Vascular tumor

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Vascular tumor may mean:

Vascular Tumors

Benign vascular tumors 1

Infantile hemangioma / Hemangioma of infancy

Pattern
  • focal
  • multifocal
  • segmental
  • indeterminate
Different types
  • superficial
  • deep
  • mixed (superficial + deep)
  • reticular / abortive / minimal growth
  • others
Association with other lesions
PHACE association /

syndrome

Posterior fossa malformations, Hemangioma, Arterial

anomalies, Cardiovascular anomalies, Eye anomalies ,

sternal clefting and ⁄ or supraumbilical raphe

LUMBAR (SACRAL,

PELVIS) association /

syndrome

Lower body hemangioma, Urogenital anomalies,

Ulceration, Myelopathy, Bony deformities, Anorectal

malformations, Arterial anomalies, and Renal anomalies

  • Most common tumor of infancy. Usually appearing after birth, infantile hemangiomas undergo a period of proliferation in few weeks after birth followed by regression and involution in first year of life. Superficial lesions appear as red or “strawberry” colored nodules, papules, or plaques while deeper hemangiomas are typically bluish or skin colored. Mixed tumors, involving both epidermis and deeper structures, may display characteristics of both. They may also be classified as focal, that appear in a specific anatomical area, and segmental that shows varied pattern of growth following developmental growth regions. Segmental type is often associated with other developmental abnormalities.[1][2][3]
  • Rarely, infantile hemangioms can cause life-threatening complications such as congestive cardiac failure, respiratory difficulty and respiratory compromise, and loss of vision. There may also be long-term sequela including permanent disfigurement and scarring. If lesions are multiple, there is an increased risk of visceral involvement. There may be an association with certain syndromes such as PHACE syndrome.[1][4]
  • Some studies have indicated autosomal-dominant and maternal patterns of inheritance. Some studies suggest that environmental factors play the key role. Some risk factors that have been identified in association with infantile hemangioma include female gender, preterm birth, low weight at birth, increasing maternal age ta birth, placenta previa, pre-eclampsia, progesterone use by mother, and Caucasian race.[5][1][6][7]
  • THE diagnosis is made clinically and a thorough investigation should be carried out for visceral hemangiomas and other associative abnormalities if suspicion arises. Majority of these lesions do not require any treatment but treatment is indicated if there is risk for complications such as visual or respiratory involvement. Elective treatment is also offered to prevent disfigurement or scarring. Recently there have been an increased usage of oral beta-blockers such as timolol over systemic glucocorticoids because of higher efficacy. Vincristine and interferon alpha have been used in some high risk hemangiomas but carry the risk of severe complications. Visceral hemangioms may require embolization or surgery if they do not respond to systemic therapy. Laser therapy especially PDL is another modality used in cases of hemangioms unresponsive to medication.[1][8][9][10][11][12][13][14][15]
  • To learn more about infantile hemagioma click here.

Congenital hemangioma

  • Rare tumor that arises in utero and presents as fully developed lesion at birth. Following birth they can regress completely, partially or not at all. So they can be classified as Rapidly involuting (RICH), Non-involuting (NICH), Partially involuting (PICH).[16][17]
    1. Rapidly involuting (RICH)
      • This fast flow tumor can be detected in utero and appears as raised gray single lesions with dilated veins, telangiectasias and a halo at birth. This tumor may be complicated by thrombocytopenia and congestive cardiac failure due to its high-flow nature. Tumor typically regresses spontaneously in 1 to 2 years of life. Sometimes it can occur in liver where it follows the same pattern of involution as that of skin.[17][18]
    2. Non-involuting (NICH)
      • Fast flow tumor that presents as well defined, plaque like lesion with pink to purple color, telangiectasias and pale borders. Typically remains stable but there have been some reports of growth and expansion.[17]
    3. Partially involuting (PICH)
      • These lesions start involution as RICH but become stable over time and persist as NICH.[19]
  • Somatic mutations in GNAQ/GNA11 are thought to cause the congenital hemangioma. GNAQ and its paralogue GNA11 function in intracellular signaling pathways as Gq alpha subunit.[17][20]
  • Diagnosis is usually clinical but imaging techniques such as MRI, CT scan, contrast-enhanced ultrasound and later biopsy can be considered if required. Surgical excision should be considered in case of complications, NICH and PICH.[21][22]

Tufted angioma

  • Benign tumor that is characterized by dense clumps of endothelial cells and capillaries located in dermis. Most lesions appear in adolescence but some can manifest at birth or late in adulthood. Clinical presentation varies but majority of lesions appear as solitary stained area or elevation that later forms red-purple or dusky red plaque while some lesions appear as firm nodules. Lesions are usually solitary, asymptomatic but tender with occasional painful episodes and located on trunk and neck in majority of the cases. Some cases of multi-focal tufted angiomas have also been reported.[23][24][25][26]
  • Tufted angioma can be associated with Kasabach-Merritt phenomenon.[26][16][23]
  • Somatic activating GNA14 c.614A>T (p.Gln205Leu) mutations have been found in some tufted angiomas. These mutations may cause the cell growth to be growth-factor independent by up-regulating the MAPK pathway.[27][28]
  • Imaging such as MRI and ultrasound can add into clinical diagnosis to differentiate tufted angioma from similar lesions such as Kaposi sarcoma, kaposiform hemangioendothelioma and infantile hemangioma. Biopsy and histopathological studies are sometimes required for accurate diagnosis. Surgical excision is the treatment modality but some recommend to only observe the lesions due to its slow growth and possible remission. Other therapies include radiation beam therapy, cryosurgery, corticosteroids and pulsed laser therapy. Vincristine and embolization has been used with success in angiomas associated with Kasabach-Merritt phenomenon.[26][29][30][31][32][33][34]

Spindle-cell hemangioma

  • Rare benign tumor that manifests as solitary or multiple nodules confined to dermis and subcutaneous tissues in almost all of the cases. Histopathologically it appears as solid areas that are cellular and consist of spindle cells seen attached to vessel walls, and cavernous spaces that can be thrombosed. Size may increase over time and patient usually complains of swelling and pain. The nodules or masses can be mobile and elastic or can be firm and immobile.[35][36][37]
  • Somatic mutations in IDH1 and IDH2 have been found to be present in 70% of spindle-cell hemangiomas. IDH1 and IDH2 are important enzymes in cell energy cycles (α-ketoglutarate and NADPH generation).[38][39]
  • Diagnosis often requires biopsy and imaging studies such as MRI to ascertain the extent of the tumor. Local excision is the treatment modality of choice with excellent prognosis in majority of the cases although recurrence is very common.[35][36][37][40][41]

