Tools
Omental Tumors
Introduction
The omentum is an intraabdominal organ connected to the spleen, stomach, pancreas, and colon, served by the left and right gastroepiploic arteries. The omentum is visceral adipose comprising a single layer of mesothelial cells sandwiched by connective tissue containing fibroblasts, adipocytes, mesothelium, endothelium, mast cells, lymphocytes, granulocytes, macrophages, blood vessels, connective tissue, and angiogenic and immunogenic pluripotent cells lines. The omentum plays a role in peritoneal homeostasis, including fluid and solute transport, tissue and cellular repair, angiogenesis, infection control, and lipid storage, and serves as a reservoir for stem cells.[1]
Immune cells move among omental regions via fenestrations. Milky spots are areas of immune cells arranged around blood vessels near fenestrations, allowing inflammatory cell egress into the peritoneal cavity; these areas are upregulated during active infection. Milky spots also aid perfusion, absorb fluid, and synthesize and release neurotransmitters associated with sympathetic nerves, including dopamine, epinephrine, norepinephrine, and choline acetyltransferase. The lymphatics from milky spots drain to the subpyloric and splenic lymph nodes.[1]
Stem cells within the omentum promote angiogenesis by producing vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF). Inflammation and hypoxia can drive VEGF expression; these cytokines promote the migration of neural stem cells to the injury site. Laminin within the omental stroma produces vasoactive growth factor and neurotrophic factor. Mechanisms have been proposed for the role of the omentum in stroke recovery, treatment for Alzheimer Disease, and increasing perfusion to ischemic limbs.[2]
The omentum is a frequent site of malignant transformation and metastatic disease. Immune cells within the milky spots are thought to mitigate inflammation and contribute to the spread of malignancy. Milky spots likely behave as secondary lymphoid organs, able to mount responses to peritoneal antigens and generate and differentiate peritoneal macrophages. Still, the omental milieu, including milky spots, mesenchymal cells, and adipocytes, is favorable for promoting metastatic disease.[3][4] Metastates to the omentum often confer a worse prognosis compared to metastases at other sites, as the omentum contributes to chemoresistance and propagation of tumor.[5]
Malignancies can arise from omental cell lines, leading to a primary omental tumor. Primary omental tumors are rare and frequently presented as case reports. Primary omental malignancies include liposarcoma, hemangiopericytoma, fibrosarcoma, leiomyosarcoma, mesothelioma, and malignant fibrous histiocytoma; indolent processes such as intraabdominal desmoid tumor have been reported.[6] More commonly, the omentum is the site of a variety of metastatic processes, most commonly uterine, ovarian, colorectal, and gastric cancers. Of note, a gastrointestinal stromal tumor may originate primarily from the omentum or be located within the omentum as metastatic disease. The omentum is also a frequent site for inflammatory processes that may be difficult to distinguish from malignancies.[7][8]
Etiology
Register For Free And Read The Full Article
Search engine and full access to all medical articles- 10 free questions in your specialty
- Free CME/CE Activities
- Free daily question in your email
- Save favorite articles to your dashboard
- Emails offering discounts
Learn more about a Subscription to StatPearls Point-of-Care
Etiology
Metastatic seeding of the omentum is common, but primary omental tumors are rare. Hemangiopericytoma, arising from the pericytes of Zimmerman, is one of the most commonly reported primary tumors of the omentum.[9][10][11] Cases of omental rhabdomyosarcoma, small cell carcinoma, malignant solitary fibrous tumor, malignant fibrous histiocytoma, lipomas, yolk sac tumor, and angiofibrolipoma have been reported.[6][12][13][14][15][16][17][18][19][20] Primary omental mesothelioma is related to asbestos exposure.[21] Gastrointestinal stromal tumors, usually metastatic to the omentum, can rarely arise primarily within the omentum.[22]
According to the 2020 World Health Organization (WHO) soft tissue tumor classification, most sarcomas originating in omentum are soft tissue tumors. Soft tissue sarcoma is derived from mesenchymal tissue cells. Liposarcoma and leiomyosarcoma are the most common intraabdominal soft tissue sarcoma but rarely occur within the omentum as a primary tumor. Liposarcoma originates from primitive mesenchymal cells and is composed of lipoblasts.[23][24][25] Desmoplastic round cell tumor of the omentum, a mesenchymal tumor, results from a chromosomal translocation that fuses the Ewing sarcoma and Wilm tumor suppressor genes, rendering an Ewing sarcoma RNA-binding protein-1.[26]
Metastatases to the omentum, common in intraabdominal and pelvic malignancies, were thought to be via direct spread, given the anatomic proximity of the omentum to the tissue of origin. However, recent studies suggest that spread may also be hematogenous and that omental metastases are correlated with a tendency toward hematogenous spread.[5]
Epidemiology
Smooth muscle tumors comprise approximately 37% of primary omental tumors.[27] Nineteen cases of liposarcoma were reported between 1936 and 2019, largely in men with an average age of 50.[24][28] Twenty-three cases of leiomyosarcoma have been reported through October 2016, presenting within the 5th decade, with a slight predilection to men.[24][29][30][31]
The WHO groups several neoplasms under extra-pleural solitary fibrous tumors (SFT), including hemangiopericytoma, lipomatous hemangiopericytoma, and giant cell angiofibroma. SFTs comprise up to 5% of all sarcomas, and omental SFT is rare. Only 14 cases of SFTs arising from the omentum have been described in the literature. Approximately 78% to 88% of omental SFT are benign. Solitary fibrous tumors typically occur between the 5th and 7th decade, with a 1:1 male-to-female ratio.[32][33][34][33][35]
Most primary omental tumors represent a small subset of their extra-omental metastatic counterparts. Fifty-four cases of omental extra gastrointestinal stromal tumors have been reported, with a median age at diagnosis of 65.[31][36][37] Omental lipomas account for 7% to 9% of all lipomas. Omental mesothelioma represents 10% of all mesothelioma.[26]
Omental metastatic disease is significantly more common than primary omental tumors. Omental metastatic disease most commonly originates from the ovaries, uterus, stomach, or colon. Approximately 10% of patients with gastric cancer have omental metastases; these patients have reduced disease-free survival.[38][39]
Pathophysiology
All primary omental tumors are rare, sporadic, and usually malignant; metastatic omental lesions are common. Primary omental tumors are typically derived from adipose, vascular, or lymphatic tissue. Tumor cells and immunologic B, T, and natural killer cells bind to milky spots that may increase tumor growth.[30][40][41][42][43][44] Tumor-associated macrophages may also promote cancer progression by secretion of chemokines that promote colonization of tumor cells. Cancer-associated fibroblasts within the omentum may facilitate the spread of cancer through transforming growth factor ß-1, promoting adhesion of cancer cells, and upregulating other growth factors.[45]
