Chest Wall Tumors

Etiology

Chest wall tumors encompass a diverse group of benign and malignant lesions arising from the osseous, cartilaginous, muscular, adipose, vascular, or neural components of the thoracic cage. The etiology reflects a complex interplay of genetic, environmental, and acquired factors leading to abnormal cellular proliferation, benign overgrowth, or malignant transformation. Primary chest wall tumors originate from local structures, including bone, muscle, fat, blood vessels, and nerve sheaths, as well as rare lesions such as myositis ossificans, elastofibroma dorsi, and extra-abdominal desmoid tumors. These extra-abdominal desmoid tumors represent a form of aggressive fibromatosis and may develop at the site of prior thoracotomy or trauma.

The cause of most chest wall tumors remains unclear, though current evidence suggests that genetic predisposition, prior irradiation, chronic inflammation, infection, trauma, diet, and lifestyle factors may influence tumor development. Hereditary cancer syndromes such as Li-Fraumeni, neurofibromatosis type 1, and multiple hereditary exostoses are associated with an increased risk of certain sarcomas. Among primary malignant chest wall tumors, chondrosarcoma, osteosarcoma, and Ewing sarcoma predominate, while benign lesions include osteochondromas, chondromas, and fibrous dysplasia. Secondary chest wall tumors, which occur more frequently than primary lesions, result from direct invasion of adjacent malignancies such as breast or lung carcinoma or from hematogenous metastases originating in distant organs, including the kidney, thyroid, or prostate. Radiation-induced sarcomas also represent a distinct etiologic subset, typically arising years after therapeutic irradiation for thoracic or breast malignancies. 

Epidemiology

Chest wall tumors are rare entities, representing approximately 1% to 2% of all primary soft tissue and bone tumors and about 5% of all thoracic neoplasms.[1][2][3] These neoplasms may be either primary or metastatic, with malignancy rates exceeding 50%.[4][5] Importantly, around 20% of these lesions are discovered incidentally on chest imaging. Although research has not definitively established sex-based differences in incidence, the age of presentation tends to influence tumor characteristics: younger patients are more likely to present with smaller, benign lesions, whereas older patients are more often affected by larger, more aggressive tumors.[6]

The incidence of primary chest wall tumors is estimated at less than 2% of the population.[1][2] Chondrosarcomas are the most common primary malignant chest wall tumors, followed by osteosarcomas, rhabdomyosarcomas, plasmacytomas, malignant fibrous histiocytomas, and Ewing sarcomas. Approximately 50% to 80% of chest wall tumors are malignant, with 55% arising from bone or cartilage and 45% from soft tissue.[4][7][8] Benign lesions, such as osteochondromas, lipomas, and fibrous dysplasia, are more common in younger individuals and are often detected incidentally.

Secondary chest wall involvement is more common than primary disease and typically results from breast carcinoma, lung carcinoma, or lymphoma. Geographically, no significant regional differences have been observed, although access to imaging and specialized oncologic care affects detection rates. Risk factors may include prior thoracic surgery, radiation exposure, and chronic inflammatory conditions.

Prognosis varies by histologic subtype and stage at diagnosis. Overall, the 5-year survival following resection of primary chest wall neoplasms is approximately 60%, with recurrence rates up to 50% and a 5-year survival of 17% in recurrent cases.[7] These epidemiologic patterns underscore the importance of early detection, accurate histopathologic classification, and coordinated multidisciplinary care to improve outcomes.

Histopathology

Chest wall tumors encompass a heterogeneous spectrum of osseous, cartilaginous, and soft-tissue neoplasms, each with distinct histopathologic and molecular characteristics. Broadly, they are classified as benign or malignant, with the latter accounting for a substantial proportion of primary chest wall lesions. Benign tumors, such as osteochondromas, chondromas, fibrous dysplasia, and lipomas, typically demonstrate well-circumscribed growth, minimal cytologic atypia, and low mitotic activity. These lesions often arise from mature cell types that maintain normal architecture, though focal calcification or ossification may occur in fibroosseous variants.

