Medication Summary
Chemotherapy is used as an adjuvant to surgery in selected patients with non–small cell lung cancer (NSCLC). Unresectable NSCLC is treated with chemotherapy or a combination of chemotherapy and radiation therapy. Molecularly targeted treatments have also become standard of care.
Aggressive antiemetic support and growth-factor support, when appropriate, are other integral parts of medical treatment of these patients. Antibiotics are commonly required for treatment of infectious complications but are not discussed in this article. Aggressive antiemetic support to prevent, not treat, nausea and vomiting is essential because of the highly emetogenic potential of chemotherapy drugs and the doses used in the treatment of NSCLC. This holds especially true for platinum-based chemotherapeutic regimens. The most common and effective agents are corticosteroids and the serotonin receptor antagonists, which include ondansetron, granisetron, and dolasetron.
Antineoplastic Agents
Class Summary
Antineoplastic agents are used either to prolong survival or to palliate symptoms in advanced or unresectable lung cancer.
Carboplatin
Carboplatin has a mechanism of action similar to that of cisplatin. It is approved for ovarian cancer but is used commonly in squamous cell carcinoma (SCC) of the head, neck, cervix, and lungs. Its main advantages over cisplatin include less nephrotoxicity and ototoxicity (not requiring extensive prehydration) and reduced likelihood of inducing nausea and vomiting. It is more likely to induce myelotoxicity.
Vinorelbine (Navelbine)
Vinorelbine is a semisynthetic vinca alkaloid that inhibits tubulin polymerization during the G2 phase of cell division, thereby inhibiting mitosis. Vinorelbine alone or in combination with cisplatin is indicated as first-line treatment of ambulatory patients with unresectable, advanced NSCLC and for stage IV NSCLC. In stage III NSCLC, vinorelbine is indicated in combination with cisplatin.
Paclitaxel
Paclitaxel is a naturally occurring chemical derived from the Pacific yew tree (Taxus brevifolia). It inhibits tubulin depolymerization in the spindle during cell division. Paclitaxel is used in combination with cisplatin for the first-line treatment of NSCLC in patients who are not candidates for potentially curative surgery or radiation therapy.
Paclitaxel protein bound (Abraxane)
Protein-bound paclitaxel is a microtubular inhibitor (albumin-conjugated formulation). It is a natural taxane, and it prevents depolymerization of cellular microtubules, which results in DNA, RNA, and protein synthesis inhibition. It is indicated for locally advanced or metastatic NSCLC, as first-line treatment in combination with carboplatin, in patients who are not candidates for curative surgery or radiation therapy.
Cisplatin
Cisplatin is an alkylating agent that causes intrastrand and interstrand cross-linking of DNA, leading to strand breakage. It has a very broad range of antitumor activity and is approved for use in testicular, ovarian, and transitional cell carcinomas. It forms the basis of currently available approved combination chemotherapy regimens for NSCLC. Administer it as a single-dose intravenous (IV) infusion or in divided doses over several days; this can be repeated only after complete hematologic recovery; cycles are typically separated by 3-4 wk.
Gemcitabine (Gemzar)
Gemcitabine is an antimetabolite that acts as an inhibitor of DNA synthesis. It is cell-cycle specific for the S phase. Gemcitabine is used as first-line treatment of patients with inoperable, locally advanced (stage IIIA or IIIB), or metastatic (stage IV) NSCLC in combination with cisplatin.
Docetaxel (Taxotere)
Docetaxel is a semisynthetic taxane, a class of drugs that inhibits cancer cell growth by promoting assembly and blocking disassembly of microtubules, thereby preventing cancer cell division, leading to cell death. It is indicated for the treatment of patients with locally advanced or metastatic NSCLC after failure of prior platinum-based chemotherapy when used alone. It can be used in combination with cisplatin for the treatment of patients with unresectable, locally advanced, or metastatic NSCLC who have not previously received chemotherapy for this condition.