Gastrointestinal stromal tumors (GISTs) and extragastrointestinal stromal tumors (EGISTs) are histopathologically and immunohistochemically similar; both neoplasms express gain-of-function mutations, and the omentum harbors Cajal cells such as CD117+ and CD34+ from which EGISTs can arise.[31][46] Omental EGIST may reflect a gastric GIST that extended outward and grew away from its origin or a de novo neoplasm of interstitial cells of Cajal precursors, possibly migrating from the gastrointestinal tract following development.[47]
The omentum creates a microenvironment conducive to metastatic tumors, and many components, including fibroblasts, macrophages, and mesenchymal stem cells, contribute to chemoresistance via their interaction with tumor cells. Omental metastases often congregate within the milky spots that communicate directly with the peritoneal cavity. In addition, omental adiposity provides an abundance of energy and releases growth factors such as leptin and other hormones, promoting adhesion, migration, and chemoresistance of metastases. Cancer-associated adipocytes, both within and external to the tumor, affect surrounding adipocytes, resulting in an altered milieu, including an increase in lipid peroxidation.[3][5][48]
For example, omental tissue secretes factors promoting gastric cancer growth, motility, invasiveness, and chemoresistance. Factors that upregulate gastric cancer via increased angiogenesis include interleukins 6 and 8. In addition, gastric cancer is thought to take up omental exosomes, thereby increasing invasiveness. Adipocytes also help promote gastric cancer metastases via the upregulation of transfer protein.[49][50]
Histopathology
Omental tumors are difficult to diagnose using radiographic criteria and the gross appearance of the lesion. Often, primary omental tumors are distinguished solely by their histologic characteristics.
The omental SFT is composed of spindle-shaped cells and collagen bundles.[34][51] These tumors are negative for immunohistochemical expression of CD117, cytokeratin, calretinin, CD99, CD68, desmin, F8, S-100, and epithelial membrane antigen and positive for CD34, α-smooth muscle actin, BCL-2, and vimentin. CD34 is a useful biomarker for SFT.[32][34] Omental SFTs are generally hypervascular, with pericytes surrounding anastomosing vessels, and hypercellular with immature cells, hemorrhage, and necrosis.[14]
EGISTs and GISTs are histopathologically similar. Seventy percent have spindle cell morphology, and 20% have epithelioid or mixed morphology with high cellularity and low mitotic activity. KIT mutations occur in tumors with spindle cell morphology, whereas the PDGFRA mutation occurs in those with epitheliod and mixed morphology, suggesting the existence of distinct molecular entities.[31][36][52]
Omental mesothelioma may demonstrate an epithelial, sarcomatoid, or biphasic pattern. Epithelioid tumors comprise 75% of cases and may be well-differentiated with a tubulopapillary pattern or solid sheets of round or polygonal cells. Such tumors may mimic carcinomas, and it can be difficult to distinguish epithelioid mesothelioma from metastatic carcinoma, particularly adenocarcinoma. Sarcomatoid omental mesothelioma may be indistinguishable from fibrosarcomas on histology alone. Immunohistochemistry can help to differentiate sarcoma and adenocarcinoma; mesothelioma tumor cells are positive for calretinin, cytokeratin, and epithelial membrane antigen and negative for S-100 protein, Leu-M1, CEA, thrombomodulin, and placental alkaline phosphatase. Calretinin is a commonly used marker to establish the diagnosis.[42]
Omental rhabdomyosarcomatous cells have round or oval hyaline inclusions containing intermediate filaments and are positive for proteins of differentiated muscle, such as desmin, vimentin, myoglobin, and actin. Liposarcoma stains for vimentin, desmin, cytokeratin, and Ki-67. Primary omental leiomyosarcoma is composed of long fusiform cells with a high mitotic index, along with areas of coagulative necrosis and myxoid change. Stains may be positive for desmin and smooth muscle actin and strongly negative for S100, CD34, and c-kit.[29][30]
Desmoplastic small round cell tumor requires immunohistochemistry to differentiate them from other entities such as Ewing Sarcoma. Desmoplastic small round cell tumor demonstrates nests of small round blue cells with scant cytoplasm and small nucleoli within desmoplastic fibrous connective tissue, staining positive for cytokeratin, desmin, vimentin, and neuron-specific enolasein.[26] Omental small cell carcinoma demonstrates small cells with scant eosinophilic cytoplasm, oval or spindle-shaped nuclei with stippled nuclear chromatin, and stains for CD56, cytokeratin, synaptophysin, and neuron-specific enolase.[13][24]
History and Physical
Primary omental tumors may remain asymptomatic for an extended period. Still, most patients eventually present with abdominal discomfort, increasing abdominal girth, a palpable abdominal mass, nausea, early satiety, and weight loss. Rarely, a tumor may rupture, provoking a systemic inflammatory response. The physical examination of a patient with a primary omental tumor may reveal a painless abdominal mass palpable in the epigastrium, hypogastrium, upper or lower right or left quadrant or involving the entire abdomen. Ascites may be present. A case report of primary omental leiomyosarcoma reported hemorrhagic pseudoascites. Some large primary omental tumors remain clinically silent.[27][28][30][31][34][35][51][53][54]
Metastatic disease involving the omentum presents as an advanced malignancy and involves systemic symptoms of weight loss, early satiety, and gastrointestinal upset. Patients may present with a significant abdominal mass, ascites, and guarding.[30][55] The most common clinical findings are abdominal discomfort (56%) and mass (35%).[7][29][56] Symptoms are not specific to the tumor of origin but instead reflect late stages of malignancy. On occasion, omental metastases may present as incidental findings on imaging.[29]
Evaluation
The ability to accurately diagnose an omental tumor based on clinical and radiographic findings is limited. Usually, a definitive diagnosis can only be made through histopathological examination of the tumor.[28][30] For example, the appearance of a well-differentiated liposarcoma on computed tomography (CT) scan or magnetic resonance imaging (MRI) is similar to fat and other abdominal tumors. In addition, the mass may be adherent to other organs, rendering the radiographic evaluation more difficult.[29][30]
Contrast CT and MRI of the abdomen and pelvis are the best imaging methods for radiographic evaluation of omental tumors. CT often reveals a multilobular, flat, pancake-like mass with enhancing solid and multicystic densities. Angiography may demonstrate a feeding artery to the tumor arising from the omental blood supply. A highly vascular lesion is more likely to be malignant than a less vascular one. While ultrasound may visualize the tumor and delineate its internal structure, such findings are nonspecific.[29][30]
Omental SFTs appear as a proliferation of fibrous tissue within the omentum, possibly abutting surrounding structures. These tumors are well vascularized, and many have a cystic component with low attenuation, signifying necrosis and calcification. However, imaging modalities cannot usually differentiate between an SFT and other mesenchymal tumors.
