The Washington Manual of Oncology, 3 Ed.

Lung Cancer

Ali Mohamed • Saiama N. Waqar

I. NON–SMALL CELL LUNG CANCER

  1. Presentation
  2. Subjective. Although patients with non–small cell lung cancer (NSCLC) can be asymptomatic at presentation and detected only by “routine” or screening radiographic examination, most patients present with symptoms related to local disease or distant metastasis. These symptoms may be secondary to a tumor in the lung, such as new or worsening cough, worsening or new dyspnea, and fever, secondary to postobstructive pneumonia. Hemoptysis, especially in the middle-aged or elderly smoker, should always raise the suspicion of lung cancer. Chest pain may signify chest wall involvement; dyspnea and hoarseness of the voice may indicate involvement of recurrent laryngeal nerve. Because of its long intrathoracic course, the left recurrent laryngeal nerve is more commonly affected than the right. Superior sulcus tumors can cause Pancoast syndrome; a triad of shoulder pain, lower brachial plexus palsy, and Horner syndrome. Swelling and engorgement of the face, upper trunk, and arms signal superior vena cava (SVC) syndrome, which is associated more with right-sided tumors. Patients with pleural effusions may have dyspnea and cough. Occasionally, dysphagia may be one of the dominant presenting symptoms secondary to mediastinal lymph node involvement. Symptoms suggesting distant metastasis are not specific and include weight loss, cachexia, and symptoms related to distant sites involved (e.g., bone pain or fractures from bone involvement, right upper quadrant abdominal pain with liver metastases, and neurologic symptoms associated with central nervous system [CNS] involvement). Paraneoplastic syndromes associated with NSCLC include hypercalcemia (which can cause constipation, abdominal pain, and confusion) and hypertrophic pulmonary osteoarthropathy with marked clubbing, joint pains, and swelling.
  3. Objective. Assessment of the performance status (PS) and signs of recent substantial weight loss carry a significant prognostic importance. The superficial lymph nodes, particularly the supraclavicular nodes, should be carefully examined, as enlargement of these nodes raises the high likelihood of metastatic involvement. Signs on examination of the chest can detect not only those signs related to pleural effusion, atelectasis, and postobstructive pneumonia, but can also help assess the severity of any underlying lung disease (e.g., chronic obstructive pulmonary disease [COPD]) that may influence subsequent management options. Careful abdominal examination may detect hepatomegaly suggesting metastatic disease. New focal neurologic signs may signify brain or spinal cord involvement.
  4. Workup and staging
  5. Laboratory data

Patients may present with laboratory abnormalities such as anemia due to chronic disease, hypercalcemia as part of a paraneoplastic syndrome, hyponatremia due to syndrome of inappropriate antidiuretic hormone syndrome, and elevated transaminases or hyperbilirubinemia due to liver metastasis. There are no reliable or clinically useful serum tumor markers for diagnosis or follow-up of lung cancer, though carcinoembryonic antigen (CEA) may be elevated in some patients.

  1. Imaging
  2. Chest radiograph (CXR). A perfectly normal CXR does not necessarily exclude lung cancer, as conventional CXR may not always identify hilar or mediastinal lesions. Lung cancer can present as a mass, peripheral nodule, hilar or mediastinal changes suggestive of lymphadenopathy, or pleural effusions. CXR may reveal areas of atelectasis suggesting endobronchial lesion, and pneumonic infiltrates may be seen in association with obstructing lesions.
  3. Computed tomography (CT) scan of the chest is the most effective noninvasive study to evaluate suspected lung cancer. Although its sensitivity to detect mediastinal metastases is variable, it has a high negative predictive value. It can also help identify local invasion (e.g., chest wall, bones, and pleura). The upper abdomen is usually included in this study, and the liver and adrenal glands should be carefully inspected for evidence of metastases.
  4. Magnetic resonance imaging (MRI) of the chest is not routinely used in the staging workup of patients with lung cancer. It is particularly helpful in the setting of suspected spinal cord, vascular, brachial plexus, or chest wall involvement. Brain MRI at presentation can help detect brain metastasis.
  5. Fluorodeoxyglucose (FDG) positron emission tomography (PET) scan is a useful adjunct tool to complete the staging workup in patients with recently diagnosed NSCLC. The FDG PET scan has been demonstrated to be superior to CT scans in identifying mediastinal lymph node involvement and distant metastasis. FDG PET scan helps identify additional sites of disease in approximately 10% to 30% of patients that were not identified by the conventional workup.
  6. Pathological diagnosis. Flexible fiber optic bronchoscopy can help determine the extent of endobronchial lesions and obtain tissue for diagnosis (washings, brushings, bronchoalveolar lavage, transbronchial biopsy). Cytologic examination of sputum is sometimes helpful in diagnosing centrally located squamous cell cancer in patients who are not candidates for CT-guided needle biopsy or bronchoscopy.