Pemetrexed disodium (Alimta)
Pemetrexed disrupts folate-dependent metabolic processes essential for cell replication. It specifically inhibits thymidylate synthase (TS), dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT), which are folate-dependent enzymes involved in de novo biosynthesis of thymidine and purine nucleotides. It is indicated for nonsquamous NSCLC as follows:
1) Initial treatment in combination with pembrolizumab and platinum chemotherapy for patients with metastatic disease with no EGFR or ALK genomic tumor aberrations
2) Initial treatment in combination with cisplatin for patients with locally advanced or metastatic disease
3) Single agent for maintenance in patients with locally advanced or metastatic disease that has not progressed after 4 cycles of platinum-based first-line chemotherapy
4) Single agent for treatment of patients with recurrent metastatic disease after prior therapy
Cyclophosphamide
Cyclophosphamide is chemically related to nitrogen mustards; as an alkylating agent, the mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.
Doxorubicin
Doxorubicin is an anthracycline that inhibits topoisomerase II and produces free radicals, which may cause destruction of DNA; the combination of these 2 events can, in turn, inhibit the growth of neoplastic cells.
Vincristine
Vincristine is a vinca alkaloid whose mechanism of action is uncertain. It may involve a decrease in reticuloendothelial cell function or an increase in platelet production. However, neither of these mechanisms fully explains the effect in thrombotic thrombocytopenic purpura and hemolytic uremic syndrome. The antineoplastic effects of vincristine are related to its binding to tubulin and inhibition of microtubule formation.
Etoposide
Etoposide inhibits topoisomerase II and causes DNA strand breakage, causing cell proliferation to arrest in the late S or early G2 portion of cell cycle; do not administer IT.
Antineoplastics, Anaplastic Lymphoma Kinase Inhibitors
Class Summary
Testing for ALK rearrangement is recommended in patients with metastatic NSCLC adenocarcinoma to determine if a therapy targeted toward ALK would be beneficial.
Crizotinib (Xalkori)
Inhibitor of receptor tyrosine kinases including, anaplastic lymphoma kinase (ALK), hepatocyte growth factor receptor (HGFR, c-Met), and recepteur d'origine nantais (RON). The gene's expression and signaling that contribute to increased cell proliferation and survival of the tumors becomes activated following the expression of ALK oncogenic fusion proteins. Indicated for locally advanced or metastatic non-small cell lung cancer (NSCLC) that is ALK positive as detected by an FDA-approved test. It is also indicated for NSCLC tumors positive for the ROS-1 gene mutation.
Ceritinib (Zykadia)
Ceritinib is a tyrosine kinase inhibitor that targets anaplastic lymphoma kinase (ALK), insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1. It is indicated for ALK-positive, metastatic NSCLC.
Alectinib (Alecensa)
Tyrosine kinase inhibitor that targets ALK and RET. The major active metabolite of alectinib, M4, showed similar in vitro potency and activity. In nonclinical studies, alectinib inhibited ALK phosphorylation and ALK-mediated activation of the downstream signaling proteins STAT3 and AKT, and decreased tumor cell viability in multiple cell lines harboring ALK fusions, amplifications, or activating mutations.. It is indicated for the treatment of patients with anaplastic lymphoma kinase (ALK)-positive, metastatic NSCLC as detected by an FDA-approved test.
Brigatinib (Alunbrig)
Brigatinib inhibits autophosphorylation of ALK and ALK-mediated phosphorylation of the downstream signaling proteins STAT3, AKT, ERK1/2, and S6 in in vitro and in vivo assays. It is indicated for ALK-positive metastatic NSCLC in patients who have progressed on or are intolerant to crizotinib.
Lorlatinib (Lorbrena)
ALK/ROS1 tyrosine kinase inhibitor indicated for ALK-positive metastatic NSCLC
PD-1/PD-L1 Inhibitors
Class Summary
PD-1 and related target PD-ligand 1 (PD-L1) are expressed on the surface of activated T cells. Under normal conditions, PD-L1/PD-1 interaction inhibits immune activation and reduces T-cell cytotoxic activity when bound. This negative feedback loop is essential for maintaining normal immune responses and limits T-cell activity to protect normal cells during chronic inflammation. Tumor cells may circumvent T-cell–mediated cytotoxicity by expressing PD-L1 on the tumor itself or on tumor-infiltrating immune cells, resulting in the inhibition of immune-mediated killing of tumor cells; therefore, inhibiting the ligand binding will enhance T-cell mediated immune response.