A lipomatous lesion is well-demarcated and homogenous or may have fibrous septations and calcification. Signs of malignancy include thicker septations, irregular shape, incursion into surrounding structures, and associated adenopathy. Positron emission tomography (PET) may help distinguish a lipoma from a well-differentiated liposarcoma.[20]
A hemangiopericytoma often has nondistinct features on imaging. Color Doppler ultrasound may reveal significant vascularization with a vascular pedicle entering the tumor. CT may reveal a well-demarcated soft tissue mass common to many omental lesions. If benign, no calcifications or invasion are evident, but when malignant, necrosis and calcifications are evident. Angiography may be helpful to identify the vessels that feed the tumor.[10]
The desmoplastic small round cell tumor has radiographic features similar to other omental masses, including a hypoechoic heterogenous mass with enhanced vascularity, regions of necrosis, hemorrhage, and calcification. MRI can often identify CT-occult lesions, and PET is used for staging.[26]
The radiological features of an EGIST may be similar to omental leiomyoma and leiomyosarcoma.[31] An EGIST appears well-circumscribed on CT and can also feature areas of low attenuation from necrosis and hemorrhage. Of note is that EGIST does not have the central gas typically demonstrated by a GIST.[37]
Needle aspiration of omental tumors is not typically helpful due to inadequate tissue sampling. Apple et al reported accurate diagnosis could be achieved with fine needle aspiration by applying a careful and strict protocol, but the protocol requires standardization and replication in many patients. Histology, including immunohistochemistry, is often required for a definitive diagnosis, as is the case to distinguish mesothelioma from adenocarcinoma and sarcoma.[34][42]
Various diagnostic modalities may be used to evaluate omental tumors. Image-guided percutaneous biopsy or laparoscopy is used to obtain tissue for diagnosis and staging. Fluorescence in situ hybridization (FISH) may be used to determine chromosomal translocation and is particularly useful when diagnosing a desmoplastic mall round cell tumor. Cancer antigen 125 (CA-125) may be elevated in some omental tumors, and while nonspecific, can be a prognostic indicator and aid in monitoring response to therapy.[26][30][34][35]
Treatment / Management
Please see the National Comprehensive Cancer Network for all available recently updated guidelines for treating cancer by type at nccn.org/guidelines.
The general approach to treating omental tumors is resection, including cytoreduction and debulking for advanced disease. Palliative surgery plus adjuvant chemoradiation has been shown to prolong survival in many cases. Most practices and treatment recommendations for primary omental tumors come from case studies and expert consensus.
The complete resection of omental liposarcoma and leiomyosarcoma results in a good prognosis. Nonstandardized chemotherapy, in addition to radiation and immunotherapy, for nonresectable disease offers variable results. Relapse is a common problem following treatment for advanced disease, and long-term survival is low.[28][29](B3)
Approximately 80% to 85% of omental SFTs are benign; malignant tumors can recur even several years after primary surgery.[34][35] The benefit of adjuvant therapy is unclear, but some reports suggest adjuvant radiotherapy may slow disease progression. Many malignant SFTs are c-kit positive, and tyrosine kinase inhibitors like imatinib and sunitinib, traditionally used when treating GISTs, have been employed to treat malignant omental SFTs.[32][34][35][47] The recommended treatment for omental GISTs is surgical resection with imatinib adjuvant therapy; this regimen has been shown to prevent relapse and prolong long-term survival.[31][46] (B3)
Cytoreductive surgery in conjunction with intraoperative hyperthermic intraperitoneal chemotherapy has been adopted for the treatment of omental mesothelioma in small clinical trials and was shown to improve median survival. Vogelzang et al conducted a multicenter, randomized, controlled phase III trial using pemetrexed-cisplatin for inoperable malignant pleural mesothelioma; this protocol has been applied to omental disease. Immunotherapy and radiotherapy are also used for omental mesothelioma.[42][57](B3)
For advanced-stage cancers that are commonly metastatic to the omentum, including uterine, gastric, ovarian, and colorectal malignancies, standard surgical care includes omentectomy. There is inconclusive evidence regarding the survival benefit of this practice. Still, expert consensus suggests that cytoreductive surgery improves overall and disease-free survival, and omentectomy provides staging and prognostic information. For example, omentectomy increased the detection of micrometastases in metastatic endometrial cancer, although the survival advantage was not significant. Given the increased chemoresistance to metastatic disease within the omentum, cytoreductive surgery remains the most effective therapy for metastases to this site.[5][50][58][59](B2)
Differential Diagnosis
Omental tumors can be mistaken for ovarian tumors and other malignancies that originate in the pelvis, as well as disseminated diseases such as lymphoma and tuberculosis. The following is a nonexhaustive list of primary and metastatic omental neoplasms.[30][42]
- Fibrosarcoma
- Spindle cell sarcoma
- Liposarcoma
- Leiomyoma
- Hemangiopericytoma
- Lipoma
- Desmoid tumor
- Fibroma
- Mesothelioma
- Leiomyosarcoma
- Myosarcoma
- Rhabdomyosarcoma
- Leiomyoblastoma
- Endothelioma
- Desmoid small round cell tumor
- Endometrial adenocarcinoma
- Ovarian cancer
- Gastric cancer
- Colorectal cancer
- Primary peritoneal cancer
- Neuroblastoma
- Primitive neuroectodermal tumors.