Epithelioid hemangioma

  • Rare benign tumor that typically presents as solitary painful nodule on head and neck. Penis is an atypical location. They can involve skin, bone and soft tissues. Histopathologically these lesions are characterized by presence of endothelial cells that resemble epithelial cells with evidence of proliferation such as large nuclei and prominent nucleoli, and often inflammatory infiltrates. Vessels are typically well-formed. Nuclear atypia is absent.[42][43][44]
  • FOS gene rearrangements such as ZFP36-FOSB fusions are found to be present in one third of epithelioid hemangioma in a study. It encodes a transcription factors that causes over-expression of vascular endothelial growth factor-D (VEGF-D).[45][46][47][48]
  • Diagnosis requires biopsy to determine characteristic histopathological features. Imaging techniques such as MRI can useful. Bone tumors often require surgery for accurate diagnosis. Surgical excision has been used in majority of cases. Other treatment modalities include radiotherapy and embolization. Recently chemoembolization and microwave ablation in combination have been used with success.[42][43][49]

Pyogenic granuloma

  • Also called as lobular capillary hemangioma, this common vascular lesion typically manifests as single, localized nodules on gingiva with sessile base but large lesions often present as lobulated or pediculated . Majority of the lesions are <2 cm in diameter and color of the lesion depending on vascularity varies from pink to purple. It can found anywhere on skin and mucous membranes such as lips, tongues, palate, and on atypical locations such asperiungual or gastrointestinal tract but gingiva is the typical location. Majority of the patients present with profuse bleeding. Others complain of painless mass, swelling, obstructive or interference related symptoms.[50][51][52][53]
  • Trauma or chronic irritation have been cited as the most common causes but it can arise due to multiple other factors such as medications, viral infections such as herpes virus type 1, Orf virus and/or human papilloma virus type 2, and BRAF mutations or use of BRAF inhibitors that can cause multiple, disseminated lesions. Medications that have been implicated in development of this lesion include oral contraceptives, retinoids, gefitinib, cabecitabine, and afatinib, BRAF inhibitors such as vemurafenib or encorafenib, and rituximab. Mutations in BRAF/RAS/GNA14 have all been associated with pyogenic granuloma, BRAF c.1799T>A has been recently described as one of the major mutations associated.[51][52][53][54][55][56][57]
  • The diagnosis is made by clinical features and then confirmed by histopatholgical features. Current standard of care is surgical excision. Other treatment modalities include curettage, electrocautery, radiosurgery, cryosurgery, sclerotherapy, or laser treatment. Topical or oral beta-blockers timolol or propranolol and topical imiquimod have also been successful.[51][52][58][59][60][61]

Hobnail hemangioma

  • Benign tumor that typically presents as solitary growth with often, but not always, tagetoid appearance of a central papule and peripheral brown ring that may or may not disappear over time. Characteristic histopathological feature include plump endothelial cells in superficial dermis that line ectatic and irregular vessels, and project into lumina like hobnails. Deeper dermis shows vessels dissecting collagen fibers. Majority of the lesions are fund on trunk and extremities with head and neck, and oral cavity as uncommon locations. Patient may present with pain, or an asymptomatic growing lesion.[62][63][64]
  • Etiology is not well understood but trauma may play a key role in pathogenesis. Some studies have found congenital etiology in some lesions.[62][63][65][66]
  • Diagnosis is based on clinical features and histopathological studies. Treatment is usually by excision. Other modalities of treatment include intermittent triamcinolone intralesional injections and pulsed dye laser treatment.[62][63]

Microvenular hemangioma

  • Rare lesion that most often manifests as single asymptomatic nodule, plaque or papule with color varying from red to bluish-red. Majority of the lesions are located on trunk and limbs. Histologically, the tumor consists of irregular and branching venous structures with inconspicuous lumina. Endothelial cells display absence of atypia and mitotic figures. Some lesions may be painful and/or tender.[67][68][69][70]
  • Etiology and pathogenesis have not been well-understood but a recent study may associate progesterone with microvenular hemangioma.[71]
  • Diagnosis requires biopsy because of rarity of this tumor. Treatment is through surgical excision.[67][68][69][70]

Anastomosing hemangioma

  • Rare tumor characterized by presence of anastomosing capillary-sized vessels with irregular fenestration, lined by endothelial cells with absence of atypia and occasional hobnailing. Majority of the lesions are found in kidneys and genitourinary tract with some being located in liver, adrenal glands and gastrointestinal tract. These tumors are typically incidental findings on radiology but some may present with back and/or flank pain with/without radiation to lower limbs.[72][73][74][75][76]
  • Etiology is not well-known but a recent study suggests muations in GNAQ genes that encodes members of G protein family.[77]
  • The diagnosis is very challenging because radiological findings of anastomosing hemangioma are similar to that of malignant tumors such as renal cell carcinoma, hepatocellular carcinoma and low grade angiosarcoma. So excision and biopsy are often suggested. There is no current guidelines for treatment but excision and local ablation are the options.[72][75][74][78][79]

Glomeruloid hemangioma

  • Characterized by red blood cells filled clumps of capillaries inside dilated vascular spaces. These collections of capillaries, lined by swollen endothelial cells, resemble renal glomeruli and stain positive for periodic acid-Schiff (PAS)-positive, diastase-resistant eosinophilic globules. Clinical presentation varies and are not discernible from other cutaneous lesions. Majority of the lesions manifest as multiple, asymptomatic pauples or nodules..[80][81]
  • Glomeruloid hemangioma is associated with POEMS syndrome in majority of the cases and rarely with Castleman's disease. Very few isolated cases of glomeruloid hemangioma have been reported.[80][81]
    • POEMS stands for peripheral neuropathy (P), organomegaly (O), endocrinopathy (E) monoclonal plasma-cells proliferative disorder (M) and skin changes (S) although diagnosis does not require presence of all of these symptoms. Other manifestations of POEMS syndrome may include sclerotic bone lesions, papilledema, edema, ascites, effusions, pulmonary hypertension, Castleman’ disease (CD), thrombocytosis and erythrocytosis, and increased serum VEGF.[82]
    • Castleman’s disease is characterized as lymphoproliferative disorder with inflammatory response involving multiple systems. Clinical presentation ranges from asymptomatic lymphadenopathy to severe systemic manifestations such as weight loss, fever and organomegaly.[83]
  • Etiology is not well-understood but some theories suggest role of vascular endothelial growth factor (VEGF), increased estrogen levels, human herpesvirus-8 and increased cytokines in its pathogenesis.[80][81]
  • Diagnosis relies on characteristic histology. Patients who present with glomeruloid hemangioma should undergo evaluation for POEMS syndrome and should be kept under follow-up because these lesions can precede full-blown POEMS syndrome in some cases.[80][81]

Papillary hemangioma

  • Rare tumor characterized by presence of papillary growths within dilated vascular channels, that contain cores of pericytes around normal capillaries. The tumor typically manifests as solitary papules in head and neck region, without any systemic manifestations.[84][85]
  • Diagnosis may require biopsy. Treatment options include excision and photodynamic therapy.[86]