Nivolumab (Opdivo)
Monoclonal antibody to programmed cell death-1 protein (PD-1). It blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2. Restores cytokine secretion and T cell activity. It is indicated for metastatic squamous and nonsquamous (including adenocarcinoma) NSCLC with progression on or after platinum-based chemotherapy. It is also indicated, in combination with ipilimumab, for metastatic NSCLC in patients whose tumors express PD-L1 (≥1%), with no EGFR or ALK tumor aberrations; and, in combination with ipilimumab and two cycles of platinum-doublet chemotherapy, for the first-line treatment of metastatic or recurrent NSCLC in patients whose tumors have no EGFR or ALK aberrations, regardless of PD-L1 expression. In addition to metastatic NSCLC, it is also indicated for resectable (tumors ≥4 cm or node positive) NSCLC in the neoadjuvant setting, in combination with platinum-doublet chemotherapy.
Pembrolizumab (Keytruda)
Pembrolizumab is a monoclonal antibody to programmed cell death-1 protein (PD-1). It blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2. It is indicated as a single agent for first-line treatment of patients with stage III NSCLC who are not candidates for surgical resection or definitive chemoradiation, or metastatic NSCLC whose tumors express PD-L1 (Tumor Proportion Score [TPS] ≥1%) as determined by an FDA-approved test, with no EGFR or ALK genomic tumor aberrations. Pembrolizumab is also indicated as a single agent for the treatment of patients with metastatic NSCLC whose tumors express PD-L1 (TPS ≥1%) as determined by an FDA-approved test, with disease progression on or after platinum-containing chemotherapy; patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving pembrolizumab.
Pembrolizumab is indicated in combination with pemetrexed and carboplatin for first-line treatment of patients with metastatic nonsquamous NSCLC irrespective of PD-L1 expression. It is also indicated first-line in combination with carboplatin and either paclitaxel or nab-paclitaxel for patients with metastatic squamous NSCLC.
Atezolizumab (Tecentriq)
Atezolizumab is a monoclonal antibody to PD-L1. It is indicated for patients with metastatic NSCLC who have disease progression during or following platinum-containing chemotherapy. Patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving atezolizumab. It is also indicated for first-line treatment for metastatic NSCLC in patients whose tumors have high PD-L1 expression (PD-L1 stained ≥50% of tumor cells [TC ≥50%] or PD-L1 stained tumor-infiltrating immune cells [IC] covering ≥10% of the tumor area [IC ≥10%]).
Durvalumab (Imfinzi)
Human IgG1 kappa monoclonal antibody that blocks PD-L1 binding to PD-1 and CD80, and therefore overcoming/preventing PD-L1-mediated inhibition/suppression of T-cell activation. It is indicated for unresectable, Stage III NSCLC in patients whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.
Also indicated in combination with tremelimumab and platinum-based chemotherapy for adults with metastatic NSCLC with no sensitizing epidermal growth factor receptor (EGFR) mutation or anaplastic lymphoma kinase (ALK) genomic tumor aberrations.
Cemiplimab (Libtayo, Cemiplimab-rwlc)
Cemiplimab is a recombinant human IgG4 monoclonal antibody that binds to PD-1 and blocks its interaction with PD-L1 and PD-L1, releasing the PD-1 pathway-mediated inhibition of the immune response, including antitumor immune response, thereby decreasing tumor growth. Binding of the PD-1 ligands PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibits T-cell proliferation and cytokine production. It is approved for first-line treatment of NSCLC who tumors have high PD-L1 expression [TPS ≥50%] with no EGFR, ROS-1, or ALK mutations.
Ipilimumab (Yervoy)
Recombinant, human cytotoxic T-lymphocyte antigen. Proposed mechanism of action is indirect, possibly through inhibition of CTLA-4 signaling, which can in turn reduce T-regulatory cell function and may contribute to a general increase in T cell responsiveness, including the anti-tumor immune response. It is indicated in combination with nivolumab, for metastatic NSCLC in patients whose tumors express PD-L1 (≥1%), with no EGFR or ALK tumor aberrations.
Anti-CLTA4 Antibodies
Class Summary
Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) blocking monoclonal antibody blocks the interaction with its ligands CD80 and CD86. This action releases CTLA-4-mediated inhibition of T-cell activation.
