The prognosis of untreated splenic hemangiosarcoma is poor. Three of 25 patients survived a year or more after the initial onset of symptoms. Splenectomy before rupture is advisable, since 5 of 19 patients survived at least 1-5 years. It is suggested that hemangiosarcoma be considered in patients with: 1) splenomegaly without evidence of malignant lymphoma or leukemia, 2) splenomegaly with microangiopathic hemolytic anemia, and 3) unexplained intraperitoneal hemorrhage.

Adolescent↗
PubMed1981

Primary hemangiosarcoma of the spleen: report of four cases.

Four cases of primary splenic hemangiosarcoma are described. The most common presenting symptoms were recurrent, fever, malaise, and abdominal pain. Three patients also had complaints referable to the urinary tract. Severe hemolytic anemia with bizarre or fragmented red blood cells on peripheral smear was noted in three patients, in two cases, for more than 1 year before diagnosis. Two patients had been treated for mammary carcinoma with ionizing radiation 10 years before developing hemangiosarcoma of the spleen. One patient had multiple congenital hemangiomas present from birth, and is thought to have developed hemangiosarcoma in a previously existing benign hemangioma. None of our patients survived more than 7 months after the diagnosis of hemangiosarcoma. The importance of early detection and treatment of this tumor is discussed.

Aged↗
PubMed2001

Expression of vascular endothelial growth factor in a human hemangiosarcoma cell line (ISO-HAS).

Vascular endothelial growth factor (VEGF), in addition to being a specific mitogen of endothelial cells in vitro, is also known to induce angiogenesis in vivo. These functions suggest that VEGF may play an important role in the growth of hemangiosarcomas. Previous studies have demonstrated the expression of VEGF and its receptors, flt-1 or KDR/flk-1, in hemangiosarcomas by immunohistochemical staining and in situ hybridization. In the present study, however, we demonstrated that tumor cells of the hemangiosarcoma cell line ISO-HAS express mRNA of VEGF and its two receptors, flt-1 and KDR, and secrete VEGF protein. VEGF mRNA expression and protein secretion were found to be enhanced by phorbol 12-myristate 13-acetate. In addition, we demonstrated that ISO-HAS cells respond to recombinant human VEGF165 with a dose-dependent up-regulation of cell proliferation and growth. These results suggest that the VEGF-VEGF receptor system plays a role in proliferation and growth of hemangiosarcoma cells.

Cell Division↗
PubMed2006

Mechanisms of 2-butoxyethanol-induced hemangiosarcomas.

Chronic exposure to 2-butoxyethanol increased liver hemangiosarcomas in male mice. The mechanism for the selective induction of hemangiosarcomas by 2-butoxyethanol is unknown but has been suggested to occur through non-DNA-reactive mechanisms. The occurrence of liver hemangiosarcomas in male mice has been linked to oxidative damage subsequent to RBC hemolysis and iron deposition and activation of macrophages (Kupffer cells) in the liver, events that exhibit a threshold in both animals and humans. 2-Butoxyethanol is metabolized to 2-butoxyacetaldehyde and 2-butoxyacetic acid, and although the aldehyde metabolite is short lived, the potential exists for this metabolite to cause DNA damage. The present study examined whether 2-butoxyethanol and its metabolites, 2-butoxyacetaldehyde and 2-butoxyacetic acid, damaged mouse endothelial cell DNA using the comet assay. No increase in DNA damage was observed following 2-butoxyethanol (1-10mM), 2-butoxyacetaldehyde (0.1-1.0mM), or 2-butoxyacetic acid (1-10mM) in endothelial cells after 2, 4, or 24 h of exposure. Additional studies examined the involvement of hemolysis and macrophage activation in 2-butoxyethanol carcinogenesis. DNA damage was produced by hemolyzed RBCs (10 x 10(6), 4 h), ferrous sulfate (0.1-1.0 microM; 2-24 h), and hydrogen peroxide (50-100 microM; 1-4 h) in endothelial cells. Hemolyzed RBCs also activated macrophages, as evidenced by increased tumor necrosis factor (TNF) alpha, while neither 2-butoxyethanol nor butoxyacetic acid increased TNF-alpha from macrophages. The effect of activated macrophages on endothelial cell DNA damage and DNA synthesis was also studied. Coculture of endothelial cells with activated macrophages increased endothelial cell DNA damage after 4 or 24 h and increased endothelial cell DNA synthesis after 24 h. These data demonstrate that 2-butoxyethanol and related metabolites do not directly cause DNA damage. Supportive evidence also demonstrated that damaged RBCs, iron, and/or products from macrophage activation (possibly reactive oxygen species) produce DNA damage in endothelial cells and that activated macrophages stimulate endothelial cell proliferation. These events coupled together provide the events necessary for the induction of hemangiosarcomas by 2-butoxyethanol.

