Lung cancer

Case scenario

Mrs Ma, aged 60, presents with a prescription for osimertinib 80 mg once daily. It is a new medicine for her. She has a history of metastatic adenocarcinoma NSCLC with right-lung primary and bone metastasis. Mrs Ma returns to the pharmacy 2 weeks later complaining of a rash and tenderness to her arms. On examination, the rash looks pustular and erythematous and only extends to her right forearm.  Mrs Ma denies any other rashes on her body or recent changes to her medicines or creams/body washes. 

Learning objectives After successful completion of this CPD activity, pharmacists should be able to: Describe the management options for lung cancer Describe how genetics can affect treatment choice Discuss the adverse effects of lung cancer treatments Describe the mechanism of action of medicines for lung cancer. Competency addressed: 1.1, 1.4, 2.1. 2.2, 3.1, 3.2. 3.3 3.5

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Introduction

Lung cancer is the most common cause of cancer-related death both worldwide and in Australia.^1,2 Lung cancer is the fifth most diagnosed cancer in Australia, with the highest mortality rate and a 5-year survival rate of around 18%.^1,2 There are two major subdivisions of lung cancer: small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC).^3–5 

NSCLC accounts for approximately 85% of all lung cancers, with the remaining being SCLC.^3–5 NSCLC arises from the epithelial cells of the lung situated within the central bronchi to terminal alveoli. The most common histologies are squamous cell carcinoma (30%), adenocarcinoma (30–40%) and large cell carcinoma (10–15%).^3–5 Squamous cell carcinoma starts near a central bronchus, while adenocarcinoma and bronchioalveolar carcinoma usually originate from peripheral lung tissue.^3–5 SCLC arises in peribronchial locations and tends to infiltrate the bronchial submucosa.^3–5

Aetiology and pathophysiology

Risk factors for lung cancer include^3–5:

• increasing age
• history of or current tobacco use
• exposure to cancer-causing substances (e.g. second-hand smoke)
• occupational exposure (e.g. asbestos, arsenic, chromium, beryllium, nickel)
• prior radiation exposure 
• air pollution
• family history
• Human immunodeficiency virus (HIV) infection
• beta carotene supplements in heavy smokers.

Although NSCLCs are associated with cigarette smoking, adenocarcinomas can be found in patients who have never smoked.^3–5 Smokers have on average a 10-fold higher risk of developing lung cancer than lifetime non-smokers.^3–5

Signs and symptoms

The most common symptoms at presentation include^3–5:

• worsening cough
• dyspnoea
• hoarseness
• chest pain
• haemoptysis
• malaise
• weight loss.
  

In SCLC, infrequently patients may present with signs and symptoms of one of the following paraneoplastic syndromes due to various peptide hormone productions^3–5:

• inappropriate antidiuretic hormone secretion
• Cushing syndrome from secretion of adrenocorticotrophic hormone
• paraneoplastic cerebellar degeneration
• Lambert-Eaton myasthenia syndrome.

Diagnosis

At initial presentation, a thorough history is required, taking note of^3–5:

• history of presenting complaint and symptoms
• past medical and medication history and allergies
• social history: occupational history (exposure to asbestos/radon), smoking (pack years)
• family history
• functional status.

Investigations to aid diagnosis and staging^3–5:

• routine blood test
• chest x-ray – investigate masses/rule out infections
• computer tomography (CT) scan, including head, chest, abdomen and pelvis
• positron emission tomography (PET) or magnetic resonance imaging (MRI) to investigate for metastases
• endobronchial ultrasound (EBUS) bronchoscopy or mediastinoscopy to determine histopathology
• respiratory function test (RFT)
• molecular testing – EGFR, ALK, ROS1 and BRAF testing
• tumour expression of PD-L1.

Staging

SCLC is defined by the spread of the cancer. Cancer that has spread beyond the supraclavicular areas is classified as extensive stage disease (ED), while cancer that has not spread is called limited stage disease (LD).⁶

The staging of NSCLC uses the American Joint Committee on Cancer (AJCC) TNM system, which stages cancer using these three key criteria⁷:

• size and extent of main tumour (T)
• spread to nearby lymph nodes (N)
• the spread of cancer to distant sites: metastasis (M).