Tremelimumab (Imjudol)
Indicated in combination with durvalumab for and platinum-based chemotherapy for adults with metastatic non-small cell lung cancer (NSCLC) with no sensitizing epidermal growth factor receptor (EGFR) mutation or anaplastic lymphoma kinase (ALK) genomic tumor aberrations.
Antineoplastics, EGFR Inhibitor
Class Summary
EGFR is expressed on the cell surface of both normal and cancer cells and plays a role in the processes of cell growth and proliferation.
Osimertinib (Tagrisso)
EGFR kinase inhibitor, which binds irreversibly to certain mutant forms of EGFR (T790M, L858R, and exon 19 deletion). It is indicated for metastatic EGFR T790M mutation–positive NSCLC in patients whose disease has progressed on or after EGFR TKI therapy. It is also used as first-line treatment for metastatic NSCLC in patients with EGFR exon 19 deletions or exon 21 L858R mutations, and as adjuvant therapy after tumor resection in NSCLC patients whose tumors have EGFR exon 19 deletions or exon 21 L858R mutations.
Gefitinib (Iressa)
Gefitinib reversibly inhibits the kinase activity of wild-type and certain activating mutations of EGFR, preventing autophosphorylation of tyrosine residues associated with the receptor, thereby inhibiting further downstream signalling and blocking EGFR-dependent proliferation. It is indicated for the treatment of patients with metastatic NSCLC whose tumors have EGFR exon 19 deletions or exon 21 (L858R) substitution mutations as detected by an FDA-approved test.
Erlotinib (Tarceva)
Erlotinib is pharmacologically classified as an HER1/EGFR tyrosine kinase inhibitor (TKI). EGFR is expressed on the cell surface of normal cells and cancer cells. It is approved for NSCLC in patients whose tumors have EGFR exon 19 deletions or exon 21 (L858R) substitution mutations as detected by an FDA-approved test for first-line treatment, maintenance treatment, or as second- or greater-line treatment after progression following at least 1 prior chemotherapy regimen. It also is indicated in combination with ramucirumab for first-line treatment of patients with metastatic NSCLC whose tumors have EGFR exon 19 deletions or exon 21 (L858R) substitution mutations.
Afatinib (Gilotrif)
Afatinib covalently binds to the kinase domains of EGFR (ErbB1), HER2 (ErbB2), and HER4 (ErbB4) and irreversibly inhibits tyrosine kinase autophosphorylation, resulting in downregulation of ErbB signaling. It demonstrates inhibition of autophosphorylation and in vitro proliferation of cell lines expressing wild-type EGFR or those expressing selected EGFR exon 19 deletion mutations or exon 21 L858R mutations, including some with a secondary T790M mutations
Afatinib is indicated for first-line treatment of patients with metastatic NSCLC whose tumors have non-resistant EGFR mutations as detected by an FDA-approved test. Additionally, afatinib is indicated for first-line use in metastatic NSCLC for 3 additional nonresistant EGFR mutations (L861Q, G719X, S768I). It is also indicated for metastatic squamous NSCLC that has progressed after platinum-based chemotherapy.
Dacomitinib (Vizimpro)
Irreversible kinase inhibitor of the human EGFR family (EGFR/HER1, HER2, and HER4) and certain EGFR-activating mutations (exon 19 deletion or the exon 21 L858R substitution mutation). It is indicated for first-line treatment of patients with metastatic NSCLC with EGFR exon 19 deletion or exon 21 L858R substitution mutations as detected by an FDA-approved test.
Amivantamab (Amivantamab-vmjw, Rybrevant)
Bispecific antibody that binds to the extracellular domains of EGFR and MET; indicated for locally advanced or metastatic NSCLC with EGFR exon 20 insertion mutations, as detected by an FDA-approved test, in adults whose disease has progressed on or after platinum-based chemotherapy. It is administered as an IV infusion.
Antineoplastics, Anti-HER2
Class Summary
Mutations in the gene encoding HER2 drive approximately 3% of nonsquamous NSCLCs and are associated with female sex, never-smoking history, and a poor prognosis, as well as with a slightly younger age and higher incidence of brain metastases than NSCLC without HER2 mutations or with other mutations. [147]
Trastuzumab deruxtecan (Enhertu)
Indicated for unresectable or metastatic HER2-mutant NSCLC based on presence of activating HER2 (ERBB2) mutations in tumor or plasma specimens in patients who have received prior systemic therapy.
