Continuing Education Activity

Primary omental tumors are a rare clinical finding, although many commonly encountered cancers frequently metastasize to the omentum. The clinical presentation of isolated omental neoplasms is subtle, and primary omental disease may remain asymptomatic and undetected until it is quite advanced. While imaging modalities may help to isolate the extent of omental disease, the findings are frequently nonspecific. Definitive diagnosis of omental tumors usually requires advanced histopathologic and immunohistochemical evaluation, and fine needle aspiration of omental lesions rarely provides adequate tissue for this analysis; surgical omentectomy is typically required. There are no standardized therapeutic protocols for primary omental neoplasms, and therapy often comprises surgery, chemotherapy, and radiation treatments. Even when remission is achieved, primary omental tumors may recur years following the initial diagnosis, as the omentum provides an environment conducive to tumor growth.

This activity for health care professionals reviews the etiology, epidemiology, pathophysiology, histopathology, clinical presentation, evaluation, and management of various primary and metastatic omental tumors. The activity also highlights the critical role of the interprofessional team in improving outcomes for patients with primary and metastatic omental neoplasms.

Objectives:

• Identify patients who may have an omental tumor based on their clinical history and radiographic findings.

• Differentiate primary omental tumors from metastatic lesions and other abdominal masses based on histopathological characteristics.

• Determine the most appropriate therapeutic strategy for a patient with an omental tumor.

• Collaborate with colleagues across specialties to ensure comprehensive and coordinated care for patients with 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

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]

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] 

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]

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]

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.