Screening and prevention

In July 2021 the Australian Government announced a $6.9 million budget to commence early scoping of a potential national lung cancer screening program to increase early diagnosis and survivorship of lung cancer.⁸ The screening program will target high-risk individuals by conducting 2-yearly low-dose computed tomography (LDCT) scans in these individuals.⁸

Primary prevention is still one of the most important strategies for reducing the burden of lung cancer in Australia. As primary healthcare professionals, pharmacists are integral in providing education and support for smoking cessation, preventing smoking uptake and providing counselling on minimising our patients’ exposure to second-hand tobacco smoke.

Smoking cessation

The pharmacist can play a major role in guiding patients through smoking cessation. Guidelines for smoking cessation are widely accessible and include the PSA’s counselling guideline for common aliments – smoking cessation.⁹ When assessing a patient, it is important to gather patient information, including medical history, current medications, readiness to quit, nicotine dependence and previous attempts to quit.

The PSA guideline outlines how to assess nicotine dependence and situations where patients may require referral, such as history of cardiovascular disease.⁹ When developing a quit strategy for patients, a combination of behavioural and medicinal interventions should be used. Patients should be provided with verbal and written information on the use of smoking cessation products and referred to Quitline for additional support packs and telephone counselling.⁹ It is important to consider the impact that smoking cessation may have on other medicines, as tobacco smoking induces CYP1A2 metabolising enzymes. As a result, smoking cessation can increase the levels of drugs metabolised by this enzyme.⁹ 

Management of lung cancer

Management of lung cancer is multimodal and includes surgery, radiation therapy, chemotherapy and targeted therapy. These therapies can be used either alone or in combination, depending on the type of lung cancer, stage of lung cancer, molecular mutations, and the patient’s performance status. 

These decisions are often made by multidisciplinary teams to help assess all aspects of the patient’s condition.^3,11

Surgery 

Patients with early-stage NSCLC disease have the best chance of cure if surgery is undertaken to remove the primary tumour.³ Surgery also allows for further testing to define the stage of cancer, and therefore guides the ongoing treatment decisions. The common surgical procedures include segmentectomy (removal of part of a lobe), lobectomy (removal of one of the lobes) or pneumonectomy (removal of part or all of lung).¹² The type of surgery is determined by the extent of disease and the cardiopulmonary reserve of the patient.¹¹

Radiation therapy 

While not always a first-line option, radiation therapy has a potential role in all stages of NSCLC, as either definitive (intention of cure) or palliative therapy (end-of-life comforting therapy). 

Radiation therapy is generally used in early-stage NSCLC in combination with chemotherapy as definitive therapy and in advanced stage NSCLC as palliative therapy.^11,12

Pharmacotherapy 

Recent advances in pharmaceutics have increased the availability of medicines to treat NSCLC. As a result, a range of targeted therapies and chemotherapy are used in the management of NSCLC. New therapies such as targeted mutation therapy have shown increased median survivals of around 25 months.³

Targeted therapies – tyrosine kinase inhibitors (TKIs)

NSCLC consists of molecular subtypes identified by genetic aberrations, which allows for use of targeted therapy. Targeted therapies produce higher response rates than immunotherapy in metastatic NSCLC, and patients should receive these agents first-line where indicated.¹³

TKIs are small molecule inhibitors which inhibit specific tyrosine kinases that are abnormally activated in some types of cancer.¹⁴ Activation of tyrosine kinases can increase survival and proliferation of malignant cells and increase angiogenesis, invasiveness, and metastatic potential of tumours.¹⁴ TKIs can target tumours harbouring targetable driver mutations.