 Mediastinoscopy is very useful in determining the status of mediastinal lymph nodes in patients who are considered to be candidates for surgical resection. Evaluation of mediastinal lymph nodes by mediastinoscopy is critical before surgical resection. Normal-appearing mediastinal lymph nodes may contain metastatic disease, and sometimes enlarged lymph nodes in the mediastinum may represent only hyperplastic lymph nodes from postobstructive pneumonia or may represent old granulomatous infection. Cervical mediastinoscopy is more accurate for staging superior mediastinal lymph nodes, whereas extended or anterior (Chamberlain) approach is better for anterior mediastinal lymph nodes. Endoscopic and endobronchial ultrasonography are being increasingly utilized to biopsy the mediastinal lymph glands. Many thoracic surgeons do not perform preoperative mediastinoscopy if the CT chest and FDG PET reveal no abnormalities in the mediastinum.

 Video-assisted thoracoscopic surgery (VATS) can be used to access peripheral nodules, suspected pleural disease, and effusions.

  1. Pathology. Specific histopathological diagnosis is essential for the appropriate treatment of each patient. The vast majority of patients fall into two major subtypes: non–small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). NSCLC accounts for 85% of lung cancers, with the most common histologies being adenocarcinoma, squamous cell carcinoma, and large cell carcinoma. The histological subtype and the molecular subtype influence treatment decisions. SCLC accounts for 13% of primary lung cancers, and the incidence has been declining.
  2. Staging. The International Staging System (ISS) uses the TNM (tumor, node, metastasis) descriptive system. T stage is subdivided into T1 (≤3 cm), T2a (>3 to ≤5 cm), T2b (>5 to ≤7 cm), T3 (tumor >7 cm, separate nodules in the same lobe, atelectasis or obstructive pneumonitis of the entire lung, or direct involvement of adjacent organs), and T4 (invasion of the mediastinum, great vessels, trachea, recurrent laryngeal nerve, esophagus, vertebral body, carina, or separate nodules in an ipsilateral different lobe). N stage is subdivided into N1 (ipsilateral peribronchial or hilar lymph node), N2 (ipsilateral mediastinal lymph node), and N3 (contralateral mediastinal, contralateral hilar or any supraclavicular node involvement supraclavicular lymph node). M stage is subdivided into M1a (contralateral nodules, pleural nodules, malignant pleural or pericardial effusion) and M1b (distant metastases). Staging is subdivided into IA (T1N0M0), IB (T2aN0M0), IIA (T1a-2aN1M0 or T2bN0M0), IIB (T2bN1M0 or T3N0M0), IIIA (T1a-2bN2M0, T3N1-2M0, or T4N0-1M0), IIIB (TanyN3Mo), and IV (M1).
  3. Therapy and prognosis
  4. Stages I and II. Tl or T2 without extrapulmonary nodal disease (i.e., N2 or N3) is treated surgically whenever complete resection is possible. Preoperative assessment should determine the stage (for potential resection), cardiopulmonary reserve, and perioperative risk of intended procedure. Suitable surgical candidates are those with estimated forced expiratory volume in 1 second (FEV1) or diffusing lung capacity for carbon monoxide (DLCO) after pneumonectomy of more than 40% and maximal O2 consumption greater than 20 ml/kg/minute. Stage of disease, age of the patient, and extent of resection significantly affect mortality, which averages approximately 3% to 7%. Lobectomy is the most commonly used procedure and is preferred over pneumonectomy when complete resection is achieved. Segmentectomy and wedge resection are associated with two- to threefold increased risk of local recurrence (and should be reserved for situations in which the tumor is <3 cm and lobectomy cannot be done). If the chest wall is involved, then en bloc resection of the tumor with the involved chest mass and a minimum of 2 cm of normal chest wall in all directions beyond the tumor are recommended. Systemic mediastinal lymph node sampling during resection should be performed first. If nodes were not involved, complete lymph node dissection is not indicated. VATS is less invasive than open thoracotomy and associated with shorter recovery time as well as less surgical complications.

 Definitive radiation therapy (RT) is an alternative for patients who are not candidates for surgery. Selection of patients for RT is based largely on the extent of the primary tumor and the prognostic factors. On the basis of retrospective data, the patterns of failure following surgery (lobectomy/pneumonectomy) or stereotactic body radiation therapy (SBRT) are comparable (J Thorac Oncol 2013;2:192). Survival after RT depends on the patient’s overall health status, radiation dose, tumor size, and complete response by 6 months after completion of RT.

 Preoperative RT is not considered appropriate in early-stage lung cancer. The role of postoperative radiotherapy (PORT) was evaluated in the PORT meta-analysis, which was a pooled analysis of 2,128 patients with lung cancer treated in nine randomized trials between 1966 and 1994, and demonstrated a 7% absolute reduction in 2-year overall survival, with the greatest detrimental effect in patients with stage I disease. In patients with Nl or N2 disease, two studies by the Lung Cancer Study Group (LCSG) and the British Medical Research Council (BMRC) concluded that PORT could improve local control but did not affect overall survival, possibly because of lack of effect on systemic disease. PORT is not recommended for patients with N0 or N1 disease, but may have some benefit in patients with N2 disease who are medically fit, and for patients with positive surgical margins.