Antineoplastics, BRAF Kinase Inhibitors
Class Summary
BRAF genes direct protein production which induces signal transmission along the RAS/MAPK pathway. RAS/MAPK pathway regulates cell growth, cell differentiation, cell migration, and apoptosis. BRAF mutations can cause dysregulation of cell growth, resulting in tumor progression [248]
Dabrafenib (Tafinlar)
Dabrafenib selectively inhibits multiple mutated BRAF kinases, BRAF V600E, BRAF V600K, and BRAF V600D. BRAF kinase inhibition primarily stunts cells growth. The combination of dabrafenib with trametinib targets two different kinases in the RAS/MEK pathway, causing greater growth inhibition of tumors with the BRAF V600 mutation.
Antineoplastics, Tyrosine Kinase Inhibitors
Entrectinib (Rozlytrek)
Entrectinib and its major metabolite inhibit tropomyosin receptor tyrosine kinases (TRKs), proto-oncogene tyrosine-protein kinase ROS1 (ROS1), and anaplastic lymphoma kinase (ALK). It is indicated for metastatic NSCLC in adults whose tumors are ROS1-positive. Entrectinib is also indicated for NTRK genetic fusion solid tumors in pediatric and adult patients for whom there are no effective treatments.
Larotrectinib (Vitrakvi)
Larotrectinib is an oral tyrosine kinase inhibitor that binds to tropomyosin receptor kinase (TrK), preventing TrK activation. This induces cellular apoptosis and inhibition of cell growth in tumors. It is currently indicated for solid tumors that have an NTRK gene fusion in adults and pediatric patients without a known acquired resistance mutation, are metastatic or where surgical resection is likely to result in severe morbidity, and have no satisfactory alternative treatments or that have progressed following treatment.
Repotrectinib (Augtyro)
Indicated for adults with locally advanced or metastatic ROS1-positive non-small cell lung cancer (NSCLC). Repotrectinib is an inhibitor of proto-oncogene tyrosine-protein kinase ROS1 (ROS1) and tropomyosin receptor tyrosine kinases (TRKs) TRKA, TRKB, and TRKC.
RET Kinase Inhibitors
Class Summary
Genomic alterations in rearranged during transfection (RET) kinase, which include fusions and activating point mutations, lead to overactive RET signaling and uncontrolled cell growth.
Selpercatinib (Retevmo)
Selpercatinib is a kinase inhibitor of wild-type rearranged during transfection (RET) and multiple mutated RET isoforms, as well as vascular endothelial growth factor receptors (VEGFR1, VEGFR3). It is indicated for metastatic RET fusion-positive NSCLC.
Pralsetinib (Gavreto)
Pralsetinib is a selective inhibitor of RET alterations and resistant mutations; specifically designed to spare VEGFR2 and other kinases with the potential to drive off-target toxicity. This RET inhibitor exhibited antitumor activity in cultured cells and animal tumor implantation models harboring oncogenic RET fusions or mutations. It is Indicated for metastatic RET gene-positive NSCLC.
MET Tyrosine Kinase Inhibitors
Class Summary
Mitogen extracellular signal-regulated kinase (MEK) protein acts downstream from Ras in the mitogen-activated protein kinase (MAPK) pathway. MAPK pathway regulates cell growth, cell differentiation, cell migration, and apoptosis. [248] Blockage of MEK protein may affect tumors with mutated Ras proteins or other proteins influenced by MAPK pathway.
Capmatinib (Tabrecta)
Capmatinib is a kinase inhibitor that targets mesenchymal-epithelial transition (MET) , including the exon 14 skipping mutation. MET tyrosine kinase stimulates cell scattering, invasion, protection from apoptosis, and angiogenesis. A variety of cancers (eg, lung, gastric) are associated with dysregulation of MET, owing to MET amplifications and exon 14 skipping mutations. Capmatinib is indicated for metastatic NSCLC in adults whose tumors have a mutation that leads to exon 14 skipping.