Epidermal growth factor receptor (EGFR) tyrosine kinase Inhibitors

EGFR mutations cause uncontrolled cancer cell proliferation. EGFR has been shown to be over-expressed in more than 60% of NSCLC cases and is associated with a poor prognosis.¹⁵ 

EGFR TKIs inhibit EGFR-dependent tumour cell proliferation and can be further classified as³:

• First-generation EGFR TKIs – bind reversibly to the TKI domain.³
  • erlotinib
  • gefitinib
• Second-generation EGFR TKIs – bind irreversibly with greater affinity to EGFR TKI domain.³
  • afatinib (also inhibits human epidermal growth factor receptor 2 and 4 [HER2, HER4])
• Third-generation TKIs – inhibit mutant eGFR, including the T790M positive EGFR (mutation causing resistance to first-and second-generation EGFR TKIs).³
  • osimertinib.

EGFR TKIs are indicated as first-line treatment for advanced stage NSCLC in patients with evidence in tumour of an activating EGFR gene mutation.¹⁶ The EURTAC study demonstrated that erlotinib had better progression-free survival (PFS) of 9.4 months versus 5.2 months with conventional first-line chemotherapy.¹⁶ Afatinib and osimertinib are indicated and PBS-listed for first-line treatment of Stage IIIB (locally advanced) or Stage IV (metastatic) NSCLC. The use of first-generation eGFR TKIs, erlotinib and gefitinib, is less favoured due to the availability of superior alternatives.²³ Osimertinib is also available on the PBS as second-line EGFR TKI therapy for patients who have progressed on prior EGFR TKI therapy and have evidence of EGFR T790M mutation in tumour material. 

Adverse effects of EGFR TKIs

As this is an emerging therapy, pharmacists should be aware of potential adverse effects of these agents. 

Outlined below are some of the common adverse effects for osimertinib (EGFR TKI) and incidences of each adverse effect²⁶: 

• diarrhoea (42%, severe 1%)
• acneiform rash (papulopustular rash), drug eruption, folliculitis, rash erythematous and maculopapular rash (41%, severe <1%)
• dry skin (31%)
• fatigue (14%, severe <1%)
• dry skin (31%)
• nail effects/paronychia (17–25%)
• QT interval prolongation (3–4%, severe <1%).

Further information on side effects and management can be found in eviQ under individual agent treatment protocols.²³

Pharmacists play a key role in management of EGFR inhibitor skin reactions. EGFR TKIs commonly cause skin reactions which present as a papulopustular rash, usually on the face and upper body, within the first 2–4 weeks of treatment.¹⁴ This could also present as itch, dry skin, paronychia, nail disorders and abnormal hair growth. It is important to note that this adverse effect occurs because of direct EGFR inhibition, and not as an allergic reaction to the therapy.²³

These reactions are treated with topical corticosteroids (hydrocortisone 1% cream) and patients may be started on a tetracycline such as doxycycline. Pre-emptive prophylactic doxycycline may be used with initiation of EGFR TKI at the discretion of the prescriber.²³ It is important to provide advice to patients on general measures to reduce skin reactions, including twice daily application of moisturiser and the use of sunscreen before going outdoors, as rash may be more severe in areas of skin exposed to sunlight.^14,23 Patients should be advised to report within 24 hours any skin changes such as rash and itch to their oncologist.

Drug interactions – osimertinib

Osimertinib is metabolised by CYP3A4 and strong inducers of this metabolising enzyme such as carbamazepine, phenytoin, rifampicin and St John’s wort may decrease exposure of osimertinib. These drugs should be avoided, but if that is not possible the dose of osimertinib should be doubled.

Osimertinib is an inhibitor of P-gp, and drugs metabolised by P-gp with a narrow therapeutic index (e.g. digoxin and dabigatran) should be monitored for signs of increased exposure. 