Intravascular papillary endothelial hyperplasia

  • Also called as Masson's tumor, this benign lesions is characterized by presence of intravascular papillary structures that are enveloped by proliferating endothelial cells. It is considered to be a reactive lesion associated with an organizing thrombus. Clinically it manifests as solitary painless mass in head-neck and the extremities especially the hand, that may grow rapidly in size and become painful and/or tender. Some lesions have been found intra-abdominallly such as in the liver that can bleed and present with anemia.[87][88][89][90]
  • This lesions appears to be associated with vascular trauma, and thrombus that may lead to chronic irritation and increased levels of fibroblast growth factor (FGF), hypoxia-inducible factor-1 (HIF-1α), and vascular endothelial growth factor (VEGF) stimulating endothelial cells proliferation.[88][89][91]
  • Histopathological studies are generally required for diagnosis and may also require immunohistochemical confirmation. Treatment is surgery with uncommon recurrence.[91][92]

Cutaneous epithelioid angiomatous nodule

  • This recently diagnosed lesion is characterized histologically as proliferating, swollen epithelioid cells and thin walled vascular channels lined by swollen endothelial cells that resemble the epithelioid cells. These cells typically contain pale pink cytoplasm, intracytoplasmic vacuoles, and vesicular nuclei. Clinically these lesions manifest as solitary nodules or papules that may grow rapidly. Rarely multiple lesions have also been reported.[93][94][95]
  • Thought to be a reactive process but no trigger has been identified yet. Immunosuppression has been proposed to be associated with this benign vascular proliferation.[93][94]
  • Diagnosis requires careful clinical and histopathological evaluation. Surgery has been the treatment used in majority of the lesions although cryotherapy has also been used. Steroids are found to be ineffective.[93][95]

Acquired elastotic hemangioma

  • First described in 2002, this rare lesion typically manifests as solitary, asymptomatic, red to purple, patches and plaques on areas damaged by sun exposure such as hands and forearms. Some patients may complain of pain or growth of the lesion. Histologically its exhibits solar elastosis and band like proliferation of capillaries in superficial dermis. These proliferating channels are arranged parallel to epidermis and endothelial cells typically display absence of atypia but may show hobnail pattern.[96][97]
  • This lesion has slight preference for females. Damage due to sun exposure such as free radical production are thought to be associated with pathogenesis. Some case reports showed use of progesterone associated with appearance of lesions in perimenopausal women.[96][97][98][99]
  • Diagnosis requires biopsy to rule out basal cell carcinoma and other similar appearing lesions. Treatment options include observation, discontinuance of progesterone, laser therapy and excision. Recurrence was not observed in any of the cases observed or treated.[97][99][96][99][100]

Locally aggressive or borderline vascular tumors

Kaposiform hemangioendothelioma

  • Locally Aggressive tumor that originates on skin and occurs primarily in childhood.[101] It is characterized by a single or multiple masses with following characteristics:
    • Deep reddish-purple color
    • Shiny, firm texture
    • Warm to the touch
    • Swollen and painful
  • May be complicated by Kasabach-Merritt phenomenon (KMP), characterized by consumption coagulopathy, thrombocytopenia, and hemolytic anemia.[102] Typical features also include low fibrinogen and elevated D-dimers.
  • Somatic activating GNA14 c.614A>T (p.Gln205Leu) mutations have been found in some KHE.[27]
  • Invasion of bone, retroperitoneum, and mediastinum has occured in some cases but no case of metastasis has been reported yet. [102]
  • Diagnostic work up may include blood tests, biopsy, contrast enhanced ultrasound and MRI or CT scan imaging.
  • Treatment Options include steroid, vincristine, interferon alpha, anti-platelet agents, sirolimus-containing therapies and surgery.[103]

Retiform hemangioendothelioma

  • First described in 1994 as a form of low grade angiosarcoma, Retiform hemangioendothelioma commonly presents as a slow growing asymptomatic solitary nodule or plaque on distal extremities in 2nd-4th decade of life.[104]
  • Must be differentiated from Angiosarcoma.
  • High level of local recurrence but very low potential for metastasis.
  • Diagnostic work up includes histopathological studies, that shows arborizing blood vessels are arranged in retiform pattern [104], and MRI.
  • Surgery is the treatment of choice, though 2/3rd cases recur. Adjuvant radiotherapy and ddjuvant chemotherapy with recombinant interferon alpha and low dose cisplatin have also been reported in selected cases. [104]

Papillary intralymphatic angioendothelioma (PILA), Dabska tumor

  • First described in 1969 by Dabska,this rare vascular neoplasm generally occurs in soft tissues but can also occur in bone. They usually appear as painless inflammatory irregular or nodular lesions below the skin surface.
  • The distinctive feature on histopathology is the intravascular growth of well-differentiated endothelial cells presenting as a matchstick columnar configuration.[105]
  • They are locally aggressive but rarely metastasize. Locally recurrence after surgery is very common.
  • Diagnostic studies may include histopathological studies, fine needle aspiration, MRI and Ct scan.[106]
  • Wide local excision is the treatment of choice. However any combination of steroids, chemotherapy, radiation therapy, and invasive procedures can be used to treat this tumor.[107]

Composite hemangioendothelioma

  • A rare vascular neoplasms, characterized by an admixture of benign, low-grade malignant, and malignant vascular components, the ratio of each component can vary. They can occur in any age group.[108]
  • They occur predominantly as long-standing lesions in the dermis and subcutis of the extremities, but can also occur at other sites, including the oral cavity and in viscera such as kidney and spleen.[109]
  • It may recur locally and has the potential to metastasize. Recurrence was found to be in 8/10 cases in some studies. [110]
  • Diagnostic work up must include biopsy because of heterogeneity of lesions and it must be differentiated from other vascular tumors.[108]
  • Surgical excision is the treatment of choice although some patients have been treated with interferon and electron beams.[108]

Pseudomyogenic hemangioendothelioma

  • A locally aggressive tumor with endothelial differentiation that usually presents as multiple asymptomatic discontinuous lesions, often at extremities.[111][112]
  • SERPINE1-FOSB fusions are characteristic that result in over-expression of truncated form of FOSB.[111] FBJ murine osteosarcoma viral oncogene homolog B, also known as Finkel-Biskis-Jinkins murine osteosarcoma viral oncogene homolog B, FOSB or FosB, is a protein that, in humans have been implicated as regulators of cell proliferation, differentiation, and transformation.[113]
  • It may mimic epithelioid sarcoma on histology but metastasis is very rare and prognosis is excellent.[112]
  • Diagnostic work up includes X-ray, MRI, CT scan and biopsy of the lesion.
  • Excision is the typical treatment but chemotherapeutic agents including gemcitabine/taxane and mammalian target of rapamycin inhibitor [114], mTOR inhibitors such as sirolimus [115], VEGFR1-4/PDGFRA inhibitors such as telatinib [111] have been used with success in various studies.