Surgical Oncology
Omentectomy and lymphadenectomy are indicated for most stage III or IV intraabdominal tumors as part of surgical staging and histologic evaluation. In addition, studies have suggested that omentectomy may improve prognosis as the omentum provides an environment that is favorable for tumor growth. Excising the omentum can eliminate the communication between cancer cells and the omental stromal elements that appear to upregulate tumor activity.[5][38] Surgical excision, whenever feasible for all primary omental tumors, is recommended.
Radiation Oncology
Radiation therapy is a part of many primary omental cancer therapeutic regimens. Radiation is an effective therapy for rhabdomyosarcoma in all locations, using a cumulative dose between 36 and 41.4 Gy for microscopic residual disease and between 50.4 and 54 Gy for gross residual disease. Sometimes, whole-body irradiation is used for desmoplastic small round cell tumors.[15][26]
Pertinent Studies and Ongoing Trials
An observational cross-sectional study compared persons with metastatic ovarian cancer of the same stage and similar characteristics, differentiated by the presence or absence of omental metastases. Of the 56 persons, 36 had omental metastases, and 20 had no omental metastases. All underwent debulking surgery. The patients had no significant difference in tumor size, CA-125 levels, or ascites. Nearly all received platinum-based chemotherapy. The overall survival rate in those with omental metastases was 43.4% compared with 93.8% in those without omental metastases. In addition, progression-free and post-recurrence survival was shorter, and the recurrence rate was higher (72.2% vs 40.0%) in the omental metastases group. The authors concluded that omental metastases are an independent risk factor for survival in patients with stage III-IV ovarian cancer.[5]
Medical Oncology
There are no standardized medical oncology regimens for primary omental cancers. Metastatic cancers are referred to the guidelines for the tissue of origin. Examples of some chemotherapy protocols for primary omental cancers reported in case studies are:
Rhabdomyosarcoma: vincristine, dactinomycin, ifosfamide.[15][16]
Liposarcoma: liposomal doxorubicin.[24]
Small cell carcinoma: cisplatin, methotrexate, vincristine (CMV regimen). This patient recurred in the stomach and was treated with oxaliplatin, leucovorin, and 5-fluorouracil.[13]
Desmoplastic small round cell tumor: P6 protocol, including vincristine, doxorubicin, and cyclophosphamide, alternating with etoposide and ifosfamide.[26][60]
Yolk sac tumor: cisplatin, etoposide, bleomycin.[6]
Prognosis
The prognosis of persons with primary and metastatic omental tumors varies with the tissue of origin, tumor biology, tumor size, and timely diagnosis. Primary omental tumors often present late in the course of the disease, at which point they are larger, more difficult to excise and pose a greater risk for recurrence.
The prognosis of omental liposarcoma is worse than liposarcoma of the extremities. In one study, the mean 5-year survival rate for liposarcoma of the trunk was 41.9% compared to 66.7% for those within the extremities. The 5-year disease-free survival for omental liposarcoma depends on the histologic type, worse for high-grade tumors, including dedifferentiated, round cell, and pleomorphic, compared with low-grade tumors such as well-differentiated and myxoid.[28][61][62]
Omental EGIST is a rare neoplasm, and its prognosis is uncertain. However, when compared to GIST, EGIST has higher mitotic indices, larger size, and more distant metastasis. In addition, EGIST may present later, given the relative lack of early symptoms.[36][46]
Malignant mesothelioma of the omentum confers a poor prognosis, and most patients die within 1 year of diagnosis, even with combined palliative therapy. In a group of patients who underwent hyperthermic intraperitoneal chemotherapy for omental mesothelioma, the median survival approached 5 years.[42]
The prognosis for small cell carcinoma in any location is poor, with a 5-year survival rate of less than 15% and a mean survival of less than 5 months, ranging from 3 to 8 months for extensive and localized disease. Solitary fibrous tumors greater than 20 cm with more than 4 mitotic figures per high power field are associated with a poor prognosis. Rather than classified as strictly benign or malignant, these tumors are thought to exist on a risk spectrum dependent on factors including patient age, tumor size, and mitotic numbers.[63]
Several studies have correlated metastatic omental disease with a worse prognosis secondary to increased chemoresistance and altered tumor biology compared with metastases in other sites. For example, in those persons with ovarian cancer metastatic to the omentum, a correlation was demonstrated between the response of omental tumors to chemotherapy and overall survival.[5] In contrast, omental metastases from gastric cancer have not been shown to alter overall or disease-free survival significantly.[64]
Complications
Intraabdominal rupture of an omental tumor has been described. Other complications arising from an omental tumor include torsion with infarction, hemorrhage, and obstruction.[35]
Consultations
Multiple specialists, including surgical oncology, medical oncology, pharmacology, palliative care medicine, gastroenterology, gynecologic oncology, histopathology, and ancillary staff, participate in the care of persons with omental neoplasms.
Deterrence and Patient Education
Primary omental neoplasms are rare and sporadic. For many primary omental tumors, there is a significant risk of recurrence, even years following diagnosis and treatment. Close ongoing surveillance of these patients is recommended.[24] In the setting of disease metastatic to the omentum, patients are referred to navigators and education specific to the primary tumor.
Pearls and Other Issues
Many primary omental tumors are diagnosed postoperatively, given the difficulty of establishing a diagnosis based on imaging modalities and physical examination findings. A surgical biopsy is often necessary to enable diagnosis and proper treatment selection. A delay in diagnosis leads to a delay in tumor-specific therapy and an increased risk of recurrence. The recurrence rate of omental tumors is high, and surveillance is essential. In the event of recurrence, repeat resection is usually recommended.