Tepotinib (Tepmetko)
Tepotinib is an inhibitor of MET tyrosine kinase, which selectively binds to MET tyrosine kinase and disrupts MET signal transduction pathways. Therefore, this disruption may induce apoptosis in tumor cells overexpressing this kinase. It is indicated for metastatic NSCLC in patients with MET exon 14 skipping mutation.
Trametinib (Mekinist)
Trametinib is a selective reversible inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and kinase activity. Trametinib inhibits activation of MEK by BRAF and inhibits MEK kinase activity BRAF V600E mutations result in constitutive activation of the BRAF pathway, which includes MEK1 and MEK2. Trametinib inhibits cell growth in BRAF V600 mutation positive tumors in vitro and in vivo. It is indicated, in combination with dabrafenib, for the treatment of patients with metastatic NSCLC with BRAF V600E mutation as detected by an FDA-approved test.
Antineoplastics, KRAS Inhibitors
Class Summary
KRAS G12C proteins continuously regenerate, so continuous inhibition is needed to prevent downstream signaling. Sotorasib and adagrasib form an irreversible, covalent bond with the unique cysteine of KRAS G12C, locking the protein in an inactive state that prevents downstream signaling without affecting wild-type KRAS. These inhibitors block KRAS signaling, inhibit cell growth, and promote apoptosis only in KRAS G12C tumor cell lines.
Adagrasib (Krazati)
It is indicated for KRAS G12C- mutated locally advanced or metastatic NSCLC in adults who have received 1 or more prior systemic therapies.
Sotorasib (Lumakras)
Indicated for KRAS G12C-mutated locally advanced or metastatic NSCLC in adults who have received 1 or more prior systemic therapies.
Antineoplastics, Monoclonal Antibodies
Bevacizumab (Avastin, Mvasi)
Bevacizumab is a murine-derived monoclonal antibody that inhibits angiogenesis by targeting and inhibiting vascular endothelial growth factor (VEGF). It inhibits new blood vessel formation, denying blood, oxygen, and other nutrients needed for tumor growth. It is indicated in combination with carboplatin and paclitaxel for the first-line treatment of patients with unresectable, locally advanced, recurrent, or metastatic nonsquamous NSCLC. Mvasi has been FDA-approved as a biosimilar to Avastin but not as an interchangeable product.
Ramucirumab (Cyramza)
Ramucirumab is a vascular endothelial growth factor receptor 2 (VEGFR2) antagonist that specifically binds VEGF receptor 2 and blocks binding of VEGFR ligands, VEGF-A, VEGF-C, and VEGF-D. As a result, it inhibits ligand-stimulated activation of VEGF2, thereby inhibiting ligand-induced proliferation, and migration of human endothelial cells. It is indicated in combination with erlotinib for first-line treatment of patients with metastatic NSCLC whose tumors have EGFR exon 19 deletions or exon 21 (L858R) substitution mutations.
Antiemetic Agents
Class Summary
Antiemetic agents are useful in the treatment of symptomatic nausea caused by chemotherapy.
Ondansetron (Zofran, Zuplenz)
Ondansetron blocks serotonin 5-HT3 receptor antagonists. It is not clear whether the effect is mediated centrally, peripherally, or both. Ondansetron is indicated in the prevention of chemotherapy-induced nausea and vomiting.
Granisetron (Granisol, Sancuso, Sustol)
Granisetron blocks serotonin 5-HT3 receptor antagonists. It is not clear whether the effect is mediated centrally, peripherally, or both. Granisetron is indicated in the prevention of chemotherapy-induced nausea and vomiting.
Dolasetron (Anzemet)
Dolasetron blocks serotonin 5-HT3 receptor antagonists. It is not clear whether the effect is mediated centrally, peripherally, or both. Dolasetron is indicated in the prevention of chemotherapy-induced nausea and vomiting.
Palonosetron (Aloxi)
Palonosetron is a selective 5-HT3 receptor antagonist with a long half-life (40 h). It is indicated for the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of chemotherapy. It blocks 5-HT3 receptors peripherally and centrally in the chemoreceptor trigger zone.
Dexamethasone
Dexamethasone is a synthetic adrenocortical steroid with multiple indications. It is widely used in prevention of nausea and vomiting caused by highly emetogenic agents (eg, cisplatin) in combination with serotonin receptor antagonists.