Polymorphous hemangioendothelioma

  • A rare vascular neoplasm, Polymorphous hemangioendothelioma occurs in lymph nodes, but a few cases have been found in extra-nodal sites such as the mediastinum, spinal cord, and liver. It is a very rare cause of persistent lymphadenopathy. The data on natural history and clinical presentation is limited due to very few number of cases reported. [116]
  • Characterized by a polymorphous blend of solid, primitive vascular and angiomatous areas in varied proportions on microscopic examination.[116]
  • Diagnotic work up includes histopathological examination, MRI and Ct scan.
  • Wide local excision[117] has been used for treatment, with radiation therapy in case of recurrence.[118]

Kaposi sarcoma

  • An AIDS-associated vascular malignancy that usually presents as mucocutaneous lesions [119] but can also occur in viscera such as lungs. It can remain confined to skin but widespread visceral involvement may occur.
  • There are three known variants
    • One variant occurs spontaneously in Jewish and Italian males in Europe and the United States.
    • Another more aggressive variant is endemic in young children is endemic in Africa.
    • A third form occurs in about 0.04% of kidney transplant patients. There is also a high incidence in AIDS patients.[120] HHV-8 is the suspected cause.[121]
  • To learn more about KS, click here.

Malignant vascular tumors

Angiosarcoma

  • Angiosarcoma(AS) is malignancy that presents with a very heterogeneous distribution in the human body with aggressive clinical course, and may appear in multiple locations, from breast to liver or skin.[122]
  • Associated with MYC gene amplification and protein overexpression.[123] Myc is a family of regulator genes and proto-oncogenes that code for transcription factors.
  • Complete surgical excision and radiotherapy are the main treatments, with a minor role of chemotherapy.[124]
  • To learn more about angiosarcoma click here.

Epithelioid hemangioendothelioma

  • A rare vascular tumor, described for the first time in 1975 by Dail and Liebow,that usually affects lung, liver and bones, although may occur many other sites in body including head and neck, breasts and lymph nodes.[125]
  • Usually Asymptomatic but patient may present with respiratory symptoms, bone pains or other symptoms depending on the site of the tumor.
  • Majority are characterized by a reciprocal t(1;3)(p36;q25) translocation. The t(1;3) results in fusion of a gene known as WWTR1 (or TAZ) to CAMTA1. These genes code for transcription factors.[126][127]
  • Imaging is crucial in forming both diagnosis and management plan. Recognition of the expression of vascular markers (Fli-1 and CD31 are endothelial-specific markers), and the microscopic evidence of vascular differentiation is of primary importance as well.[125]
  • Surgery has been used as primary treatment modality depending upon the location of the tumor, with radiotherapy being used in some cases.