Enhancing Healthcare Team Outcomes
Primary omental tumors remain rare and difficult to diagnose, and there are no standardized treatment regimens. Therefore a flexible, patient-centered treatment plan as developed within an inter-disciplinary team remains the best approach.
Tumors metastatic to the omentum are advanced and often resistant to protocol developed for the tumor of origin. The treatment of these complex malignancies requires an experienced team well-versed in oncological options, multi-modal therapies, and clinical trials.
References
Ishigaki K, Kumano K, Fujita K, Ueno H. Cellular basis of omentum activation and expansion revealed by single-cell RNA sequencing using a parabiosis model. Scientific reports. 2021 Jul 6:11(1):13958. doi: 10.1038/s41598-021-93330-5. Epub 2021 Jul 6 [PubMed PMID: 34230565]
Li X, Ding Y, Haddad YW, Geng X. The Greater Omentum: Multifaceted Interactions in Neurological Recovery and Disease Progression. Aging and disease. 2024 Feb 19:():. doi: 10.14336/AD.2024.0213. Epub 2024 Feb 19 [PubMed PMID: 38421824]
Liu J, Geng X, Li Y. Milky spots: omental functional units and hotbeds for peritoneal cancer metastasis. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine. 2016 May:37(5):5715-26. doi: 10.1007/s13277-016-4887-3. Epub 2016 Jan 29 [PubMed PMID: 26831659]
Koppe MJ, Nagtegaal ID, de Wilt JH, Ceelen WP. Recent insights into the pathophysiology of omental metastases. Journal of surgical oncology. 2014 Nov:110(6):670-5. doi: 10.1002/jso.23681. Epub 2014 Jun 24 [PubMed PMID: 24962271]
Iwagoi Y, Motohara T, Hwang S, Fujimoto K, Ikeda T, Katabuchi H. Omental metastasis as a predictive risk factor for unfavorable prognosis in patients with stage III-IV epithelial ovarian cancer. International journal of clinical oncology. 2021 May:26(5):995-1004. doi: 10.1007/s10147-021-01866-3. Epub 2021 Jan 29 [PubMed PMID: 33512628]
Fischerova D, Indrielle-Kelly T, Burgetova A, Bennett RJ, Gregova M, Dundr P, Nanka O, Gambino G, Frühauf F, Kocian R, Borcinova M, Cibula D. Yolk Sac Tumor of the Omentum: A Case Report and Literature Review. Diagnostics (Basel, Switzerland). 2022 Jan 25:12(2):. doi: 10.3390/diagnostics12020304. Epub 2022 Jan 25 [PubMed PMID: 35204394]
Level 3 (low-level) evidenceSchwartz RW, Reames M, McGrath PC, Letton RW, Appleby G, Kenady DE. Primary solid neoplasms of the greater omentum. Surgery. 1991 Apr:109(4):543-9 [PubMed PMID: 2008659]
Level 3 (low-level) evidenceMeza-Perez S, Randall TD. Immunological Functions of the Omentum. Trends in immunology. 2017 Jul:38(7):526-536. doi: 10.1016/j.it.2017.03.002. Epub 2017 Jun 1 [PubMed PMID: 28579319]
Shahid S, Khan H, Mehmood M, Rage KA, Saeed S. Malignant haemangiopericytomas of omentum presenting as left inguinal hernia: A case report. Annals of medicine and surgery (2012). 2021 Feb:62():298-301. doi: 10.1016/j.amsu.2021.01.070. Epub 2021 Jan 23 [PubMed PMID: 33552488]
Level 3 (low-level) evidenceVasdeki D, Bompou E, Diamantis A, Anagnostou A, Tepetes K, Efthimiou M. Haemangiopericytoma of the greater omentum: a rare tumour requiring long-term follow-up. Journal of surgical case reports. 2018 May:2018(5):rjy087. doi: 10.1093/jscr/rjy087. Epub 2018 May 14 [PubMed PMID: 29977504]
Level 3 (low-level) evidenceArchid R, Schneider CC, Adam P, Othman A, Zieker D, Königsrainer A. Hemangiopericytoma/solitary fibrous tumor of the greater omentum: A case report and review of the literature. International journal of surgery case reports. 2016:23():160-2. doi: 10.1016/j.ijscr.2016.04.028. Epub 2016 Apr 21 [PubMed PMID: 27138450]
Level 3 (low-level) evidenceAlteerah IA, Azzuz RH, Moftah MA, Hasen YM, Eldruki SI. Primary Pleomorphic Omental Rhabdomyosarcoma in an Adult: A Report of a Unique Case. Cureus. 2022 Jan:14(1):e21576. doi: 10.7759/cureus.21576. Epub 2022 Jan 24 [PubMed PMID: 35228935]
Level 3 (low-level) evidenceFeng JF, Guo YH, Chen WY, Chen DF, Liu J. Primary small cell carcinoma of the lesser omentum. The Kaohsiung journal of medical sciences. 2012 Feb:28(2):115-9. doi: 10.1016/j.kjms.2011.10.028. Epub 2012 Jan 14 [PubMed PMID: 22313540]
Guo YC, Yao LY, Tian ZS, Shi B, Liu Y, Wang YY. Malignant solitary fibrous tumor of the greater omentum: A case report and review of literature. World journal of clinical cases. 2021 Jan 16:9(2):445-456. doi: 10.12998/wjcc.v9.i2.445. Epub [PubMed PMID: 33521114]
Level 3 (low-level) evidencePathak P, Nautiyal M, Sachan PK, Shirazi N. Omental rhabdomyosarcoma (primary rhabdoid tumor of greater omentum): a rare case report. Surgical case reports. 2015:1(1):73. doi: 10.1186/s40792-015-0077-6. Epub 2015 Sep 2 [PubMed PMID: 26366369]
