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Bring the potential of ROZLYTREK® to life
Learn how ROZLYTREK can benefit your patients
Learn how ROZLYTREK can benefit your patients
Graham, a 55-year-old man, presented to his GP with marked shortness of breath which was restricting his daily activities (ECOG PS 2)
Many different genetic alterations have been found in lung cancer cells.1 Molecular testing is recommended to characterise the type of lung cancer and identify targeted treatment options.2
Initial treatment:
Although these targets represent the most common forms of lung cancer, several other molecular targets such as NTRK gene fusions are known to present somatic variants with therapeutic potential3,4
Testing with FISH/IHC did not reveal any clinically-relevant gene alterations
NGS has the high sensitivity, accuracy and throughput necessary to test for key therapeutic targets including all gene fusions.2,5–10 Gene fusions have been reported in approximately 20% of all cancers and ESMO guidelines recommend testing all patients with metastatic NSCLC for ROS1 gene fusion.11,12
Furthermore, NTRK is an evolving biomarker in NSCLC.12 NTRK1–3 are rare oncogenic drivers occurring at low prevalence (< 1%) in a variety of tumours including NSCLC – typically in adenocarcinomas and never-smokers.12
NGS testing results:
NGS identified NTRK1-SQSTM1 fusion. Approximately 0.1–1% of NSCLC patients have NTRK gene fusions.13
Graham, a 55-year-old man, presented to his GP with marked shortness of breath which was restricting his daily activities (ECOG PS 2)
Question 2:
Knowing the patient has CNS disease with an NTRK gene fusion, what treatment would you choose?
Treatment options for advanced/metastatic NSCLC include surgery, chemotherapy, radiation therapy, immunotherapy and targeted therapy.3,4
A TRK inhibitor with proven CNS activity in patients with NTRK fusion+ solid tumours, such as ROZLYTREK, may be the most appropriate choice for this patient.15,16
ROZLYTREK has shown activity in NTRK fusion+ NSCLC.3 It is a potent, selective TRK inhibitor demonstrating antitumour activity within the CNS.15 ROZLYTREK crosses the blood–brain barrier to deliver a clinically meaningful response in patients with NTRK gene fusions and CNS metastasis.15,16
ROZLYTREK is a potent, selective TRK inhibitor demonstrating antitumour activity within the CNS.15 ROZLYTREK crosses the blood–brain barrier to deliver a clinically meaningful response in patients with NTRK gene fusions and CNS metastasis.15,16
Heidi is a 25-year-old primary teacher who has been experiencing bloody discharge from her left nipple for around 6 months
Question 1:
Would you perform molecular testing at this stage?
There is no clear consensus on the treatment of secretory breast cancer, but surgery seems to be the primary treatment currently.17
Surgery may be combined with chemotherapy and radiotherapy.17
Many different genetic alterations have been found in breast cancer cells.18 Molecular testing is recommended to characterise the type of breast cancer and identify targeted treatment options.19
Testing with FISH/IHC did not reveal any clinically-relevant gene alterations
Targeted therapies including TRK inhibitors have shown activity in NTRK fusion+ breast cancers15
NGS testing results:
Molecular testing identified ETV6-NTRK3 gene fusion which was classified as a secretory breast carcinoma.
Secretory breast carcinoma is a rare condition that accounts for < 0.1% of all cases of invasive breast cancer.22
NTRK fusions are found in more than 25 different cancers and are highly prevalent in secretory breast carcinoma (> 90%)23
Molecular testing is recommended to characterise the type of breast cancer and identify targeted treatment options.19
NGS has the high sensitivity, accuracy and throughput necessary to test for key therapeutic targets, including all gene fusions.18,24
Heidi is a 25-year-old primary teacher who has been experiencing bloody discharge from her left nipple for around 6 months
Question 2:
Knowing the patient has CNS disease with an NTRK gene fusion, what treatment would you choose?
There is currently no consensus regarding treatment for secretory breast carcinoma, and treatment options may depend on the person's age and the size of the tumour.17 Options may include surgery to remove the tumour or mastectomy, surgery to also remove nearby lymph nodes, radiotherapy, and chemotherapy.17
A TRK inhibitor for patients with NTRK fusion+ secretory breast carcinoma, such as ROZLYTREK, may be the most appropriate choice for this patient.15
ROZLYTREK is a potent, selective TRK inhibitor, and delivers a clinically meaningful response in patients with NTRK gene fusions.15
ROZLYTREK is a potent, selective TRK inhibitor, and delivers a clinically meaningful response in patients with NTRK gene fusions.15
Marcus is a 48-year-old engineer who presented to his doctor with a palpable and painful lump on the left thigh
After instruction of an MRI and biopsy, the results suggested an undifferentiated sarcoma with a 6 cm resectable tumour – histologic grade G1, stage IB
Question 1:
Would you perform molecular testing at this stage?