Among the osseous and cartilaginous tumors, chondrosarcoma represents the most common primary malignant tumor of the chest wall, typically demonstrating hyaline cartilage formation and ring-and-arc calcifications on imaging. Histologically, it exhibits a lobulated architecture with atypical chondrocytes in lacunae, nuclear hyperchromasia, and a myxoid or hyaline matrix. Grading is based on cellularity, nuclear atypia, and mitotic activity, with high-grade tumors showing increased pleomorphism and necrosis. Osteosarcoma, arising from bone-forming cells, is characterized by malignant osteoid production by anaplastic spindle cells and may contain areas of calcified bone matrix or hemorrhage. Ewing sarcoma, a small round blue cell tumor, is defined by sheets of uniform cells with scant cytoplasm and the hallmark EWSR1-FLI1 translocation, confirmed by molecular testing.[9]

Within the soft-tissue compartment, undifferentiated pleomorphic sarcoma and liposarcoma represent malignant entities with variable morphology and clinical behavior. Desmoid-type fibromatosis, though histologically benign, is locally aggressive and frequently associated with CTNNB1 mutations; immunohistochemistry typically demonstrates nuclear β-catenin expression.[10] Elastofibroma dorsi, another benign lesion, reveals collagen and elastic fibers interspersed with adipose tissue in a distinctive checkerboard pattern.

Soft-tissue sarcomas of the chest wall often display infiltrative borders and variable necrosis, with histologic grade a strong prognostic indicator of recurrence and metastasis. Histopathologic evaluation remains critical for diagnosis, prognostication, and therapeutic decision-making. Immunohistochemistry and molecular genetic testing (eg, EWSR1, MDM2, or SS18 rearrangements) have become essential tools for differentiating morphologically similar tumors. Accurate histologic classification directly informs surgical planning, adjuvant therapy selection, and overall prognosis, underscoring the central role of pathology in the multidisciplinary management of chest wall tumors.

History and Physical

A careful history and physical examination are essential for evaluating patients presenting with a chest wall mass. The clinical presentation varies with tumor size, growth rate, and tissue of origin, and many lesions are discovered incidentally on chest imaging. When symptomatic, patients most commonly report localized pain, soreness, swelling, impaired movement, or a palpable lump. Pain is the most frequent complaint, particularly in malignant or invasive tumors, and may be constant, progressive, and aggravated by respiration or movement. This discomfort often reflects periosteal irritation, nerve compression, or cortical bone destruction.

In contrast, benign lesions are typically painless and slowly enlarging. A thorough history should assess for prior trauma, thoracotomy, radiation exposure, or chronic infection, which may suggest secondary or reactive lesions such as desmoid-type fibromatosis. Systemic symptoms such as fever, weight loss, or malaise are less common but may accompany aggressive or metastatic disease.

On physical examination, findings depend on the tumor's location and its involvement of adjacent structures. Inspection may reveal visible asymmetry, localized swelling, or distortion of the thoracic contour. Palpation can detect a firm, fixed, nontender mass, often immobile when attached to deeper tissues. The texture of the lesion may offer diagnostic clues: a hard, immobile mass suggests a bony or cartilaginous origin, while a rubbery or pliable mass may indicate soft-tissue involvement. Overlying erythema, ulceration, or warmth may occur with malignancy or inflammation. Decreased breath sounds on auscultation can indicate compression of the underlying lung or pleura. The described findings primarily reflect the tumor’s mass effect and are not diagnostic of a specific pathology; however, they can guide imaging and biopsy decisions.

Additional clues suggesting malignancy include rapid enlargement, persistent pain, fixation to surrounding structures, and associated systemic manifestations. Tumors invading the ribs or sternum may limit chest wall expansion or cause pleuritic pain. At the same time, invasion of the neurovascular bundle or brachial plexus may produce neuropathic pain, paresthesias, or upper extremity weakness. Large intrathoracic extensions can compress adjacent organs, resulting in dyspnea, cough, or venous congestion. Together, a comprehensive history and physical examination provide critical context for diagnostic imaging, tissue sampling, and multidisciplinary management planning in patients with suspected chest wall tumors.

Evaluation

Following a thorough history and physical examination, the diagnostic workup for chest wall tumors centers on a combination of imaging, laboratory studies, and histopathologic confirmation. Laboratory evaluation is generally nonspecific but can help identify systemic involvement or paraneoplastic processes. Basic studies, such as a complete blood count, comprehensive metabolic panel, erythrocyte sedimentation rate, and C-reactive protein, may be obtained to assess for anemia, systemic inflammation, or hepatic involvement. Serum alkaline phosphatase and lactate dehydrogenase levels may be elevated in osteogenic or highly metabolically active tumors, such as osteosarcoma or Ewing sarcoma, respectively. However, laboratory testing is adjunctive, as definitive diagnosis relies on imaging and tissue sampling.