Level 3 (low-level) evidenceChammout A, Alshutaihi MS, Kelarji AB, Naser M, Mouselli A, Alyousfi R. Adult omental alveolar rhabdomyosarcoma: An unusual site. A case report and literature review. Annals of medicine and surgery (2012). 2022 Sep:81():104464. doi: 10.1016/j.amsu.2022.104464. Epub 2022 Aug 18 [PubMed PMID: 36147128]
Level 3 (low-level) evidencePérez-Navarro JV, Flores-Cardoza A, Anaya-Prado R, González-Izquierdo Jde J, Ramírez-Barba EJ. [Angiofibrolipoma of the greater omentum: case report and literature review]. Cirugia y cirujanos. 2009 May-Jun:77(3):229-32 [PubMed PMID: 19671276]
Level 3 (low-level) evidenceAddeo P, De Palma GD, Masone S, Mascolo M, Persico G. Malignant fibrous histiocytoma of the greater omentum. Surgery. 2011 Mar:149(3):455-6. doi: 10.1016/j.surg.2009.10.001. Epub 2009 Oct 27 [PubMed PMID: 19863985]
Kweon JH, Choi CS, Im CJ, Seo GS, Choi SC. Malignant fibrous histiocytoma arising from the omentum presenting as hemoperitoneum. Gut and liver. 2010 Jun:4(2):241-4. doi: 10.5009/gnl.2010.4.2.241. Epub 2010 Jun 16 [PubMed PMID: 20559528]
Li JXJ, Giddings HL, Owen G. Omental lipoma: a rare cause of a giant intra-abdominal mass. Journal of surgical case reports. 2022 Apr:2022(4):rjac160. doi: 10.1093/jscr/rjac160. Epub 2022 Apr 25 [PubMed PMID: 35481249]
Level 3 (low-level) evidenceSousa B, Silva J, Monteiro N, Romano M, Araújo E. Malignant Peritoneal Mesothelioma: A Case Report. Cureus. 2023 Aug:15(8):e42902. doi: 10.7759/cureus.42902. Epub 2023 Aug 3 [PubMed PMID: 37664365]
Level 3 (low-level) evidenceKataoka M, Saitoh T, Kawashima K, Yazaki T, Sonoyama H, Okimoto E, Oka A, Mishima Y, Mishiro T, Oshima N, Shibagaki K, Tobita H, Moriyama I, Ishimura N, Nagase M, Hirahara N, Tajima Y, Ishihara S. Primary Extragastrointestinal Stromal Tumor of Greater Omentum with Intraperitoneal Bleeding. Internal medicine (Tokyo, Japan). 2021 Nov 1:60(21):3413-3419. doi: 10.2169/internalmedicine.6519-20. Epub 2021 May 22 [PubMed PMID: 34024850]
Gogolev AB, Urezkova MM, Kudaibergenova AG. [Changes in the WHO classification (2020) of soft tissue tumors]. Arkhiv patologii. 2023:85(1):43-50. doi: 10.17116/patol20238501143. Epub [PubMed PMID: 36785961]
Gao Y, Qin Y, Wang Y, Quan X, Wei X, Yao J. Primary liposarcoma of the omentum: A case report. Medicine. 2022 Jan 7:101(1):e28344. doi: 10.1097/MD.0000000000028344. Epub [PubMed PMID: 35029880]
Level 2 (mid-level) evidenceSaijo F, Sato K, Handa T, Narushima Y, Matsumura N, Iwama N, Nakayama F, Tokumura H. First Account of Primary Leiomyosarcoma of the Lesser Omentum since Establishment of c-Kit Mutations in Gastrointestinal Stromal Tumors. Case reports in surgery. 2019:2019():2426092. doi: 10.1155/2019/2426092. Epub 2019 Nov 4 [PubMed PMID: 31781464]
Level 3 (low-level) evidenceBohara S, Jha P, Bhat PS, Malla S, Karki S, Jha SK, Basukala S, Rawal SB. Intra-abdominal omental mass as a desmoplastic round cell tumor: A rare case report. Clinical case reports. 2023 Nov:11(11):e8191. doi: 10.1002/ccr3.8191. Epub 2023 Nov 15 [PubMed PMID: 38028068]
Level 3 (low-level) evidenceWeinberger HA, Ahmed MS. Mesenchymal solid tumors of the omentum and mesentery: report of four cases. Surgery. 1977 Nov:82(5):754-9 [PubMed PMID: 918865]
Level 3 (low-level) evidenceHashimoto S, Arai J, Nishimuta M, Matsumoto H, Fukuoka H, Muraoka M, Nakashima M, Yamaguchi H. Resection of liposarcoma of the greater omentum: A case report and literature review. International journal of surgery case reports. 2019:61():20-25. doi: 10.1016/j.ijscr.2019.06.067. Epub 2019 Jul 8 [PubMed PMID: 31306901]
Level 3 (low-level) evidenceBrañes A, Bustamante C, Valbuena J, Pimentel F, Quezada N. Primary leiomyosarcoma of the greater omentum: a case report. International journal of surgery case reports. 2016:28():317-320. doi: 10.1016/j.ijscr.2016.10.025. Epub 2016 Oct 14 [PubMed PMID: 27771602]
Level 3 (low-level) evidenceBarel O, Qian C, Manolitsas T. Primary leiomyosarcoma of the omentum presenting as an ovarian carcinoma, case report and review of the literature. Gynecologic oncology reports. 2016 Aug:17():75-8. doi: 10.1016/j.gore.2016.07.002. Epub 2016 Jul 7 [PubMed PMID: 27489871]
Level 2 (mid-level) evidenceFagkrezos D, Touloumis Z, Giannila M, Penlidis C, Papaparaskeva K, Triantopoulou C. Extra-gastrointestinal stromal tumor of the omentum: a rare case report and review of the literature. Rare tumors. 2012 Jun 26:4(3):e44. doi: 10.4081/rt.2012.e44. Epub 2012 Aug 8 [PubMed PMID: 23087800]
Level 3 (low-level) evidenceUrabe M, Yamagata Y, Aikou S, Mori K, Yamashita H, Nomura S, Shibahara J, Fukayama M, Seto Y. Solitary fibrous tumor of the greater omentum, mimicking gastrointestinal stromal tumor of the small intestine: a case report. International surgery. 2015 May:100(5):836-40. doi: 10.9738/INTSURG-D-14-00141.1. Epub [PubMed PMID: 26011203]