 Adjuvant chemotherapy was not standard of care until the last decade, since older adjuvant chemotherapy regimens studied did not show a survival benefit. From 1996 to 2005, a series of randomized studies of adjuvant chemotherapy in NSCLC were performed, using platinum doublets and triplets. An absolute 5-year survival benefit of 5.4% with adjuvant chemotherapy was found in a pooled analysis by the LACE collaborative group. This analysis included the five largest clinical trials that used adjuvant cisplatin-based chemotherapy after surgical resection [International Adjuvant Lung Cancer Trial (IALT), intergroup JBR.10 trial, Adjuvant Navelbine International Trialists Association (ANITA), European Big Lung trial, and the Adjuvant Lung Project Italy (ALPI)]. The survival benefit from adjuvant chemotherapy was greatest with the regimen of cisplatin and vinorelbine, with the most significant effect seen in patients with stage II and III NSCLC. Adjuvant chemotherapy should be considered for patients with stage II and III disease. The role of adjuvant chemotherapy in stage IB disease is controversial. American Society for Clinical Oncology (ASCO) and National Comprehensive Cancer Network (NCCN) recommended careful consideration for adjuvant chemotherapy in stage IB rather than routine use. So far, no prospective studies have demonstrated overall improvement in survival with molecularly targeted therapies in patients with completely resected NSCLC. The ongoing ALCHEMIST study, an NCI-sponsored study, will evaluate the benefit of adding molecularly targeted therapies in this setting in molecularly defined subgroups.

  1. Stage III. Stage IIIA includes T3 Nl or N2 nodal disease. Patients with superior sulcus syndrome without mediastinal lymph gland involvement or disease involving the spine are candidates for surgery following induction chemoradiation.

 Among patients with stage IIIA, surgery is the standard therapy for those with T3N1, followed by adjuvant chemotherapy, whereas the role of surgery is controversial for patients with stage IIIAN2, with no survival improvement from surgery after chemoradiotherapy in two large studies, the Intergroup 0139 and the European Organization for Research and Treatment of Cancer (EORTC) 08941. At present, definitive chemoradiation is considered standard of care for patients with T4, N2, or N3 involvement. When mediastinal involvement is detected only at the time of resection, surgery should be followed by adjuvant chemotherapy with or without sequential RT. Patients with superior sulcus syndrome without mediastinal lymph gland involvement or disease involving the spine are candidates for surgery following induction chemoradiation.

 RT alone is not an optimal therapy in patients with unresectable stage III NSCLC and good PS, as the 5-year survival rates are only 5%.

 It has been shown that the addition of chemotherapy to RT improves survival in patients with stage III NSCLC over RT alone. Chemotherapy administered concurrent with radiation is superior to induction chemotherapy followed by sequential thoracic radiation, due to improved survival, though at the cost of increased toxicity with increased incidence of acute esophagitis and pneumonitis. Common regimens in use include cisplatin and etoposide concurrent with radiation and carboplatin and paclitaxel concurrent with thoracic radiation. The role of consolidation chemotherapy with docetaxel was evaluated by the HOG-LUN 01-24 trial, where three cycles of docetaxel versus observation were given after concurrent chemoradiation using cisplatin and etoposide with thoracic radiation to 59.4 Gy (1.8 Gy/fraction). The updated results showed no significant difference in survival between the two groups, but more toxicities on the docetaxel arm (Ann Oncol 2012;23:1730–1738). Currently, concurrent chemoradiation with cisplatin-based doublet is recommended in patients with good PS and unresectable stage III disease. Although consolidation chemotherapy (chemotherapy after chemoradiotherapy) is commonly used, it has not been shown to improve outcomes in randomized clinical trials. For patients with poor PS, thoracic radiation alone or sequential chemotherapy followed by radiation are administered for symptom palliation and survival prolongation. Given the high incidence of eventual brain metastasis in patients with stage III disease, the role of prophylactic cranial irradiation (PCI) has been examined in this patient population. Although PCI resulted in decreased incidence of brain metastasis, there was no survival benefit from PCI in these patients. The RTOG 1306 study is examining the role of induction-targeted therapy followed by chemoradiotherapy in patients with locally advanced NSCLC.