The initial imaging study in the evaluation of a suspected chest wall mass is typically a chest radiograph, which provides a prompt, widely available screening tool to assess the lesion’s size, extent, and relationship to adjacent structures. Chest radiography may demonstrate cortical bone destruction, rib expansion, or a soft-tissue opacity consistent with a chest wall mass. This modality can also help identify pulmonary invasion or confirm the lesion's osseous origin. However, computed tomography (CT) is significantly more sensitive and specific than radiography for characterizing these features and delineating tumor margins, calcifications, and bony involvement.[11][12]

After chest radiography, magnetic resonance imaging (MRI) with gadolinium is the preferred cross-sectional modality for local staging and surgical planning. MRI provides superior contrast resolution for soft-tissue structures, enabling assessment of tumor extent, neurovascular involvement, fascial-plane invasion, necrosis, and postoperative or postradiation changes. According to the American College of Radiology Appropriateness Criteria for Soft-Tissue Masses, MRI with and without intravenous (IV) contrast is rated as “usually appropriate” for chest wall neoplasms. At the same time, CT is reserved for cases where MRI is contraindicated or when high-resolution bone detail is required.[13] CT also facilitates evaluation of the pleura, mediastinum, and lymph nodes, providing valuable information on vascularity and the lesion’s anatomical relationships.[12]

MRI is superior to CT in differentiating neoplastic from inflammatory or infectious processes, as it can delineate the internal components of complex lesions and identify distinct tissue characteristics such as necrosis, hemorrhage, or myxoid stroma.[14] Positron emission tomography (PET) is increasingly used for metabolic characterization, staging, and assessment of treatment response, particularly in high-grade sarcomas or metastatic disease. PET can also detect occult metastases or recurrent disease during surveillance.[15]

Despite the advances in imaging, radiologic findings alone are insufficient for definitive diagnosis. Histologic confirmation remains essential and should be obtained through a biopsy tailored to the lesion size and location. Lesions smaller than 5 cm are typically amenable to excisional biopsy. In comparison, larger lesions (>5 cm) are best approached with core needle or incisional biopsy to minimize contamination of surrounding tissue and preserve resection options.[5] For excisional biopsies, achieving a wide negative margin of at least 2 cm is critical to reduce recurrence risk and ensure accurate histopathologic evaluation.[12]

Treatment / Management

Managing chest wall tumors presents both clinical and surgical challenges due to the anatomic complexity of the thoracic cage and the diversity of tumor histologies. Surgical resection is the standard of care for benign lesions. At the same time, malignant tumors require a multidisciplinary approach that integrates surgery, radiation, and systemic therapy to optimize local control and preserve function.

For most primary chest-wall sarcomas, including chondrosarcoma and other soft-tissue sarcomas, surgery remains the cornerstone of treatment. The primary objective is an en bloc resection with histologically clear margins (R0 resection), as margin status is the most significant predictor of local recurrence and overall survival. When resection margins are close or microscopically positive, or when additional high-risk features are present, adjuvant radiotherapy is recommended to improve local control. Contemporary clinical series consistently reinforce the prognostic importance of achieving R0 resection to optimize outcomes.[16](B2)

Neoadjuvant therapy is sometimes employed to downstage locally advanced tumors, facilitate complete resection, or assess tumor biology, particularly for high-grade soft-tissue sarcomas. The role of chemotherapy varies by histologic subtype and grade, with the most significant benefit observed in chemosensitive tumors such as Ewing sarcoma, osteosarcoma, and rhabdomyosarcoma. Non–small cell lung cancers with direct chest-wall invasion may also be managed surgically in appropriately selected patients. In such cases, an en bloc resection of the involved lung parenchyma and chest wall components is performed within a multimodality framework that typically integrates systemic therapy and/or radiotherapy, depending on disease stage and patient-specific factors.