References

  1. ↑ 1.0 1.1 1.2 1.3 Smith C, Friedlander SF, Guma M, Kavanaugh A, Chambers CD (July 2017). "Infantile Hemangiomas: An Updated Review on Risk Factors, Pathogenesis, and Treatment". Birth Defects Res. 109 (11): 809–815. doi:10.1002/bdr2.1023. PMC 5839165. PMID 28402073. Vancouver style error: initials (help)
  2. ↑ Chiller KG, Passaro D, Frieden IJ (December 2002). "Hemangiomas of infancy: clinical characteristics, morphologic subtypes, and their relationship to race, ethnicity, and sex". Arch Dermatol. 138 (12): 1567–76. PMID 12472344.
  3. ↑ Greenberger S, Bischoff J (September 2011). "Infantile hemangioma-mechanism(s) of drug action on a vascular tumor". Cold Spring Harb Perspect Med. 1 (1): a006460. doi:10.1101/cshperspect.a006460. PMC 3234458. PMID 22229118.
  4. ↑ Rotter A, Samorano LP, Rivitti-Machado MC, Oliveira Z, Gontijo B (June 2018). "PHACE syndrome: clinical manifestations, diagnostic criteria, and management". An Bras Dermatol. 93 (3): 405–411. doi:10.1590/abd1806-4841.20187693. PMC 6001075. PMID 29924216. Vancouver style error: initials (help)
  5. ↑ Castrén E, Salminen P, Vikkula M, Pitkäranta A, Klockars T (November 2016). "Inheritance Patterns of Infantile Hemangioma". Pediatrics. 138 (5). doi:10.1542/peds.2016-1623. PMID 27940781.
  6. ↑ Haggstrom AN, Drolet BA, Baselga E, Chamlin SL, Garzon MC, Horii KA, Lucky AW, Mancini AJ, Metry DW, Newell B, Nopper AJ, Frieden IJ (March 2007). "Prospective study of infantile hemangiomas: demographic, prenatal, and perinatal characteristics". J. Pediatr. 150 (3): 291–4. doi:10.1016/j.jpeds.2006.12.003. PMID 17307549.
  7. ↑ Drolet BA, Swanson EA, Frieden IJ (November 2008). "Infantile hemangiomas: an emerging health issue linked to an increased rate of low birth weight infants". J. Pediatr. 153 (5): 712–5, 715.e1. doi:10.1016/j.jpeds.2008.05.043. PMID 18940356.
  8. ↑ Darrow DH, Greene AK, Mancini AJ, Nopper AJ (October 2015). "Diagnosis and Management of Infantile Hemangioma: Executive Summary". Pediatrics. 136 (4): 786–91. doi:10.1542/peds.2015-2482. PMID 26416928.
  9. ↑ Ceisler EJ, Santos L, Blei F (2004). "Periocular hemangiomas: what every physician should know". Pediatr Dermatol. 21 (1): 1–9. PMID 14871317.
  10. ↑ Tal R, Dotan M, Lorber A (June 2016). "Approach to haemangiomatosis causing congestive heart failure". Acta Paediatr. 105 (6): 600–4. doi:10.1111/apa.13359. PMID 26859502.
  11. ↑ Hogeling M, Adams S, Wargon O (August 2011). "A randomized controlled trial of propranolol for infantile hemangiomas". Pediatrics. 128 (2): e259–66. doi:10.1542/peds.2010-0029. PMID 21788220.
  12. ↑ Bennett ML, Fleischer AB, Chamlin SL, Frieden IJ (September 2001). "Oral corticosteroid use is effective for cutaneous hemangiomas: an evidence-based evaluation". Arch Dermatol. 137 (9): 1208–13. PMID 11559219.
  13. ↑ Perez J, Pardo J, Gomez C (2002). "Vincristine--an effective treatment of corticoid-resistant life-threatening infantile hemangiomas". Acta Oncol. 41 (2): 197–9. PMID 12102167.
  14. ↑ Schiestl C, Neuhaus K, Zoller S, Subotic U, Forster-Kuebler I, Michels R, Balmer C, Weibel L (April 2011). "Efficacy and safety of propranolol as first-line treatment for infantile hemangiomas". Eur. J. Pediatr. 170 (4): 493–501. doi:10.1007/s00431-010-1324-2. PMID 20936416.
  15. ↑ Chinnadurai S, Sathe NA, Surawicz T (March 2016). "Laser treatment of infantile hemangioma: A systematic review". Lasers Surg Med. 48 (3): 221–33. doi:10.1002/lsm.22455. PMID 26711436.
  16. ↑ 16.0 16.1 "www.issva.org" (PDF).
  17. ↑ 17.0 17.1 17.2 17.3 Ayturk UM, Couto JA, Hann S, Mulliken JB, Williams KL, Huang AY, Fishman SJ, Boyd TK, Kozakewich HP, Bischoff J, Greene AK, Warman ML (April 2016). "Somatic Activating Mutations in GNAQ and GNA11 Are Associated with Congenital Hemangioma". Am. J. Hum. Genet. 98 (4): 789–95. doi:10.1016/j.ajhg.2016.03.009. PMC 4833432. PMID 27058448.
  18. ↑ Berenguer B, Mulliken JB, Enjolras O, Boon LM, Wassef M, Josset P, Burrows PE, Perez-Atayde AR, Kozakewich HP (2003). "Rapidly involuting congenital hemangioma: clinical and histopathologic features". Pediatr. Dev. Pathol. 6 (6): 495–510. PMID 15018449.
  19. ↑ Nasseri E, Piram M, McCuaig CC, Kokta V, Dubois J, Powell J (January 2014). "Partially involuting congenital hemangiomas: a report of 8 cases and review of the literature". J. Am. Acad. Dermatol. 70 (1): 75–9. doi:10.1016/j.jaad.2013.09.018. PMID 24176519.
  20. ↑ "Error 403".
  21. ↑ Ramphul K, Mejias SG, Ramphul-Sicharam Y, Sonaye R (April 2018). "Congenital Hemangioma: A Case Report of a Finding Every Physician Should Know". Cureus. 10 (4): e2485. doi:10.7759/cureus.2485. PMC 6003795. PMID 29922526.
  22. ↑ Thimm MA, Rhee D, Takemoto CM, Karnsakul W, Cuffari C, Guerrerio AL, Garcia A, Gearhart J, Huisman T, Hwang M (October 2018). "Diagnosis of congenital and acquired focal lesions in the neck, abdomen, and pelvis with contrast-enhanced ultrasound: a pictorial essay". Eur. J. Pediatr. 177 (10): 1459–1470. doi:10.1007/s00431-018-3197-8. PMID 29971555. Vancouver style error: initials (help)
  23. ↑ 23.0 23.1 Prasuna A, Rao PN (2015). "A tufted angioma". Indian Dermatol Online J. 6 (4): 266–8. doi:10.4103/2229-5178.160259. PMC 4513407. PMID 26225332.
  24. ↑ Jones EW, Orkin M (February 1989). "Tufted angioma (angioblastoma). A benign progressive angioma, not to be confused with Kaposi's sarcoma or low-grade angiosarcoma". J. Am. Acad. Dermatol. 20 (2 Pt 1): 214–25. PMID 2644316.
  25. ↑ Pesapane F, Nazzaro G, Alberti-Violetti S, Gianotti R (2015). "A case of acquired tufted angioma in adulthood". An Bras Dermatol. 90 (3 Suppl 1): 16–8. doi:10.1590/abd1806-4841.20153733. PMC 4540497. PMID 26312663.
  26. ↑ 26.0 26.1 26.2 Bandyopadhyay D, Saha A (2015). "Multifocal Annular Tufted Angioma: An Uncommon Clinical Entity". Indian J Dermatol. 60 (4): 422. doi:10.4103/0019-5154.160528. PMC 4533571. PMID 26288441.
  27. ↑ 27.0 27.1 Lim YH, Bacchiocchi A, Qiu J, Straub R, Bruckner A, Bercovitch L, Narayan D, McNiff J, Ko C, Robinson-Bostom L, Antaya R, Halaban R, Choate KA (August 2016). "GNA14 Somatic Mutation Causes Congenital and Sporadic Vascular Tumors by MAPK Activation". Am. J. Hum. Genet. 99 (2): 443–50. doi:10.1016/j.ajhg.2016.06.010. PMC 4974082. PMID 27476652.