Initial treatment:
Surgery (wide excision with negative margins (R0) when possible) is the standard of care for sarcoma, associated with radiation therapy and chemotherapy.26 High-risk patients tend to relapse within 2–3 years.26
Many different genetic alterations have been found in sarcoma cells.27 Broad molecular testing to further characterise the tumour profile could support additional treatment options.28
Specific driver molecular abnormalities have been identified in up to 40% of soft tissue sarcomas,29 with < 5% of sarcoma cases presenting with NTRK fusions.30
Standard diagnosis of sarcoma consists of imaging assessments (MRI, CT or PET) and tissue biopsy to determine histological type, stage and resectability of the tumour.26,31
Molecular testing is recommended to characterise the type of sarcoma and identify targeted treatment options, with immunohistochemistry being a valuable screening tool.32
Targeted agents such as tyrosine kinase inhibitors are becoming important treatment options for soft tissue sarcomas.33
NGS testing results:
Molecular testing identified an TPM3-NTRK1 gene fusion as soft tissue sarcoma.
p53, RB, PI3K and IDH gene mutations are the most prevalent mutations identified in sarcomas.34
However, NTRK gene fusions are also oncogenic drivers in a variety of tumour types, including adult and paediatric sarcomas.32
Molecular testing is recommended to characterise the type of sarcoma and identify targeted treatment options, and immunohistochemistry is a valuable screening tool.32
Marcus is a 48-year-old engineer who presented to his doctor with a palpable and painful lump on the left thigh
After instruction of an MRI and biopsy, the results suggested an undifferentiated sarcoma with a 6cm resectable tumour – histologic grade G1, stage IB
Question 2:
Knowing the patient has CNS disease with an NTRK gene fusion, what treatment would you choose?
Chemotherapy, radiotherapy and, if possible, resection of metastases are the standard treatment options for advanced/metastatic soft tissue sarcoma.26
However, targeted agents such as tyrosine kinase inhibitors are becoming important treatment options for soft tissue sarcomas.33
A TRK inhibitor also with proven CNS activity in patients with NTRK fusion+ solid tumours, such as ROZLYTREK, may be the most appropriate choice for this patient.15
ROZLYTREK is a potent, selective TRK inhibitor demonstrating antitumour activity within the CNS.16 ROZLYTREK crosses the blood-brain barrier to deliver a clinically meaningful response in patients with NTRK gene fusions and CNS metastasis.15,16
TRK inhibitors provide effective treatment options for patients with sarcomas harboring NTRK gene fusions.32
ROZLYTREK is a potent, selective TRK inhibitor demonstrating antitumour activity within the CNS. 15,16 ROZLYTREK crosses the blood-brain barrier to deliver a clinically meaningful response in patients with NTRK gene fusions and CNS metastasis.15,16
This medicinal product is subject to additional monitoring. This will allow quick identification of new safety information. Healthcare professionals are asked to report any suspected adverse reactions. See section 4.8 of the SmPC for details on how to report adverse reactions.
Footnotes
ALK, anaplastic lymphoma kinase; BRCA, BReast CAncer gene; CD31/34, cluster of differentiation 31/34; CNS, central nervous system; CT, computed tomography; ECOG PS, Eastern Cooperative Oncology Group performance status; EGFR, epidermal growth factor receptor; ER, oestrogen receptor; FISH, fluorescence in situ hybridisation; HER, human epidermal growth factor receptor; HER2, human epidermal growth factor receptor 2; IDH, isocitrate dehydrogenase mutation; IHC, immunohistochemistry; MRI, magnetic resonance imaging; NGS, next-generation sequencing; NSCLC, non-small cell lung cancer; NTRK, neurotrophic tyrosine receptor kinase; PD-L1, programmed death-ligand 1; PET, positron emission tomography; PI3K, phosphoinositide 3-kinase; PR, progesterone receptor; RB, retinoblastoma; ROS1, c-ros oncogene 1; S-100, dysregulated S100 expression is a common feature in several human cancers; SMA, smooth muscle actin; TPM3, tropomyosin 3; TRK, tropomyosin receptor kinase.
References