Several chest wall neoplasms respond best to combined or nonsurgical management strategies. Ewing sarcoma of the chest wall, including Askin tumors, is treated with systemic chemotherapy followed by local control through surgery and/or radiotherapy, with the approach guided by tumor response and resectability.[17] Similarly, rhabdomyosarcoma of the trunk or chest requires multimodal therapy combining chemotherapy and radiotherapy, occasionally supplemented by conservative surgery to preserve function. Durable local control in these tumors is a significant determinant of long-term outcome.[18] 

Solitary plasmacytoma of bone or soft tissue is generally treated with definitive radiotherapy, typically 40 to 50 Gy, depending on tumor size. At the same time, surgery is reserved for diagnostic confirmation, mechanical instability, or decompression. Desmoid-type fibromatosis of the extra-abdominal chest wall is now best managed with an initial strategy of active surveillance, as recommended by the National Comprehensive Cancer Network and the Desmoid Tumor Working Group, with surgery, radiotherapy, or systemic therapy reserved for progressive or symptomatic disease.[10](B3)

Surgical margin width remains an important prognostic determinant. For low-grade or benign lesions, a 2 cm margin is often adequate, whereas malignant tumors require at least a 4 cm margin to reduce the risk of local recurrence.[12] Following tumor resection, chest wall stabilization and reconstruction are critical to maintaining respiratory mechanics and protecting intrathoracic organs.[19] Reconstruction is guided by defect size, location, and depth rather than rigid dimensional criteria. Most experts recommend reconstruction when defects exceed 5 cm in diameter or 100 cm² in area, involve more than 3 anterior ribs, more than 4 posterior ribs, or compromise structural integrity, especially with full-thickness anterolateral or sternal resections or posterior defects below the fourth rib.[20][21]

Reconstruction options include rigid prosthetic materials, such as titanium plates or methyl methacrylate “sandwich” constructs, and nonrigid meshes made from biologic or biosynthetic materials. The choice depends on the need for stability and the risk of infection; biologic meshes are preferred in contaminated or irradiated fields because they reduce the risk of infection and improve integration. Soft-tissue coverage is typically achieved with regional muscle or musculocutaneous flaps, most commonly the pectoralis major, latissimus dorsi, or rectus abdominis, to restore contour and protect prosthetic materials.[22](B2)

These complex reconstructions carry a risk of perioperative morbidity and mortality, often related to incomplete resection, wound complications, or underlying comorbidities. Despite these challenges, surgery with complete resection remains the best curative option for primary and select secondary chest wall tumors, particularly when integrated within a multidisciplinary care pathway that includes medical and radiation oncology.[23][24] Combined-modality treatment—tailored to tumor histopathology, grade, and patient factors—offers the highest likelihood of achieving durable local control and long-term survival.

Differential Diagnosis

The differential diagnosis of chest wall tumors is extensive, encompassing a wide range of benign and malignant entities that may arise primarily from the osseous, cartilaginous, or soft-tissue structures of the thoracic cage, as well as from secondary involvement by adjacent thoracic or metastatic disease. Nonneoplastic conditions, including infectious, inflammatory, and posttraumatic processes, must also be considered, as they can clinically or radiographically mimic neoplastic masses. The differential may be narrowed by integrating key diagnostic criteria, including overall prevalence, characteristic clinical features, mineralization patterns, specific anatomic location, and intrinsic MRI characteristics that correlate with histopathologic findings.[25]

Benign chest wall lesions are more common and generally exhibit slow growth, well-circumscribed borders, and lack invasive features. The most frequent benign tumors include osteochondromas, chondromas, fibrous dysplasia, and desmoid-type fibromatosis (extra-abdominal desmoid tumors).[2] Osteochondromas, typically arising from the ribs or sternum, display cortical and medullary continuity with the parent bone on imaging.

Chondromas, which consist of mature hyaline cartilage, can be difficult to distinguish radiographically from low-grade chondrosarcomas; however, the absence of cortical destruction and soft-tissue extension favors a benign diagnosis. Fibrous dysplasia is characterized by fibroosseous proliferation with a ground-glass appearance on CT. In contrast, desmoid tumors are locally aggressive fibroblastic proliferations that typically show low-to-intermediate signal intensity on T1-weighted MRI and variable signal intensity on T2-weighted imaging, reflecting varying degrees of collagenization.

Malignant chest wall tumors typically exhibit rapid growth, bone destruction, and soft-tissue extension. The most common primary malignant neoplasms include soft-tissue sarcomas, chondrosarcomas, and Ewing sarcoma.[7] Chondrosarcomas display characteristic “ring-and-arc” calcifications on CT, reflecting mineralization of the hyaline cartilage matrix, whereas Ewing sarcoma, most often affecting children and young adults, typically shows a permeative pattern of bone destruction and a soft-tissue mass; MRI reveals heterogeneous marrow and soft-tissue involvement.