  28. ↑ "GNA14 G protein subunit alpha 14 [Homo sapiens (human)] - Gene - NCBI".
  29. ↑ Ghosh SK, Bandyopadhyay D, Ghosh A, Biswas SK, Barma KD (July 2011). "Acquired multifocal tufted angiomas in an immunocompetent young adult". Indian J Dermatol. 56 (4): 412–4. doi:10.4103/0019-5154.84741. PMC 3179005. PMID 21965850.
  30. ↑ Osio A, Fraitag S, Hadj-Rabia S, Bodemer C, de Prost Y, Hamel-Teillac D (July 2010). "Clinical spectrum of tufted angiomas in childhood: a report of 13 cases and a review of the literature". Arch Dermatol. 146 (7): 758–63. doi:10.1001/archdermatol.2010.135. PMID 20644037.
  31. ↑ Chiu CS, Yang LC, Hong HS, Kuan YZ (2007). "Treatment of a tufted angioma with intense pulsed light". J Dermatolog Treat. 18 (2): 109–11. doi:10.1080/09546630601028752. PMID 17520468.
  32. ↑ Yesudian PD, Parslew R, Klafowski J, Gould D, Pizer B (February 2008). "Tufted angioma-associated Kasabach-Merritt syndrome treated with embolization and vincristine". Plast. Reconstr. Surg. 121 (2): 692–3. doi:10.1097/01.prs.0000298541.92722.5d. PMID 18301012.
  33. ↑ Silva C, Schettini A, Santos M, Chirano C (2017). "Tufted angioma". An Bras Dermatol. 92 (5): 742–743. doi:10.1590/abd1806-4841.20175896. PMC 5674719. PMID 29166525. Vancouver style error: initials (help)
  34. ↑ Kimura R, Yoshida Y, Wakumoto K, Yamada N, Yamamoto O (October 2017). "Successful treatment of tufted angioma with low-dose electron beam radiation therapy: Report of two cases". J. Dermatol. 44 (10): e262–e263. doi:10.1111/1346-8138.13936. PMID 28623854.
  35. ↑ 35.0 35.1 Murakami K, Yamamoto K, Sugiura T, Kirita T (2018). "Spindle Cell Hemangioma in the Mucosa of the Upper Lip: A Case Report and Review of the Literature". Case Rep Dent. 2018: 1370701. doi:10.1155/2018/1370701. PMC 5892276. PMID 29780644.
  36. ↑ 36.0 36.1 Chavva S, Priya MH, Garlapati K, Reddy GS, Gannepalli A (June 2015). "Rare Case of Spindle Cell Haemangioma". J Clin Diagn Res. 9 (6): ZD19–21. doi:10.7860/JCDR/2015/11998.6080. PMC 4525619. PMID 26266229.
  37. ↑ 37.0 37.1 Minagawa T, Yamao T, Shioya R (2011). "Spindle cell hemangioendothelioma of the temporal muscle resected with zygomatic osteotomy: a case report of an unusual intramuscular lesion mimicking sarcoma". Case Rep Surg. 2011: 481654. doi:10.1155/2011/481654. PMC 3350060. PMID 22606579.
  38. ↑ Pansuriya TC, van Eijk R, d'Adamo P, van Ruler MA, Kuijjer ML, Oosting J, Cleton-Jansen AM, van Oosterwijk JG, Verbeke SL, Meijer D, van Wezel T, Nord KH, Sangiorgi L, Toker B, Liegl-Atzwanger B, San-Julian M, Sciot R, Limaye N, Kindblom LG, Daugaard S, Godfraind C, Boon LM, Vikkula M, Kurek KC, Szuhai K, French PJ, Bovée JV (November 2011). "Somatic mosaic IDH1 and IDH2 mutations are associated with enchondroma and spindle cell hemangioma in Ollier disease and Maffucci syndrome". Nat. Genet. 43 (12): 1256–61. doi:10.1038/ng.1004. PMC 3427908. PMID 22057234.
  39. ↑ Lu C, Ward PS, Kapoor GS, Rohle D, Turcan S, Abdel-Wahab O, Edwards CR, Khanin R, Figueroa ME, Melnick A, Wellen KE, O'Rourke DM, Berger SL, Chan TA, Levine RL, Mellinghoff IK, Thompson CB (February 2012). "IDH mutation impairs histone demethylation and results in a block to cell differentiation". Nature. 483 (7390): 474–8. doi:10.1038/nature10860. PMC 3478770. PMID 22343901.
  40. ↑ Gray SS, Eltorky MA, Riascos RF, Montilla RD (June 2012). "Spindle cell hemangioma reoccurrence in the hand: case report". Hand (N Y). 7 (2): 194–9. doi:10.1007/s11552-012-9397-1. PMC 3351523. PMID 23730241.
  41. ↑ Perkins P, Weiss SW (October 1996). "Spindle cell hemangioendothelioma. An analysis of 78 cases with reassessment of its pathogenesis and biologic behavior". Am. J. Surg. Pathol. 20 (10): 1196–204. PMID 8827025.
  42. ↑ 42.0 42.1 Barber E, Domes T (September 2014). "Painful erections secondary to rare epithelioid hemangioma of the penis". Can Urol Assoc J. 8 (9–10): E647–9. doi:10.5489/cuaj.1833. PMC 4164556. PMID 25295139.
  43. ↑ 43.0 43.1 Tsikopoulos K, Perdikakis E, Georgiannos D, Bisbinas I (March 2018). "Epithelioid hemangioma of the scapula treated with chemoembolization and microwave ablation: Α case report". Acta Orthop Traumatol Turc. 52 (2): 157–161. doi:10.1016/j.aott.2017.01.003. PMC 6136344. PMID 28159479.
  44. ↑ Gong QX, Fan QH, Xie J, Su ZL, Zhang MH, Zhang ZH (September 2013). "[Epithelioid hemangioma: a clinicopathologic analysis of 7 cases]". Zhonghua Bing Li Xue Za Zhi (in Chinese). 42 (9): 593–8. PMID 24314244.
  45. ↑ Milde-Langosch K (November 2005). "The Fos family of transcription factors and their role in tumourigenesis". Eur. J. Cancer. 41 (16): 2449–61. doi:10.1016/j.ejca.2005.08.008. PMID 16199154.
  46. ↑ Durchdewald M, Angel P, Hess J (November 2009). "The transcription factor Fos: a Janus-type regulator in health and disease". Histol. Histopathol. 24 (11): 1451–61. doi:10.14670/HH-24.1451. PMID 19760594.
  47. ↑ Marconcini L, Marchio S, Morbidelli L, Cartocci E, Albini A, Ziche M, Bussolino F, Oliviero S (August 1999). "c-fos-induced growth factor/vascular endothelial growth factor D induces angiogenesis in vivo and in vitro". Proc. Natl. Acad. Sci. U.S.A. 96 (17): 9671–6. PMC 22268. PMID 10449752.
  48. ↑ Huang SC, Zhang L, Sung YS, Chen CL, Krausz T, Dickson BC, Kao YC, Agaram NP, Fletcher CD, Antonescu CR (October 2015). "Frequent FOS Gene Rearrangements in Epithelioid Hemangioma: A Molecular Study of 58 Cases With Morphologic Reappraisal". Am. J. Surg. Pathol. 39 (10): 1313–21. doi:10.1097/PAS.0000000000000469. PMC 4567921. PMID 26135557.
  49. ↑ Gérard V, Tomasella M, Kurth W, Brands G, Lognard M (April 2015). "[Epithelioid hemangioma, a rare bone tumor]". Rev Med Liege (in French). 70 (4): 169–71. PMID 26054166.
  50. ↑ Marla V, Shrestha A, Goel K, Shrestha S (2016). "The Histopathological Spectrum of Pyogenic Granuloma: A Case Series". Case Rep Dent. 2016: 1323798. doi:10.1155/2016/1323798. PMC 4921146. PMID 27382492.