Acetaldehyde↗
PubMedDate not supplied

Efficacy and toxicity of VAC chemotherapy (vincristine, doxorubicin, and cyclophosphamide) in dogs with hemangiosarcoma.

Fifteen dogs with hemangiosarcoma were treated with a combination of vincristine, doxorubicin, and cyclophosphamide after incisional or excisional biopsy. The median survival for all fifteen dogs was 172 days (mean survival = 316 days). The median survival for those dogs with splenic hemangiosarcoma was 145 days (mean survival = 271 days) as compared with previously published median survival times in dogs with splenic hemangiosarcoma treated with surgery alone of 19 to 65 days. Toxicities included neutropenia (11/15), severe gastroenteritis (4/15), cardiotoxicity (3/15), and sepsis (2/15). The authors conclude that vincristine, doxorubicin, and cyclophosphamide chemotherapy may be an efficacious treatment modality in dogs with hemangiosarcoma and is associated with acceptable toxicity.

Animals↗
PubMedDate not supplied

Cutaneous hemangiosarcoma in 25 dogs: a retrospective study.

Hemangiosarcomas confined to the skin and underlying muscle were surgically excised in 25 dogs. Tumors were staged based on their histological location (ie, dermal, hypodermal, and deep). Dermal (stage I) hemangiosarcomas were small, most commonly ventral-abdominal or prepucial in location, and were associated with prolonged survival times (median survival, 780 days). Tumors with hypodermal (stage II) and underlying muscular involvement (stage III) were grouped together because of their larger size, bruise-like appearance, lack of anatomic predilection, biological behavior, and shorter survival times (median survival of 172 and 307 days for dogs with stages II and III, respectively). We conclude that dermal hemangiosarcomas may be effectively treated with surgery alone, whereas hemangiosarcomas located within the hypodermal tissues bear a poor prognosis and warrant wide surgical excision with adjuvant chemotherapy.

Animals↗
PubMed1980

Microangiopathic hemolytic anemia associated with radiation-induced hemangiosarcomas.

A retrospective study of red blood cell parameters in 53 dogs with experimental radiation-induced hemangiosarcoma showed 24 had anemia. Morphologic alterations in red blood cells in peripheral blood films from anemic dogs included signs of regeneration (anisocytosis and polychromasia), hypochromasia, red cell fragmentation and acanthocytosis. The degree and type of red cell changes varied from dog to dog and generally correlated with the principal site of tumor involvement. Blood from dogs with tumors principally involving liver had red cell regeneration, fragmentation and acanthocytosis. Blood from dogs with tumors primarily involving the heart had only red cell fragmentation. Blood films from dogs with skeletal and pulmonary hemangiosarcomas were similar to blood films from dogs with hepatic hemangiosarcoma except that red cell alterations generally were less severe. Scanning and transmission electron micrographic evaluation of neoplastic tissue showed large amounts of fibrin within neoplastic vascular sinuses and disruption and distortion of red blood cells traversing these abnormal vascular beds. The red blood cell fragmentation syndrome associated with radiation-induced hemangiosarcomas therefore was considered to be a microangiopathic hemolytic anemia of localized origin.

Anemia, Hemolytic↗