Osteosarcoma and undifferentiated pleomorphic sarcoma are additional considerations, particularly in older adults, and may demonstrate variable mineralization or necrosis. Secondary or metastatic lesions are an important component of the differential, as the chest wall can be involved by direct extension from adjacent structures (eg, breast carcinoma, pleural mesothelioma, or lung cancer) or by hematogenous metastases from distant primaries, such as renal cell carcinoma, thyroid carcinoma, or melanoma. Infectious etiologies, such as tuberculous osteomyelitis or actinomycosis, and inflammatory processes, including postthoracotomy changes or chronic osteitis, can also simulate neoplastic lesions both clinically and radiographically.

Surgical Oncology

The overarching surgical objective in managing chest wall tumors is to achieve an en bloc resection with histologically negative (R0) margins, ensuring oncologic adequacy while preserving chest wall stability, respiratory mechanics, and overall function. The extent of resection is carefully individualized based on the tumor’s histopathologic type, local invasiveness, and anatomic relationships to surrounding structures, particularly the pleura, ribs, sternum, and neurovascular bundles. Surgical margins must be wide enough to minimize the risk of recurrence, yet conservative enough to prevent unnecessary morbidity and functional impairment.

When margins are positive, close, or indeterminate, or when tumors demonstrate high-risk histologic features such as high-grade sarcomas or extensive local infiltration, adjuvant radiotherapy is recommended to improve local disease control and reduce recurrence rates. In select cases where chest wall invasion results from primary intrathoracic malignancies, such as non–small cell lung carcinoma or breast carcinoma, resection of the involved chest wall should be pursued within a multidisciplinary framework that integrates systemic therapy, radiation, and surgical planning to optimize outcomes. Treatment strategies are thus personalized, taking into account tumor biology, disease stage, and patient comorbidities to achieve the best possible balance between oncologic clearance and postoperative quality of life.[26]

Radiation Oncology

Radiation therapy is an integral component of the multidisciplinary management of chest wall tumors, serving both curative and adjuvant roles depending on tumor histology, resectability, and stage. For many soft-tissue sarcomas of the chest wall, radiotherapy is incorporated preoperatively to facilitate margin-negative resection and tumor downstaging, or postoperatively to reduce the risk of local recurrence in cases with close or positive margins. In specific tumor types, such as solitary plasmacytoma, definitive radiotherapy alone remains the standard of care, achieving excellent local control without the morbidity of extensive surgery. Similarly, in Ewing sarcoma and rhabdomyosarcoma, radiotherapy represents a critical pillar of multimodal therapy, complementing systemic chemotherapy and surgery to maximize survival and preserve function.

Recent advancements in radiation delivery techniques, particularly intensity-modulated radiation therapy and proton beam therapy, have refined the precision and safety of chest wall irradiation. Proton therapy, in particular, offers a dosimetric advantage by minimizing exposure to critical thoracic structures, such as the heart and lungs, and to reconstructive prosthetics, making it especially valuable for large, complex truncal lesions. Emerging clinical trials are investigating hypofractionated regimens and preoperative proton therapy protocols to improve tumor control, functional preservation, and quality of life, underscoring the evolving sophistication of radiation therapy in chest wall tumor management.[17][27]

Pertinent Studies and Ongoing Trials

Several ongoing and recent clinical trials are particularly relevant to chest wall and truncal soft-tissue sarcomas. However, most protocols enroll these tumors under the broader category of soft-tissue sarcoma rather than designating the chest wall as a distinct site. Among these, a phase II prospective study is evaluating the role of preoperative proton therapy in extremity and body-wall sarcomas, with a focus on optimizing target coverage and reducing late treatment effects in trunk and chest-wall cohorts.