  51. ↑ 51.0 51.1 51.2 Thada SR, Pai KM, Agarwal P (May 2014). "A huge oral pyogenic granuloma with extensive alveolar bone loss and 'sun-ray' appearance mimicking a malignant tumour". BMJ Case Rep. 2014. doi:10.1136/bcr-2013-202367. PMC 4039851. PMID 24859551.
  52. ↑ 52.0 52.1 52.2 Wollina U, Langner D, França K, Gianfaldoni S, Lotti T, Tchernev G (July 2017). "Pyogenic Granuloma - A Common Benign Vascular Tumor with Variable Clinical Presentation: New Findings and Treatment Options". Open Access Maced J Med Sci. 5 (4): 423–426. doi:10.3889/oamjms.2017.111. PMC 5535648. PMID 28785323.
  53. ↑ 53.0 53.1 Kamal R, Dahiya P, Puri A (January 2012). "Oral pyogenic granuloma: Various concepts of etiopathogenesis". J Oral Maxillofac Pathol. 16 (1): 79–82. doi:10.4103/0973-029X.92978. PMC 3303528. PMID 22434943.
  54. ↑ Simmons BJ, Chen L, Hu S (November 2016). "Pyogenic granuloma association with isotretinoin treatment for acne". Australas. J. Dermatol. 57 (4): e144–e145. doi:10.1111/ajd.12418. PMID 27885661.
  55. ↑ Inoue A, Sawada Y, Nishio D, Nakamura M (February 2017). "Pyogenic granuloma caused by afatinib: Case report and review of the literature". Australas. J. Dermatol. 58 (1): 61–62. doi:10.1111/ajd.12423. PMID 26603180.
  56. ↑ Henning B, Stieger P, Kamarachev J, Dummer R, Goldinger SM (June 2016). "Pyogenic granuloma in patients treated with selective BRAF inhibitors: another manifestation of paradoxical pathway activation". Melanoma Res. 26 (3): 304–7. doi:10.1097/CMR.0000000000000248. PMID 27116335.
  57. ↑ Groesser L, Peterhof E, Evert M, Landthaler M, Berneburg M, Hafner C (February 2016). "BRAF and RAS Mutations in Sporadic and Secondary Pyogenic Granuloma". J. Invest. Dermatol. 136 (2): 481–6. doi:10.1038/JID.2015.376. PMID 26802240.
  58. ↑ Giblin AV, Clover AJ, Athanassopoulos A, Budny PG (2007). "Pyogenic granuloma - the quest for optimum treatment: audit of treatment of 408 cases". J Plast Reconstr Aesthet Surg. 60 (9): 1030–5. doi:10.1016/j.bjps.2006.10.018. PMID 17478135.
  59. ↑ Al-Mohaya MA, Al-Malik AM (December 2016). "Excision of oral pyogenic granuloma in a diabetic patient with 940nm diode laser". Saudi Med J. 37 (12): 1395–1400. doi:10.15537/smj.2016.12.15941. PMC 5303780. PMID 27874157.
  60. ↑ Malik M, Murphy R (December 2014). "A pyogenic granuloma treated with topical timolol". Br. J. Dermatol. 171 (6): 1537–8. doi:10.1111/bjd.13116. PMID 24836966.
  61. ↑ Millsop JW, Trinh N, Winterfield L, Berrios R, Hutchens KA, Tung R (March 2014). "Resolution of recalcitrant pyogenic granuloma with laser, corticosteroid, and timolol therapy". Dermatol. Online J. 20 (3). PMID 24656264.
  62. ↑ 62.0 62.1 62.2 Hiremath SK, Charantimath S, Byakodi S, Bijjal S, Byakodi R, Sapra G (July 2013). "Oral hobnail hemangioma: a case report". Arch Iran Med. 16 (7): 428–30. doi:013167/AIM.0013 Check |doi= value (help). PMID 23808782.
  63. ↑ 63.0 63.1 63.2 Yoon SY, Kwon HH, Jeon HC, Lee JH, Cho S (November 2011). "Congenital and multiple hobnail hemangiomas". Ann Dermatol. 23 (4): 539–43. doi:10.5021/ad.2011.23.4.539. PMC 3229956. PMID 22148030.
  64. ↑ Takayama R, Ueno T, Futagami A, Ansai S, Fukumoto T, Saeki H (2015). "Hobnail Hemangioma: A Case Report". J Nippon Med Sch. 82 (3): 151–5. doi:10.1272/jnms.82.151. PMID 26156669.
  65. ↑ Morganroth GS, Tigelaar RE, Longley BJ, Luck LE, Leffell DJ (February 1995). "Targetoid hemangioma associated with pregnancy and the menstrual cycle". J. Am. Acad. Dermatol. 32 (2 Pt 1): 282–4. PMID 7829718.
  66. ↑ Christenson LJ, Stone MS (June 2001). "Trauma-induced simulator of targetoid hemosiderotic hemangioma". Am J Dermatopathol. 23 (3): 221–3. PMID 11391103.
  67. ↑ 67.0 67.1 Mansur AT, Demirci GT, Ozbal Koc EA, Yildiz S (January 2018). "An unusual lesion on the nose: microvenular hemangioma". Dermatol Pract Concept. 8 (1): 7–11. doi:10.5826/dpc.0801a02. PMC 5808364. PMID 29445567.
  68. ↑ 68.0 68.1 Requena L, Sangueza OP (December 1997). "Cutaneous vascular proliferation. Part II. Hyperplasias and benign neoplasms". J. Am. Acad. Dermatol. 37 (6): 887–919, quiz 920–2. PMID 9418757.
  69. ↑ 69.0 69.1 Koch PS, Goerdt S, Peitsch WK (March 2015). "Solitary red-purple plaque on the chest of a 7-year-old boy: a quiz. Microvenular haemangioma". Acta Derm. Venereol. 95 (3): 378–82. doi:10.2340/00015555-1953. PMID 25138781.
  70. ↑ 70.0 70.1 Kim YC, Park HJ, Cinn YW (2003). "Microvenular hemangioma". Dermatology (Basel). 206 (2): 161–4. doi:10.1159/000068453. PMID 12592086.
  71. ↑ Juan YC, Chen CJ, Hsiao CH, Chiu TM (July 2018). "A microvenular hemangioma with a rare expression of progesterone receptor immunocreativity and a review of the literature". J. Cutan. Pathol. doi:10.1111/cup.13322. PMID 30019384.
  72. ↑ 72.0 72.1 Jin LU, Liu J, Li Y, Sun S, Mao X, Yang S, Lai Y (February 2016). "Anastomosing hemangioma: The first case report in the bladder". Mol Clin Oncol. 4 (2): 310–312. doi:10.3892/mco.2015.699. PMC 4734195. PMID 26893881.
  73. ↑ Ross M, Polcari A, Picken M, Sankary H, Milner J (September 2012). "Anastomosing hemangioma arising from the adrenal gland". Urology. 80 (3): e27–8. doi:10.1016/j.urology.2012.05.032. PMID 22840861.
  74. ↑ 74.0 74.1 Lin J, Bigge J, Ulbright TM, Montgomery E (November 2013). "Anastomosing hemangioma of the liver and gastrointestinal tract: an unusual variant histologically mimicking angiosarcoma". Am. J. Surg. Pathol. 37 (11): 1761–5. doi:10.1097/PAS.0b013e3182967e6c. PMID 23887160.
  75. ↑ 75.0 75.1 Cheon PM, Rebello R, Naqvi A, Popovic S, Bonert M, Kapoor A (June 2018). "Anastomosing hemangioma of the kidney: radiologic and pathologic distinctions of a kidney cancer mimic". Curr Oncol. 25 (3): e220–e223. doi:10.3747/co.25.3927. PMC 6023565. PMID 29962849.
  76. ↑ Perdiki M, Datseri G, Liapis G, Chondros N, Anastasiou I, Tzardi M, Delladetsima JK, Drakos E (January 2017). "Anastomosing hemangioma: report of two renal cases and analysis of the literature". Diagn Pathol. 12 (1): 14. doi:10.1186/s13000-017-0597-4. PMC 5260082. PMID 28118845.
  77. ↑ Bean GR, Joseph NM, Gill RM, Folpe AL, Horvai AE, Umetsu SE (May 2017). "Recurrent GNAQ mutations in anastomosing hemangiomas". Mod. Pathol. 30 (5): 722–727. doi:10.1038/modpathol.2016.234. PMID 28084343.