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Non–small cell lung cancer. Symptoms and signs of lung cancer.
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Non–small cell lung cancer. Diagnostic approach for possible lung cancer.
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Staging workup for non–small cell lung cancer.
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Treatment recommendations and future research directions in the management of non–small cell lung cancer.
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Non–small cell lung cancer. Performance status scales for patients with cancer.
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Non–small cell lung cancer. Prognostic factors for lung cancer.
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Non–small cell lung cancer. Bronchoscopy. A large central lesion was diagnosed as non–small cell carcinoma.
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Non–small cell lung cancer. Left pleural effusion and volume loss secondary to non–small cell carcinoma of the left lower lobe. The pleural effusion was sampled and found to be malignant; therefore, the lesion is inoperable.
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Non–small cell lung cancer. Left upper collapse is almost always secondary to endobronchial bronchogenic carcinoma.
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Non–small cell lung cancer. Complete left lung collapse secondary to bronchogenic carcinoma of left mainstem bronchus.
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Non–small cell lung cancer. A cavitating right lower lobe squamous cell carcinoma.
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Non–small cell lung cancer. CT scan shows cavitation and air-fluid level.
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Non–small cell lung cancer. Patient has right lower lobe opacity. This is not well circumscribed and was found to be a squamous cell carcinoma.
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Lung cancer, small cell. Contrast-enhanced CT scan of the chest shows a large left lung and a hilar mass, with invasion of the left pulmonary artery.
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Lung cancer, small cell. Coronal positron emission tomogram shows abnormal areas of increased metabolic activity in the left hilar and left adrenal regions consistent with a hilar tumor with left adrenal metastasis.
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Lung cancer, small cell. Whole-body nuclear medicine bone scanning with anterior and posterior images reveal multiple abnormal areas of increased radiotracer activity in the pelvis, spine, ribs, and left scapula. These findings are consistent with bony metastatic disease. The bones are commonly affected in patients with small-cell lung cancer.
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Lung squamous carcinoma 4x: low power magnification of moderately differentiated squamous cell carcinoma showing irregular nests of tumor cells with focal areas of keratinization (pink-orange areas).
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Lung squamous carcinoma 20x: higher power magnification of moderately differentiated squamous cell carcinoma showing focal areas of keratinization (pink-orange areas) just to the right of center.
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Lung adenocarcinoma 4x: low power magnification of moderately differentiated adenocarcinoma showing rounded nests of pale staining tumor cells with gland lumina within some of the clusters.
Tables
Organization |
Criteria set |
American Cancer Society (2023) |
• Asymptomatic • Age 50 to 80 years • Currently smoke or formerly smoked • ≥20 pack-year smoking history |
CHEST (American College of Chest Physicians)(2021) |
• Asymptomatic • Age 55 to 77 years with ≥30 pack-year smoking history or age 50-80 years with ≥20 pack-year smoking history • Currently smoke or quit within the past 15 years • Do not meet other criteria, but clinical risk prediction calculations/life expectancy estimates/life-year gained calculations suggest high net benefit from screening |
National Comprehensive Cancer Network (2023) |
• Age ≥50 y • ≥20 pack-year history of smoking cigarettes • Use of risk calculators may identify additional candidates for screening |
U.S. Preventive Services Task Force (2021) |
• Age 50 to 80 years • 20 pack-year smoking history • Currently smoke or have quit within the past 15 years • Do not have a health problem that substantially limits life expectancy or the ability or willingness to have curative lung surgery. |
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- Overview
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- Approach Considerations
- Laboratory Studies
- Chest Radiography
- Computed Tomography
- Magnetic Resonance Imaging
- Bone Scintigraphy
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- Sputum Cytologic Studies
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- PD-1/PD-L1 Inhibitors
- Anti-CLTA4 Antibodies
- Antineoplastics, EGFR Inhibitor
- Antineoplastics, Anti-HER2
- Antineoplastics, BRAF Kinase Inhibitors
- Antineoplastics, Tyrosine Kinase Inhibitors
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- Antineoplastics, KRAS Inhibitors
- Antineoplastics, Monoclonal Antibodies
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