In addition, the FAST-02 trial is a United States multicenter feasibility study of FLASH proton therapy for patients with painful thoracic bone metastases.[28] Enrollment for this trial was reported complete in 2025, and it builds directly on the feasibility data generated in the FAST-01 study. Such research holds particular promise for improving palliation in patients with chest-wall osseous disease while minimizing toxicity to surrounding structures.[29]

Prognosis

Prognosis for patients with chest wall tumors is highly variable and depends on multiple factors, including tumor histology, grade, size, margin status, and the presence or absence of metastases at diagnosis. Primary chest wall malignancies generally carry a poorer prognosis than benign lesions or metastatic deposits from more indolent primary tumors. Among malignant tumors, chondrosarcoma, the most common primary chest wall sarcoma, tends to have a relatively favorable prognosis, with 5-year survival rates approaching 70% to 80% following complete (R0) resection. In contrast, osteosarcoma, Ewing sarcoma, and undifferentiated pleomorphic sarcoma are associated with more aggressive biological behavior and a higher risk of both local recurrence and distant metastasis, with 5-year survival rates ranging from 30% to 60% depending on stage and response to multimodality therapy.[4][7][16][17]

The status of surgical margins remains the single most important prognostic determinant for local control and overall survival. Achieving a margin-negative (R0) resection significantly improves outcomes, whereas positive or close margins markedly increase the risk of recurrence, often necessitating adjuvant radiotherapy. A tumor size greater than 5 cm, high histologic grade, and deep or multifocal involvement are also independent predictors of poorer prognosis. Recurrence rates may reach 50% in certain high-grade sarcomas, reducing the 5-year survival to as low as 17% in recurrent disease.[7][29]

Benign lesions such as osteochondromas, chondromas, or desmoid-type fibromatosis have an excellent long-term outlook but may recur locally, particularly when excision margins are incomplete. Desmoid tumors, although nonmetastatic, can be locally aggressive and challenging to eradicate, leading to significant morbidity despite a generally favorable survival rate. For secondary chest wall involvement from lung, breast, or other metastatic cancers, prognosis is primarily dictated by the biology and stage of the primary malignancy, though carefully selected patients undergoing en bloc resection for isolated chest wall invasion can achieve meaningful long-term survival. Overall, multidisciplinary management, incorporating surgery, radiotherapy, systemic therapy, and coordinated postoperative surveillance, has improved both survival and quality of life. Advances in proton therapy, targeted molecular therapy, and reconstructive techniques continue to enhance functional outcomes while reducing morbidity, reflecting the growing emphasis on personalized, outcome-driven care in chest wall oncology.

Complications

Complications following the management of chest wall tumors encompass a wide range of surgical, oncologic, and functional challenges that may occur in both the immediate postoperative period and long-term follow-up. The complexity of chest wall resection and reconstruction, often involving extensive soft tissue, bony, and respiratory structures, predisposes patients to a high rate of morbidity, with reported complication rates ranging from 30% to 50%, depending on tumor size, location, comorbidities, and the extent of reconstruction.[19][22][23]

Early postoperative complications include wound-related issues such as infection, seroma, hematoma, wound dehiscence, and flap necrosis, particularly when large prosthetic or biologic materials are used for reconstruction. Respiratory compromise is another critical concern, as extensive resections may alter chest wall stability and impair ventilation. Inadequate reconstruction can lead to paradoxical chest wall motion, atelectasis, pneumonia, and prolonged ventilatory dependence. The risk of pulmonary complications increases with resections involving 3 or more ribs or full-thickness anterolateral defects, emphasizing the need for meticulous reconstruction to maintain thoracic mechanics.[19][20][21]

Cardiopulmonary complications, including arrhythmias, respiratory failure, and pulmonary embolism, may arise secondary to pain, limited mobility, or the physiologic stress of surgery. Bleeding and vascular injury can occur intraoperatively, especially when tumors invade major vessels, requiring careful preoperative imaging and intraoperative planning. Chronic pain syndromes and intercostal neuralgia are frequent late complications due to nerve injury or scar formation, potentially necessitating multimodal pain management or referral to pain specialists.

Oncologic complications include local recurrence, often linked to incomplete or close margins, and metastatic progression, which can occur months to years after initial resection. Reconstruction-related complications vary by material: prosthetic meshes can become infected or dislodged, whereas biologic grafts may undergo partial resorption or fail to integrate. In cases of radiotherapy, radiation-induced fibrosis, delayed wound healing, and secondary malignancies represent additional risks.[7][16][17][27]

Finally, functional and cosmetic complications, such as chest wall deformity, shoulder dysfunction, or scoliosis, can significantly affect quality of life, particularly in younger or highly active individuals. These outcomes underscore the importance of interdisciplinary coordination among surgeons, radiation and medical oncologists, anesthesiologists, and rehabilitation specialists to optimize perioperative care, minimize complications, and promote long-term functional recovery.