  1. Stage IV
  2. Initial therapy. Systemic chemotherapy improves survival in patients with previously untreated NSCLC over best supportive care (BSC). Some of the commonly used combination regimens in the treatment of NSCLC are listed in Appendix II. It is important that both the patient and the physician realize that the goal of systemic chemotherapy is not to cure the disease but rather to achieve palliation of symptoms and prolongation of survival without unacceptable toxicity. Patients with squamous NSCLC should be considered for platinum-based doublet therapy. The chemotherapy options include a platinum agent in combination with either a taxane (paclitaxel, docetaxel), vinorelbine, or gemcitabine and produce identical improvement in survival with slight differences in toxicity profile (N Engl J Med 2002;346:92). Carboplatin is commonly used in the United States in view of its favorable toxicity profile. A recent phase III trial showed higher response rates and less neurotoxities with albumin-bound paclitaxel (nab-paclitaxel) plus carboplatin when compared with solvent-based paclitaxel (sb-paclitaxel) plus carboplatin (J Clin Oncol 2012;30:2055). The combination of pemetrexed and a platinum doublet (cisplatin or carboplatin) is reasonable choice for patients with metastatic nonsquamous NSCLC. The addition of bevacizumab to carboplatin–paclitaxel regimen was associated with improved overall survival in patients with advanced nonsquamous NSCLC and no brain metastases (N Engl J Med 2006;355:2542). The addition of cetuximab to platinum-doublet chemotherapy is associated with modest survival benefit, which may be related to the expression of epidermal growth factor receptor (EGFR; Lancet Oncol 2012;13:33). If tolerated, systemic chemotherapy should be given for four to six cycles in the absence of progressive disease. There is no evidence to indicate that prolonged courses of doublet chemotherapy result in improved survival. In elderly and patients with poor PS (PS2), single-agent chemotherapy (gemcitabine, vinorelbine, or a taxane) is appropriate.
  3. Molecularly targeted therapy. Patients with known driver mutation(s) should be treated with single-agent target therapy.

i. EGFR. Initial studies with first generation reversible EGFR tyrosine kinase inhibitors (gefitinib and erlotinib) were conducted in molecularly unselected patients with previously treated NSCLC. The response rates for gefitinib were 11% and 18%, respectively, in the two Iressa Dose Evaluation in Advanced Lung Cancer (IDEAL) trials. However, gefitinib was not found to improve survival compared with placebo in the Iressa Survival Evaluation in Lung Cancer (ISEL) study. Erlotinib, another EGFR TKI, was found to improve both PFS and OS compared with placebo in the BR.21 study, and was approved by the U.S. Food and Drug Administration (FDA) in previously treated molecularly unselected patients, based on the results of this study. Clinical predictors for response to EGFR TKI include adenocarcinoma histology, female gender, East Asian ethnicity, and never smoker or previous light smoker status. Presence of activating EGFR tyrosine kinase mutations in the tumor, including deletion in exon 19 and L858R mutation involving exon 21 render the receptor constitutively active and predict for response to EGFR TKI therapy.

Gefitinib was the first EGFR TKI to be compared with chemotherapy in the frontline setting in light or never smokers in the Iressa Pan Asia Study (IPASS). Subset analysis confirmed improved response rates (71.2% vs. 47.3%) and significant progression-free survival advantage in patients with EGFR mutations (mainly exon 19 deletion or the exon 21 L858R mutation) who were treated with gefitinib compared with chemotherapy (J Clin Oncol 2011;29:2866). The OPTIMAL and EURTAC trials confirmed the progression-free survival and objective response rate advantages of erlotinib (EGFR TKI) in EGFR-mutant patients. Afatinib is a second-generation irreversible EGFR inhibitor that also targets HER2 and HER4 and was recently approved by the FDA for treatment of patients with activating EGFR tyrosine kinase mutations, based on the results of the phase III Lux-Lung 3 trial. In this study, afatinib was compared with cisplatin and pemetrexed in the frontline setting and was associated with significant improvement in PFS (11.1 vs. 6.9 months; HR 0.58, p=0.001) (J Clin Oncol 2013;31:3327). Most recently, it has been shown that this effect was specifically more pronounced in the subset of patients with exon 19 deletions.

However, despite the initial response, virtually all patients with EGFR-mutant NSCLC eventually develop disease progression on EGFR TKI therapy. Mechanisms of secondary resistance include EGFR T790M mutation (50% of patients), PIK3CA mutations, and gene amplifications of MET and HER2. Studies of third-generation EGFR TKIs (AZD 9291 and CO 1686) designed to target the T790M mutation have shown very promising results so far.

ii. Anaplastic lymphoma kinase (ALK) gene rearrangements. EML4-ALK is a novel fusion gene that is present in 3% of patients with advanced NSCLC. Additional partners of ALK fusion that have been described include TGF, KIF5B, and KLC1. ALK gene fusions are more commonly seen in younger patients with adenocarcinoma histology who report no history of tobacco smoking and have wild-type EGFR.

Crizotinib produces an impressive response rate of 57% in patients with ALK FISH–positive tumors. In a randomized second-line clinical trial comparing crizotinib with docetaxel or pemetrexed in ALK-positive patients, crizotinib was associated with a significant improvement in median PFS (7.7 vs. 3 months; HR 0.49, p < 0.001). Among the patients randomized to chemotherapy in this trial, pemetrexed was associated with improved PFS compared with docetaxel (4.2 vs. 2.6 months) (N Engl J Med 2013;368:2385). Crizotinib is currently being compared to chemotherapy with platinum plus pemetrexed in patients with ALK-positive tumors, in the frontline setting.