Level 3 (low-level) evidenceYin H, Ye D, Zhu Y, Geng C. Solitary Fibrous Tumor of the Great Omentum: A Case Report and Literature Review. Current medical imaging. 2022:18(4):417-420. doi: 10.2174/1573405617666211108111624. Epub [PubMed PMID: 34749624]
Level 3 (low-level) evidenceZong L, Chen P, Wang GY, Zhu QS. Giant solitary fibrous tumor arising from greater omentum. World journal of gastroenterology. 2012 Nov 28:18(44):6515-20. doi: 10.3748/wjg.v18.i44.6515. Epub [PubMed PMID: 23197901]
Level 3 (low-level) evidenceRodriguez Tarrega E, Hidalgo Mora JJ, Paya Amate V, Vega Oomen O. Solitary fibrous tumor of the greater omentum mimicking an ovarian tumor in a young woman. Gynecologic oncology reports. 2016 Aug:17():16-9. doi: 10.1016/j.gore.2016.04.004. Epub 2016 Apr 26 [PubMed PMID: 27354994]
Sawaki A. Rare gastrointestinal stromal tumors (GIST): omentum and retroperitoneum. Translational gastroenterology and hepatology. 2017:2():116. doi: 10.21037/tgh.2017.12.07. Epub 2017 Dec 19 [PubMed PMID: 29354773]
Sajjanar AB, Katole NT, Vagha SJ. KIT (CD117) Positive Huge Primary Malignant Extra Gastrointestinal Stromal Tumors (EGISTs) Arising From Jejunal Mesentery: A Rare Case Report. Cureus. 2022 Dec:14(12):e33168. doi: 10.7759/cureus.33168. Epub 2022 Dec 31 [PubMed PMID: 36742272]
Level 3 (low-level) evidenceHaverkamp L, Brenkman HJ, Ruurda JP, Ten Kate FJ, van Hillegersberg R. The Oncological Value of Omentectomy in Gastrectomy for Cancer. Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract. 2016 May:20(5):885-90. doi: 10.1007/s11605-016-3092-4. Epub 2016 Feb 19 [PubMed PMID: 26895951]
Xu H, Cui SS, Ran L, Liu Y, Hu C, Xu Y, Tian Y. Incidence of omental metastasis in uterine serous carcinoma: a systematic review and meta-analysis. Journal of gynecology obstetrics and human reproduction. 2022 Jun:51(6):102395. doi: 10.1016/j.jogoh.2022.102395. Epub 2022 Apr 28 [PubMed PMID: 35489712]
Level 1 (high-level) evidenceSorensen EW, Gerber SA, Sedlacek AL, Rybalko VY, Chan WM, Lord EM. Omental immune aggregates and tumor metastasis within the peritoneal cavity. Immunologic research. 2009 Dec:45(2-3):185-94. doi: 10.1007/s12026-009-8100-2. Epub 2009 Feb 28 [PubMed PMID: 19253004]
Level 3 (low-level) evidenceJoe DH, Yang JM, Kim HS, Kim SS, Choi SW, Choi SH, Lee S, Lim KW. A case of primary leiomyosarcoma of the lesser omentum. The Korean journal of internal medicine. 1999 Jan:14(1):88-90 [PubMed PMID: 10063320]
Level 3 (low-level) evidenceShin MK, Lee OJ, Ha CY, Min HJ, Kim TH. Malignant mesothelioma of the greater omentum mimicking omental infarction: a case report. World journal of gastroenterology. 2009 Oct 14:15(38):4856-9 [PubMed PMID: 19824125]
Level 3 (low-level) evidenceMiyamoto T, Murphy B, Zhang N. Intraperitoneal metastasis of ovarian cancer: new insights on resident macrophages in the peritoneal cavity. Frontiers in immunology. 2023:14():1104694. doi: 10.3389/fimmu.2023.1104694. Epub 2023 Apr 25 [PubMed PMID: 37180125]
Krishnan V, Tallapragada S, Schaar B, Kamat K, Chanana AM, Zhang Y, Patel S, Parkash V, Rinker-Schaeffer C, Folkins AK, Rankin EB, Dorigo O. Omental macrophages secrete chemokine ligands that promote ovarian cancer colonization of the omentum via CCR1. Communications biology. 2020 Sep 22:3(1):524. doi: 10.1038/s42003-020-01246-z. Epub 2020 Sep 22 [PubMed PMID: 32963283]
Neilson LJ, Cartwright D, Risteli M, Jokinen EM, McGarry L, Sandvik T, Nikolatou K, Hodge K, Atkinson S, Vias M, Kay EJ, Brenton JD, Carlin LM, Bryant DM, Salo T, Zanivan S. Omentum-derived matrix enables the study of metastatic ovarian cancer and stromal cell functions in a physiologically relevant environment. Matrix biology plus. 2023 Dec:19-20():100136. doi: 10.1016/j.mbplus.2023.100136. Epub 2023 Nov 22 [PubMed PMID: 38223308]
Todoroki T, Sano T, Sakurai S, Segawa A, Saitoh T, Fujikawa K, Yamada S, Hirahara N, Tsushima Y, Motojima R, Motojima T. Primary omental gastrointestinal stromal tumor (GIST). World journal of surgical oncology. 2007 Jun 12:5():66 [PubMed PMID: 17565683]
Level 3 (low-level) evidenceKanamori K, Yamagata Y, Honma Y, Date K, Wada T, Hayashi T, Otsuki S, Sekine S, Yoshikawa T, Katai H, Nishida T. Extra-gastrointestinal stromal tumor arising in the lesser omentum with a platelet-derived growth factor receptor alpha (PDGFRA) mutation: a case report and literature review. World journal of surgical oncology. 2020 Jul 23:18(1):183. doi: 10.1186/s12957-020-01961-1. Epub 2020 Jul 23 [PubMed PMID: 32703220]