  78. ↑ Abboudi H, Tschobotko B, Carr C, DasGupta R (2017). "Bilateral Renal Anastomosing Hemangiomas: A Tale of Two Kidneys". J Endourol Case Rep. 3 (1): 176–178. doi:10.1089/cren.2017.0018. PMC 5734139. PMID 29279869.
  79. ↑ Peng X, Li J, Liang Z (September 2017). "Anastomosing haemangioma of liver: A case report". Mol Clin Oncol. 7 (3): 507–509. doi:10.3892/mco.2017.1341. PMC 5543263. PMID 28808574.
  80. ↑ 80.0 80.1 80.2 80.3 Gupta J, Kandhari R, Ramesh V, Singh A (March 2013). "Glomeruloid hemangioma in normal individuals". Indian J Dermatol. 58 (2): 160. doi:10.4103/0019-5154.108088. PMC 3657245. PMID 23716835.
  81. ↑ 81.0 81.1 81.2 81.3 Gupta V, Rai A, Mridha AR, Sharma VK (2016). "Multiple glomeruloid hemangiomas without POEMS syndrome". Indian J Dermatol Venereol Leprol. 82 (4): 442–4. doi:10.4103/0378-6323.181461. PMID 27279314.
  82. ↑ Nozza A (2017). "POEMS SYNDROME: an Update". Mediterr J Hematol Infect Dis. 9 (1): e2017051. doi:10.4084/MJHID.2017.051. PMC 5584767. PMID 28894560.
  83. ↑ Kahn F, Fagerström A, Segelmark M, Bakoush O (June 2008). "Irreversible Kidney Damage due to Multicentric Castleman's Disease". Libyan J Med. 3 (2): 101–3. doi:10.4176/080108. PMC 3074288. PMID 21499466.
  84. ↑ Suurmeijer AJ (February 2010). "Papillary hemangiomas and glomeruloid hemangiomas are distinct clinicopathological entities". Int. J. Surg. Pathol. 18 (1): 48–54. doi:10.1177/1066896908323504. PMID 18805868.
  85. ↑ Suurmeijer AJ, Fletcher CD (November 2007). "Papillary haemangioma. A distinctive cutaneous haemangioma of the head and neck area containing eosinophilic hyaline globules". Histopathology. 51 (5): 638–48. doi:10.1111/j.1365-2559.2007.02847.x. PMID 17927585.
  86. ↑ Schmidt-Erfurth UM, Kusserow C, Barbazetto IA, Laqua H (July 2002). "Benefits and complications of photodynamic therapy of papillary capillary hemangiomas". Ophthalmology. 109 (7): 1256–66. PMID 12093647.
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  88. ↑ 88.0 88.1 Kim S, Jun JH, Kim J, Kim DW, Jang YH, Lee WJ, Chung HY, Lee SJ (2013). "HIF-1α and VEGF expression correlates with thrombus remodeling in cases of intravascular papillary endothelial hyperplasia". Int J Clin Exp Pathol. 6 (12): 2912–8. PMC 3843272. PMID 24294378.
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  90. ↑ Hong SG, Cho HM, Chin HM, Park IY, Yoo JY, Hwang SS, Kim JG, Park WB, Chun CS (April 2004). "Intravascular papillary endothelial hyperplasia (Masson's hemangioma) of the liver: a new hepatic lesion". J. Korean Med. Sci. 19 (2): 305–8. doi:10.3346/jkms.2004.19.2.305. PMC 2822318. PMID 15082910.
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  95. ↑ 95.0 95.1 Dastgheib L, Aslani FS, Sepaskhah M, Saki N, Motevalli D (March 2013). "A young woman with multiple cutaneous epithelioid angiomatous nodules (CEAN) on her forearm: a case report and follow-up of therapeutic intervention". Dermatol. Online J. 19 (3): 1. PMID 23551998.
  96. ↑ 96.0 96.1 96.2 Hicks T, Katz I (October 2016). "First description of the dermatoscopic features of acquired elastotic hemangioma-a case report". Dermatol Pract Concept. 6 (4): 35–37. doi:10.5826/dpc.0604a08. PMC 5108644. PMID 27867745.
  97. ↑ 97.0 97.1 97.2 Cohen PR, Hinds BR (December 2017). "Acquired Elastotic Hemangioma: Case Series and Comprehensive Literature Review". Cureus. 9 (12): e1994. doi:10.7759/cureus.1994. PMC 5832390. PMID 29507844.
  98. ↑ Requena L, Kutzner H, Mentzel T (September 2002). "Acquired elastotic hemangioma: A clinicopathologic variant of hemangioma". J. Am. Acad. Dermatol. 47 (3): 371–6. PMID 12196746.
  99. ↑ 99.0 99.1 99.2 Tong PL, Beer TW (December 2010). "Acquired elastotic hemangioma: ten cases with immunohistochemistry refuting a lymphatic origin in most lesions". J. Cutan. Pathol. 37 (12): 1259–60. doi:10.1111/j.1600-0560.2010.01610.x. PMID 20950363.
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  105. ↑ © 1999 Lippincott Williams & Wilkins, Inc.
  106. ↑ https://www.dovemed.com/diseases-conditions/papillary-intralymphatic-angioendothelioma-pila/
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  108. ↑ 108.0 108.1 108.2 Rokni GR, Montazer F, Sharifian M, Goldust M (December 2017). "Composite hemangioendothelioma of the forehead and right eye; a case report". BMC Dermatol. 17 (1): 15. doi:10.1186/s12895-017-0067-4. PMC 5727897. PMID 29233122.
  109. ↑ Shang Leen SL, Fisher C, Thway K (July 2015). "Composite hemangioendothelioma: clinical and histologic features of an enigmatic entity". Adv Anat Pathol. 22 (4): 254–9. doi:10.1097/PAP.0000000000000079. PMID 26050262.
  110. ↑ https://www.jpatholtm.org/upload/pdf/kjp-40-2-142.pdf
  111. ↑ 111.0 111.1 111.2 van IJzendoorn D, Sleijfer S, Gelderblom H, Eskens F, van Leenders G, Szuhai K, Bovée J (June 2018). "Telatinib Is an Effective Targeted Therapy for Pseudomyogenic Hemangioendothelioma". Clin. Cancer Res. 24 (11): 2678–2687. doi:10.1158/1078-0432.CCR-17-3512. PMID 29511030. Vancouver style error: initials (help)
  112. ↑ 112.0 112.1 Raftopoulos E, Royer M, Warren M, Zhao J, Rush W (August 2018). "Pseudomyogenic Hemangioendothelioma: Case Report and Review of the Literature". Am J Dermatopathol. 40 (8): 597–601. doi:10.1097/DAD.0000000000001104. PMID 29406432.
  113. ↑ https://en.wikipedia.org/wiki/FOSB
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  116. ↑ 116.0 116.1 El Hussein S, Omarzai Y (May 2017). "Multifocal Polymorphous Hemangioendothelioma of the Liver: Case Report and Review of Literature". Int. J. Surg. Pathol. 25 (3): 266–270. doi:10.1177/1066896916679517. PMID 27913780.
  117. ↑ Tadros M, Rizk SS, Opher E, Thompson LD (June 2003). "Polymorphous hemangioendothelioma of the neck". Ann Diagn Pathol. 7 (3): 165–8. PMID 12808568.
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  126. ↑ Errani C, Zhang L, Sung YS, Hajdu M, Singer S, Maki RG, Healey JH, Antonescu CR (August 2011). "A novel WWTR1-CAMTA1 gene fusion is a consistent abnormality in epithelioid hemangioendothelioma of different anatomic sites". Genes Chromosomes Cancer. 50 (8): 644–53. doi:10.1002/gcc.20886. PMC 3264678. PMID 21584898.
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