Resistance mechanisms to ALK inhibitors can be categorized as ALK-dominant, due to an ALK-resistant mutation or ALK copy number gain, or ALK-nondominant due to a second oncogene. Ceritinib is a selective oral tyrosine kinase inhibitor of ALK, which is 20 times as potent as crizotinib in inhibiting ALK. Ceritinib has activity both in patients who are ALK-inhibitor naïve (Overall Response Rate, ORR 70%) and in patients who have received prior ALK-inhibitor treatment (ORR 55%). Ceritinib crosses the blood–brain barrier and may be a good option for patients with brain metastasis, with ORR of 54% in target brain lesions. In view of the impressive ORR, ceritinib received accelerated approval by the FDA. Several novel ALK inhibitors are in development.

iii. Other targetable molecular alterations in NSCLC. ROS1 gene rearrangements are seen in 2% of patients with lung adenocarcinoma, and are also observed more commonly in never smokers. Crizotinib is an inhibitor of ROS1, in addition to MET and ALK. The response rate to crizotinib in patients whose tumors carry ROS1 gene fusions is 57%. KIF5B-RET gene fusion occurs in 1% of lung adenocarcinomas and represents novel targets in lung adenocarcinoma. Patients whose tumors carry RET gene fusions tend to be never smokers and younger, with small poorly differentiated primary tumors with N2 nodal involvement. A phase II study of cabozantinib, an inhibitor of RET tyrosine kinase activity, is ongoing. In the preliminary report of the first three patients enrolled, two patients had partial response (PR) and the third had stable disease.

BRAF mutations are also seen in 2% of lung adenocarcinomas, with half of them comprising of BRAF V600E mutations, while the remainder are characterized as non-V600E mutations. The response to BRAF inhibitor dabrafenib in patients with BRAF V600E mutations is 40% based on preliminary data from the BRF113928 study.

HER2 mutations involving exon 20 occur in 1% to 2% of patients with NSCLC. These mutations tend to occur in never smokers, and mostly in women. Afatinib, an inhibitor of HER1, HER2, and HER4 is associated with 100% disease control rate in a four-patient case series of HER2 mutation–positive lung adenocarcinoma, while trastuzumab-based therapies resulted in 96% disease control rate in 15 patients. The largest study of patients with HER2 mutation–positive patients with lung cancer is ongoing, in which patients are being treated with neratinib, an inhibitor of HER2, in combination with temsirolimus, an inhibitor of mTOR.

KRAS mutations are the most frequently observed somatic molecular alterations in lung adenocarcinoma (30%), occurring mostly in codons 12 and 13. KRAS mutations have proven difficult to target. The Biomarker-integrated Approaches of Targeted Therapy for Lung Cancer Elimination (BATTLE) trial included 14 patients with mutations in either BRAF or KRAS treated with sorafenib, with a disease control rate of 79%. A phase II study randomized patients with KRAS-mutant NSCLC to receive second-line docetaxel alone versus docetaxel in combination with selumetinib, an inhibitor of MEK. The selumetinib had an improved response rate (16%) compared with the docetaxel arm (0%), but the study failed to meet its primary end point of improvement in OS with addition of selumetinib to docetaxel.

  1. Maintenance therapy. Frontline platinum-based doublet therapy is usually administered for four to six cycles, following which patients with significant side effects, fatigue, and decline in PS can be observed with serial imaging studies, with institution of second-line therapy at the time of disease progression. On the other hand, patients with good performance status with no disease progression following frontline platinum-doublet therapy who desire additional treatment can be considered for maintenance therapy. When the maintenance agent used is the same one used in conjunction with platinum in the frontline setting, it is called “continuation maintenance,” whereas if the agent used for maintenance was not included in frontline therapy, it is termed maintenance therapy. Pemetrexed is a well-tolerated agent that has been studied as both switch maintenance following platinum-doublet therapy (Lancet 2009;374:1432) and continuation maintenance in the PARAMOUNT trial following four cycles of cisplatin and pemetrexed (J Clin Oncol2013;23:2895), with improvement in both PFS and OS.
  2. Second-line therapy. Prior treatment, presence of driver mutations, and the patient’s overall health are important factors that impact the subsequent therapies for patients developing progressive disease after first-line chemotherapy. Docetaxel improves survival compared to BSC and chemotherapy with vinorelbine or ifosfamide, and pemetrexed has been found to be equivalent to docetaxel in the second-line setting (J Clin Oncol 2004;22:1589). Erlotinib improved survival compared with BSC in unselected previously treated patients (N Engl J Med 2005;353:123). However, single-agent chemotherapy is preferable to EGFR TKI in patients without EGFR mutation. The future for NSCLC therapy will depend on our better understanding of the tumor signaling pathways and inhibition of these pathways with novel agents or immunotherapy.
  3. Role of surgery or RT in stage IV NSCLC. An isolated metastatic lesion (e.g., brain) can be surgically resected before systemic therapy. Surgical intervention is also indicated in certain situations (e.g., metastatic lesion in weight-bearing bones, stabilization of spine). RT is indicated for palliation of the following:

i. Atelectatic lobe, especially in COPD patients. Re-expansion is expected in 60% to 70% of patients if atelectasis has been present for less than 2 weeks.