Level 3 (low-level) evidenceLi Z, Fang X, Wang S. Omentum provides a special cell microenvironment for ovarian cancer. Cancer reports (Hoboken, N.J.). 2023 Oct:6(10):e1858. doi: 10.1002/cnr2.1858. Epub 2023 Aug 21 [PubMed PMID: 37605299]
Tan Y, Lin K, Zhao Y, Wu Q, Chen D, Wang J, Liang Y, Li J, Hu J, Wang H, Liu Y, Zhang S, He W, Huang Q, Hu X, Yao Z, Liang B, Liao W, Shi M. Adipocytes fuel gastric cancer omental metastasis via PITPNC1-mediated fatty acid metabolic reprogramming. Theranostics. 2018:8(19):5452-5468. doi: 10.7150/thno.28219. Epub 2018 Oct 29 [PubMed PMID: 30555557]
Kersy O, Loewenstein S, Lubezky N, Sher O, Simon NB, Klausner JM, Lahat G. Omental Tissue-Mediated Tumorigenesis of Gastric Cancer Peritoneal Metastases. Frontiers in oncology. 2019:9():1267. doi: 10.3389/fonc.2019.01267. Epub 2019 Nov 18 [PubMed PMID: 31803630]
Bouhabel S, Leblanc G, Ferreira J, Leclerc YE, Dubé P, Sidéris L. Solitary fibrous tumor arising in the mesentery: a case report. World journal of surgical oncology. 2011 Oct 31:9():140. doi: 10.1186/1477-7819-9-140. Epub 2011 Oct 31 [PubMed PMID: 22035205]
Level 3 (low-level) evidencePhiza A, Gurpinder S, Simrandeep S, Sushma B. Primary mesenteric gastrointestinal stromal tumour with concomitant mesenteric tuberculosis: Careful histopathology is essential. Tropical doctor. 2022 Apr:52(2):343-345. doi: 10.1177/00494755221076947. Epub 2022 Feb 14 [PubMed PMID: 35156872]
Vats M, Pandey D, Ahlawat H, Akhtar A, Singh N. Multiple Primary Dedifferentiated Liposarcoma of the Jejunal Mesentery: A Case Report and Review of Literature. Journal of clinical and diagnostic research : JCDR. 2016 Jan:10(1):XD01-XD04. doi: 10.7860/JCDR/2016/15009.7090. Epub 2016 Jan 1 [PubMed PMID: 26894164]
Level 3 (low-level) evidenceIshida J, Ishida H, Konno K, Komatsuda T, Abe K. Primary leiomyosarcoma of the greater omentum. Journal of clinical gastroenterology. 1999 Mar:28(2):167-70 [PubMed PMID: 10078829]
Level 3 (low-level) evidenceTsutsumi H, Ohwada S, Takeyoshi I, Izumi M, Ogawa T, Fukusato T, Morishita Y. Primary omental liposarcoma presenting with torsion: a case report. Hepato-gastroenterology. 1999 May-Jun:46(27):2110-2 [PubMed PMID: 10430407]
Level 3 (low-level) evidenceDixon AY, Reed JS, Dow N, Lee SH. Primary omental leiomyosarcoma masquerading as hemorrhagic ascites. Human pathology. 1984 Mar:15(3):233-7 [PubMed PMID: 6698542]
Level 3 (low-level) evidenceHarb A, King E, Lloyd H, Harb Z, Payne JG. Primary omental mesothelioma: a rare but important differential diagnosis in previous asbestos exposure. Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract. 2010 Feb:14(2):423-5. doi: 10.1007/s11605-009-0910-y. Epub 2009 May 8 [PubMed PMID: 19424765]
Turan T, Ureyen I, Karalök A, Taşçı T, Ilgın H, Keskin L, Kose MF, Tulunay G. What is the importance of omental metastasis in patients with endometrial cancer? Journal of the Turkish German Gynecological Association. 2014:15(3):164-72. doi: 10.5152/jtgga.2014.13109. Epub 2014 Aug 8 [PubMed PMID: 25317045]
Level 2 (mid-level) evidenceChen M, Guo P, Tan J, Liu D, Yao S. The role of omentectomy in the surgical treatment of uterine serous carcinoma. European journal of obstetrics & gynecology and reproductive biology: X. 2019 Oct:4():100084. doi: 10.1016/j.eurox.2019.100084. Epub 2019 Jul 10 [PubMed PMID: 31517308]
Wei G, Shu X, Zhou Y, Liu X, Chen X, Qiu M. Intra-Abdominal Desmoplastic Small Round Cell Tumor: Current Treatment Options and Perspectives. Frontiers in oncology. 2021:11():705760. doi: 10.3389/fonc.2021.705760. Epub 2021 Sep 15 [PubMed PMID: 34604040]
Level 2 (mid-level) evidenceSoufi M, Mdaghri J, Benamr S, Lahlou MK, Massrouri R, Essadel A, Mohammadine el H, Taghy A, Settaf A, Chad B. Giant liposarcoma of the omentum mimicking an ovarian tumor. A case report. The Indian journal of surgery. 2012 Oct:74(5):425-7. doi: 10.1007/s12262-012-0718-y. Epub 2012 Aug 11 [PubMed PMID: 24082602]
Level 3 (low-level) evidenceMeloni F, Feo CF, Profili S, Cossu ML, Meloni GB. Omental Well-Differentiated Liposarcoma: US, CT and MR Findings. International journal of biomedical science : IJBS. 2009 Sep:5(3):302-4 [PubMed PMID: 23675151]
Level 3 (low-level) evidenceIngle A, Reddy S, Reddy VK. Omental Solitary Fibrous Tumor: A Rare Tumor at Rare Site. Journal of laboratory physicians. 2021 Sep:13(3):283-285. doi: 10.1055/s-0041-1731942. Epub 2021 Jul 9 [PubMed PMID: 34602796]
Metwally IH, Abdelkhalek M, Shetiwy M, Elalfy AF, Abouzid A, Elbalka SS, Hamdy M, Abdallah A. Significance of Omental Infiltration in Gastric Cancer Patients: a Retrospective Cohort Study. Journal of gastrointestinal cancer. 2020 Sep:51(3):861-867. doi: 10.1007/s12029-019-00310-0. Epub [PubMed PMID: 31677057]
Level 2 (mid-level) evidence