Anaplastic lymphoma kinase (ALK) fusion inhibitors

ALK gene mutation occurs in 2–7% of NSCLC resulting in constitutive activity and oncogenesis.^3,5 Crizotinib is a first-generation ALK TKI which has activity against ALK mutations.¹⁵ It is also important to note that crizotinib has other molecular targets that are significant in NSCLC, such as the c-ROS oncogene 1 (ROS-1) and has recently also been approved for treatment of patients with evidence of ROS1 gene rearrangement in tumour material in Stage IIIB (locally advanced) or Stage IV (metastatic) NSCLC.²³ 

Second-generation ALK inhibitors target ALK mutations with higher affinity and include ceritinib, alectinib and brigatinib. These are preferred agents for treatment of ALK positive Stage IIIB (locally advanced) or Stage IV (metastatic) NSCLC.²³ Lorlatinib is a third-generation ALK TKI that was approved in November 2018 for patients who have progressed on crizotinib and another ALK inhibitor or after progression using alectinib or ceritinib as a first-line ALK inhibitor.³ This was based on the study by Solomon et al showing overall response rate (ORR) of 48% and median response rate of 12.5 months with lorlatinib in patients who previously received one or more ALK inhibitors.³

Emerging molecular targets

ROS, BRAF, RET, MET, NTRK and KRAS G12C mutations are other mutations that may initiate and maintain the growth of cancer cells. These gene mutations may be tested for in NSCLC due to emerging new TKIs being developed and approved for use in Australia that target these mutations.  

Targeted therapy – monoclonal antibodies 

Vascular endothelial growth factor (VEGF) receptor inhibitors 

Bevacizumab is a monoclonal antibody (MAB) that targets the VEGF, inhibiting the formation of new blood vessels and reducing vascularisation and growth of tumours.¹⁴ Study E4599 (bevacizumab + carboplatin + paclitaxel vs carboplatin + paclitaxel) showed that the addition of bevacizumab resulted in a statistically significant improvement in overall survival and PFS.¹⁷ Consequently, bevacizumab is indicated for advanced or metastatic NSCLC in combination with carboplatin and paclitaxel and for continuing treatment, as monotherapy in a patient who does not have progressive disease.¹¹

Immunotherapy PD1 and PDL1 inhibitors 

The immune system is capable of anticancer activity; however, immune checkpoints or ‘brakes’ generated from the tumour can suppress the immune system’s activity.³ Immune checkpoint inhibitors release the ‘brakes’ of the immune system, allowing for full activity against the tumour.³ Pharmaceutical agents execute this through inhibition of T-cell antigen 4 (CTLA-4), program death ligand 1 (PDL-1) and its receptor (PD-1).¹⁴ Pembrolizumab, nivolumab (PD1 inhibitors), atezolizumab, and durvalumab (PDL-1 inhibitors) are immune checkpoint inhibitors approved for use in NSCLC. These agents may be used according to PBS restrictions for advanced stage disease in combination with chemotherapy, for patients with no targetable mutations, advanced stage disease following progression of first-line maintenance therapy for patients with locally advanced, un-resectable disease.^11,12

The use of these agents in these settings is supported by several clinical trials. The IMpower150 trial, compared combination atezolizumab, bevacizumab, carboplatin and paclitaxel (ABCP) versus bevacizumab plus chemotherapy as first-line therapy.¹⁹ This study showed improved median overall survival in the ABCP arm compared to the bevacizumab
plus chemotherapy arm (19.2 months versus 14.7 months).¹⁹

Adverse effects of PD1 and PDL1 Inhibitors

As immunotherapy boosts the immune response, an adverse effect of this may be over-stimulation of the immune system resulting in immune-related adverse events (irAE). These present as a range of autoimmune toxicities affecting any body system. Reactions may affect any organ system, including the liver, kidneys, skin (rash), endocrine (hypo- or hyperthyroidism), lungs (pneumonitis) and gastrointestinal tract (diarrhoea and colitis). Early identification and swift management are key in avoiding life-threatening severity. 