ii. Hemoptysis, intractable cough, and pain.

iii. Metastatic disease. Bone: RT is used to alleviate pain and prevent impending fracture or compression syndrome. In case of pathologic fracture, RT is used in conjunction with orthopedic fixation to maintain function and activity. Brain: for solitary brain metastasis, better survival and function is seen when the lesion is resected before RT.

  1. Follow-up. The recommendations with regard to surveillance imaging for patients who have been treated for NSCLC with no evidence of clinical or radiographical disease are somewhat arbitrary. NCCN guidelines recommend history, physical exam, and chest CT (with or without contrast) every 6 to 12 months for 2 years, then history, physical exam, and noncontrast CT chest annually. Routine PET CT or brain MRI is not recommended.
  2. Background. Lung cancer is the second most common cancer and the leading cause of death due to malignancy in both men and women in the United States. An estimated 228,000 new cases will be diagnosed in 2013, with 160,000 deaths.
  3. Risk factors
  4. Tobacco use. Cigarette smoking is responsible for 90% of lung cancer cases, and 1 out of 10 individuals who smoke will develop lung cancer. The risk of developing lung cancer is directly related to the duration of smoking and persists for a long time, even after stopping smoking.
  5. RT. Patients treated with thoracic RT for breast cancer or lymphoma were shown to have a higher incidence of lung cancer.
  6. Coexisting lung diseases. These include COPD, chronic infections (e.g., tuberculosis), and others (e.g., alpha-1 antitrypsin deficiency, diffuse pulmonary fibrosis).
  7. Genetic factors. Lung cancer can be familial, and people with first-degree relatives diagnosed with lung cancer are at higher risk of developing it. However, the underlying gene abnormalities are ill-defined.
  8. Environmental exposure to asbestos, arsenic, chromium, hydrocarbons, radon, and uranium in mining workers and, less clearly, silicosis in smokers.
  9. Age. Incidence of lung cancer increases with age.
  10. Screening. The National Lung Cancer Screening Trial (NLST) demonstrated a 20% relative reduction in lung cancer specific mortality in high-risk population (old adult with 30 pack-year history of smoking) with the use of screening low-dose CT, compared with chest X-ray (N Engl J Med 2011;365:395). Currently, most of the medical societies recommend annual screening for lung cancer with low-dose CT scan in high-risk groups after an informed risk–benefit discussion.
  11. Research initiatives. There is an ongoing effort to identify driver mutations in NSCLC and develop molecularly targeted therapies (see section on Molecularly Targeted Therapy). The Cancer Genome Atlas (TCGA) group has recently published results of comprehensive genomic analyses of squamous cell NSCLC and adenocarcinoma histology. In addition, there is great interest in applying immunotherapy in the treatment of lung cancer, including the use of the anti-CTLA4 drug ipilimumab, blockers of PD1 and PDL1, and lung cancer vaccines. Early results from studies involving PD-1 /PDL1- inhibitors show a response rate of 20% with relatively few toxicities. Some of the responses appear to be very durable.
  12. SCLC
  13. Presentation
  14. Subjective. Small cell lung cancer is primarily a disease of smokers, and is characterized by rapid doubling time, and early propensity to metastasize to lymph nodes and distant sites. Presenting symptoms often include shortness of breath, wheezing, cough, hemoptysis, chest pain, and postobstructive pneumonia. As the mediastinal lymph nodes are involved very commonly, patients can present with SVC syndrome (10% of patients at the time of diagnosis), hoarseness from recurrent laryngeal nerve compression or invasion, and dysphagia. Thirty percent of patients at some point in their disease course will have brain metastases; 90% of such patients will be symptomatic from brain metastases. Patients may present with bone pain due to painful bony metastasis.
  15. Objective. The importance of a good physical examination in these patients cannot be emphasized enough because more than two-thirds of patients have obvious distant metastases, some of which can be recognized in the physical examination. This may include hepatomegaly, subcutaneous nodules, focal neurologic signs, palpable adenopathy, palpable subcutaneous or breast metastatic deposits, and bony tenderness. The most common sites of extrathoracic disease include bone (19% to 38% of all presenting patients), liver (17% to 34%), bone marrow (17% to 23%), and CNS (0% to 14%). Patients with liver metastasis may have abnormalities on hepatic function profile. Bone marrow involvement may be present, and when severe, can result in cytopenias. Paraneoplastic syndromes are also much more common in SCLC than NSCLC.
  16. Workup and staging
  17. Workup. The physician should aim for a cost-effective workup that adequately stages the tumor for necessary therapeutic decisions. The key question is whether the patient has limited or extensive-stage disease, with the former being treated with thoracic radiation in addition to chemotherapy and the latter treated initially with chemotherapy alone. Therefore, once metastasis has been documented with extensive-stage disease, there is no need to document any other metastatic locations unless they are symptomatic, requiring palliative therapy.

 The typical radiographic appearance of SCLC is small primary tumors with large hilar and mediastinal lymph node involvement. Pleural effusions occur less frequently, though if present, upstage the patient to the “extensive stage” category.

 Staging for SCLC includes a CT scan of the chest and abdomen with contrast, to evaluate for primary tumor, nodal metastasis, and metastasis to liver and adrenal glands. Given the high propensity for brain metastasis in these patients, brain imaging (CT with contrast or brain MRI) should be performed for all patients at presentation. When distant metastasis is not apparent on these imaging studies, a PET scan should be performed. PET scans have been shown to upstage limited stage–SCLC to extensive stage–SCLC in up to 19% of patients (Cancer Imaging 2012;11:253).

  1. Staging. The Veterans Administration Lung Group staging system currently in use in North America categorizes patients into limited-stage and extensive-stage disease. Limited stage is defined as tumor confined to one hemithorax and regional lymph nodes and is often subjectively defined by what can fit into one RT portal. Extensive stage is defined as any disease outside limited stage. Generally, 30% to 40% of patients will have limited-stage, and 60% to 70%, extensive-stage disease. The same TNM staging system for NSCLC can be used in SCLC.
  2. Therapy and prognosis
  3. Limited stage
  4. Therapy. The current standard of care is combined-modality therapy with chemotherapy and RT.

i. Chemotherapy. Although patients with SCLC respond to chemotherapy initially, almost all will relapse and die from the disease. Combination chemotherapy results in higher response rates and longer survival than does single-agent chemotherapy. The overall response rate to treatment for limited-stage SCLC is estimated to be 80% to 90%. The combination of cisplatin and etoposide (PE) has been repeatedly demonstrated to yield similar or improved results as compared with any other studied combination, and is easily one of the most commonly used chemotherapeutic regimens for patients with SCLC. In addition, this combination is tolerated well when administered in conjunction with thoracic radiation. We typically administer PE for four to six cycles for those patients who have no evidence of progressive disease. A meta-analysis indicated that carboplatin can replace cisplatin without differences in outcome (J Clin Oncol 2012;30:1692).

ii. RT. Administration of thoracic RT in conjunction with systemic chemotherapy has been shown to improve survival. A meta-analysis of 13 trials including 2,140 patients with limited disease demonstrated a higher survival rate for combined-modality approach with the combination of chemotherapy and thoracic RT as compared with combination chemotherapy alone, with the 3-year survival increasing from 8.9% to 14.3% (N Engl J Med 1992;327:1618). The intergroup 0096 study demonstrated improved survival with 1.5 Gy twice daily thoracic radiation to a dose of 45 Gy in 3 weeks, compared with 1.8 Gy once daily radiation to a total dose of 45Gy in 5 weeks (26% vs. 16%) (N Engl J Med 1999;340:265). The schedule of RT and temporal coordination with chemotherapy may be of some importance, with early RT associated with improved survival compared with treatment starting at the third or fourth cycles of chemotherapy (J Clin Oncol 2004;22:4785).

iii. PCI. For those limited-stage patients who demonstrate a complete response to induction chemotherapy, PCI should be considered to reduce the incidence of brain metastasis and improve survival. A meta-analysis of 987 patients demonstrated a 16% decrease in mortality, 5.4% increase in 3-year survival, decreased incidence of brain metastasis, and prolonged disease-free survival in limited-stage patients who received PCI after complete response to induction chemotherapy (N Engl J Med 1999;341:476). The EORTC 08993 randomized 286 patients with any response to induction chemotherapy to PCI or observation. PCI was associated with improved 1-year overall survival from 13.3% to 27.1% (N Engl J Med 2007;357:664). Late neurocognitive dysfunction may develop, and careful consideration is imperative when treatment is offered to the elderly and patients with poor PS. Administering PCI after chemoradiation and in low doses per fractions could further reduce the risk of neurologic sequelae.

  1. Surgery. Surgery followed by adjuvant chemotherapy is an option for patients with very limited disease, defined as T1-2N0M0.
  2. Extensive stage
  3. Therapy. The current standard of care is platinum-based chemotherapy doublet, which has a 60% to 80% response rate. The combination PE is a commonly used regimen in patients with extensive-stage SCLC. The COCIS meta-analysis showed no significant differences in outcomes for patients treated with etoposide and either cisplatin or carboplatin (J Clin Oncol 2012;30:1692). Maintenance chemotherapy has not been shown to improve overall survival.