Management of irAE requires referral to the patient’s medical oncologist without delay and will generally include treatment with corticosteroids and holding or permanently stopping the product depending on the grade of reaction.¹⁴ Further information on signs and symptoms of irAE can be found in eviQ.²³

Chemotherapy NSCLC

Chemotherapy in NSCLC generally includes the use of a platinum-based drug (carboplatin or cisplatin) in combination with another agent such as etoposide, pemetrexed, paclitaxel, gemcitabine or docetaxel.¹² The role of chemotherapy in NSCLC varies significantly according to the stage of cancer and the ability to resect the cancer. To summarise, chemotherapy is generally used post- surgery in early-stage disease in combination with radiation for curative intent or in advanced-stage disease for patients without targetable mutations to increase survival and improve quality of life. Concurrent radiation and chemotherapy is more efficacious than sequential chemoradiation but increases the risk of adverse effects, particularly esophagitis.¹¹

Chemotherapy SCLC

Patients diagnosed with SCLC often have extensive disease at the time of diagnosis.

As a result, the goal of treatment is the prolongation of survival and palliation of symptoms.¹² In extensive disease, where patients are appropriate for chemotherapy, the standard regime is a platinum drug plus etoposide for 4­–6 cycles in combination with radiation. These patients may also receive prophylactic cranial irradiation if disease responds well to chemotherapy.²⁰ Patients who present with limited stage SCLC
may be managed with concurrent chemotherapy and thoracic irradiation.¹²

Palliative care

The aim of palliative care is to improve the quality of life by reducing symptoms
of cancer and slowing the spread of the cancer without the goal of curing the disease. These symptoms, which directly impact quality of life, include dyspnoea, cough, anorexia and fatigue.³ The involvement of a palliative care team can assist patients with advanced lung cancer in managing the symptoms as well as pain, nausea and end-of-life decisions.²¹

Management of adverse effects of lung cancer treatment

Each mode of therapy has significant adverse effects which are amplified by the use of these modalities in combination.  Supportive care medications aim to prevent and manage these adverse effects. Pharmacists can play a role in the recognition of adverse effects of chemotherapy and immunotherapy and in ensuring appropriate referral and management. Patients experiencing adverse effects should be referred to their oncologist for further assessment.¹⁴

Patient resources 

Patients undergoing treatment at a medical oncology centre are often supported by a team of doctors, nurses and allied health professionals who are willing to help. If patients have concerns regarding their treatment or adverse effects, they should be referred urgently
to their treatment centre for direction.

Useful resources include: 

• eviQ-Cancer Institute NSW (www.eviq.org.au)
• Cancer Council (www.cancer.org.au)
• Lung Foundation Australia (lungfoundation.com.au)
• MacMillan Cancer Support UK (www.macmillan.org.uk).

Knowledge to practice 

The safe delivery of cancer treatment requires a multidisciplinary approach, and often care is shared between hospital specialists, hospital cancer care pharmacists, general practitioners and pharmacists.²² Communication between this team is key in ensuring best outcomes for the patient. 

The accessibility of pharmacists allows them to play a key role in the care of patients with lung cancer. One of the most significant roles is that of encouraging smoking cessation. However, the emergence of oral therapies has resulted in the accessibility of cancer care medications in the community pharmacy. These medications require close clinical review for appropriateness, including screening for potential drug interactions and interactions with current medications, as well as complementary and alternative medicines. Patients commenced on these oral anti-cancer therapies in the community should be provided with detailed counselling and written information of treatment regime and adverse-effect management (accessible via eviQ).²³ Patients receiving treatment from a cancer care centre may also present to community pharmacy, and therefore pharmacists can play a key role in early identification and management of adverse effects.

Case scenario continued You explain to Mrs Ma that the rash she has is common in people who take osimertinib and reassure her that prompt treatment with OTC hydrocortisone 1% cream and doxycycline will bring it under control. You emphasise that she should contact her oncologist without delay for assessment and prescription of the antibiotic so that the rash does not become worse.