 Although the JCOG 9511 study showed improved survival from the combination of cisplatin and irinotecan compared with PE, confirmatory studies in the United States showed no difference in outcomes from the two regimens (Cancer 2010;116:5710).

i. Relapsed SCLC. In spite of a high response rate, most patients with SCLC eventually have relapse of the disease and die of progressive disease. There are two categories of relapsed SCLC: sensitive relapse, that is, those who relapse 3 months after the completion of therapy, and resistant relapse, that is, those who have progressive disease during initial chemotherapy or those who have relapse within 3 months of completion of therapy. Although the response rates for the subgroup of patients with sensitive relapse is approximately 25%, fewer than 10% of patients with resistant relapse respond to salvage therapy. A number of single agents have been reported to be active in this setting including irinotecan (16% to 47%), paclitaxel (29%), docetaxel (25%), oral etoposide (23%), gemcitabine (6% to 16%), vinorelbine (15%), and temozolomide (16%). Topotecan is the only approved regimen for salvage chemotherapy in sensitive relapse patients. A phase III trial comparing topotecan with cyclophosphamide, adriamycin, and vincristine (CAV) reported similar survival and response rates, but lesser toxicity with topotecan (J Clin Oncol 1999;17:658). A randomized study comparing oral and intravenous topotecan showed similar outcomes, with median overall survivals of 33 and 35 weeks, respectively (J Clin Oncol 2006;25:2086).

  1. Prognosis. Unfavorable prognostic factors include extensive stage, poor PS, older age, hyponatremia, male gender, and elevated serum lactate dehydrogenase (LDH) and alkaline phosphatase. Of these, stage and PS are most powerfully associated with prognosis. The most important risk factor for treatment-related mortality, which can approach 5% in aggressive limited-stage therapy, is PS. Additionally, amplification of the c-myconcogene is linked with shorter survival.

The natural history of the progression of this disease is that of rapid growth and early dissemination. The median survival of patients with limited-stage SCLC is 15 to 20 months. The reported 5-year survival varies from 10% to 13%. Median survival in extensive stage is 8 to 13 months, but only 2 to 4 months if untreated. From 50% to 80% of patients who survive longer than 2 years will have metastases to the brain.

  1. Background
  2. Epidemiology. The incidence of SCLC has been declining over the last few decades, accounting for only 13% of all newly diagnosed lung cancer cases (J Clin Oncol 2006;24:4539). It is a disease of the elderly, with age peaks at 70 to 74 years in men and 60 to 69 years in women. In addition, there has been a dramatic increase in the incidence among women, with a current incidence ratio of 1:1 between men and women.
  3. Risk factors. Almost all patients with this cancer have a history of tobacco abuse: only 2% of 500 patients treated at the National Cancer Institute in one series denied ever smoking. Exposure to radioactive radon in mining also may be a risk factor.
  4. Follow-up
  5. Secondary malignancies. These patients are at high risk of developing other malignancies related to smoking. The cumulative risk of a second malignancy 15 years after diagnosis of SCLC is 70%. Overall, in 20% of long-term survivors in one large analysis, secondary malignancies developed. The risk of having a second primary lung cancer increases with time (14.4% after 10 years). If a new lung mass develops in a long-term survivor, the physician must obtain a biopsy to rule out a new primary malignancy that may not be SCLC. Additionally, these patients are at increased risk for other tobacco-related malignancies such as cancer of the upper aerodigestive tract (12.6% after 10 years).
  6. Smoking. These patients should be strongly encouraged to stop smoking. Once a smoker quits, the risk of any type of lung cancer begins to decline, but it takes at least a decade for such patients to approach a risk equivalent to that of a nonsmoker.

SUGGESTED READINGS

Gerber D, Schiller J. Maintenance chemotherapy for advanced non-small-cell lung cancer: new life for an old idea. J Clin Oncol 2013;31:1009–1020.

Govindan R, Ding L, Griffith M, et al. Genomic landscape of non-small cell lung cancer in smokers and never-smokers. Cell 2012;150:1121–1134.

Kris MG, Johnson BE, Berry LD, et al. Using multiplexed assays of oncogenic drivers in lung cancer to select targeted drugs. JAMA 2014;311:1998–2006.

Mok TS, Wu L-Y, Thongprasert S, et al. Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N Engl J Med 2009;361:947–957.

National Lung Screening Trial Research T; Aberle DR, Adams AM, et al. Reduced lung-cancer mortality with low-dose computed tomographic screening. N Engl J Med 2011;365:395–409.

Sequist LV, Yang JC-H, Yamamoto N, et al. Phase III study of afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations. J Clin Oncol 2013;3327–3334.

Shaw AT, Kim D-W, Nakagawa K, et al. Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N Engl J Med 2013;368:2385–2394.

Turrisi AT 3rd, Kim K, Blum R, et al. Twice-daily compared with once-daily thoracic radiotherapy in limited small-cell lung cancer treated concurrently with cisplatin and etoposide. N Engl J Med 1999;340:265–271.



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