Resources

• Guidelines for pharmacists providing smoking cessation support: 
  https://my.psa.org.au/s/article/Guidelines-for-pharmacists-providing-smoking-cessation-support
• APF non-prescription medicine treatment guideline – Nicotine replacement therapy for smoking cessation: https://apf.psa.org.au/non-prescription-medicine-guides/nicotine-replacement-therapy-smoking-cessation/nicotine-replacement

References

1. Lung Foundation Australia. Lung cancer in Australia. 2018. At: https://lungfoundation.com.au/wp-content/uploads/2018/09/Infographic-Lung-cancer-Oct2018.pdf
2. Australian Government Cancer Australia. Lung Cancer in Australia Statistics. At: www.canceraustralia.gov.au/affected-cancer/cancer-types/lung-cancer/lung-cancer-australia-statistics
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4. NIH National Cancer Institute. Non-small cell lung cancer treatment (PDQ®) – health professional version. At: www.cancer.gov/types/lung/hp/non-small-cell-lung-treatment-pdq
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8. Australian Government Cancer Australia. Lung cancer screening. 2021. At: www.canceraustralia.gov.au/about-us/lung-cancer-screening
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10. The Royal Australian College of General Practitioners. Supporting smoking cessation: A guide for health professionals. 2nd edn. East Melbourne: RACGP; 2019.
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12. Cancer Council Australia Lung Cancer Guidelines Working Party. Clinical practice guidelines for the treatment of lung cancer. 2017. Sydney: Cancer Council Australia. At: https://wiki.cancer.org.au/australia/Guidelines:Lung_cancer
13. Mazieres J, Drilon A, Lusque A, et al. Immune checkpoint inhibitors for patients with advanced lung cancer and oncogenic driver alterations: results from the IMMUNOTARGET registry. Ann Oncol 2019;30(8):1321–8.
14. Rossi S, ed. Australian medicines handbook. Adelaide: Australian Medicines Handbook; 2020.
15. Hasovits C, Pavlakis. EGFR-targeted therapy and resistance. Cancer Forum 2013;27:(2).
16. Rosell R, Carcereny E, Gervais R, et al. Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial. Lancet Oncol 2012;13(3):239–46.
17. Sandler A, Yi J, Dahlberg S, et al. Treatment outcomes by tumor histology in Eastern Cooperative Group Study E4599 of bevacizumab with paclitaxel/carboplatin for advanced non-small cell lung cancer. J Thorac Oncol 2010;5(9):1416–23.
18. Langer CJ, Gadgeel SM, Borghaei H, et al. Carboplatin and pemetrexed with or without pembrolizumab for advanced, non-squamous non-small-cell lung cancer: a randomised, phase 2 cohort of the open-label KEYNOTE-021 study. Lancet Oncol 2016;17(11):1497–1508.
19. Reck M, Mok TSK, Nishio M, et al. Atezolizumab plus bevacizumab and chemotherapy in non-small-cell lung cancer (IMpower150): key subgroup analyses of patients with EGFR mutations or baseline liver metastases in a randomised, open-label phase 3 trial. Lancet Respir Med 2019;7(5):387–401.
20. National Comprehensive Cancer Network. NCCN clinical practice guidelines in oncology. Small cell lung cancer. Version 2.2014. 2014; At: www.nccn.org/professionals/physician_gls/pdf/sclc.pdf
21. Cancer Council Australia. Types of cancer. Lung cancer. 2020. At: www.cancer.org.au/cancer-information/types-of-cancer/lung-cancer
22. Carrington C. Safe use of oral cytotoxic medicines. Aust Prescr 2013;36:9–12 At: www.nps.org.au/australian-prescriber/articles/safe-use-of-oral-cytotoxic-medicines
23. Cancer Institute NSW. eviQ Cancer Treatments Online 2017. At: www.eviq.org.au
24. Haanen, JB, F Carbonnel, C Robert, et al. Management of toxicities from immunotherapy: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol 2017;28(suppl_4):iv119–iv142.
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DANIELLE WOOLLEY BPharm (Hons) is pharmacist team leader at Royal Brisbane and Women’s Hospital and has practised in cancer care for the past 4 years.

VIVIAN DAY BPharm (Hons), GradDip (Clin Pharm) is a senior cancer care pharmacist at the Royal Brisbane and Women’s Hospital. She has been a pharmacist for 10 years, four of them in oncology, and is pursuing a postgraduate master’s degree in oncology.