Clinical Trial Announcement

Total Page：16

File Type：pdf, Size：1020Kb

CLINICAL TRIAL ANNOUNCEMENT PHASE 2 TRIAL OF TESEVATINIB IN SUBJECTS WITH NSCLC and BRAIN or LEPTOMENINGEAL METASTASIS This study will enroll subjects with brain metastases (BM) or leptomeningeal metastases (LM) occurring while being treated with erlotinib or afatinib or gefitinib. For more information, contact the Neuro-Oncology The objective of this trial is to evaluate the clinical activity of tesevatinib in subjects Clinical Trial Team at: with non-small cell lung cancer (NSCLC), activating EGFR mutations, and BM or [email protected] LM. 310-829-8265 Clinical Trial Investigators Tesevatinib (formerly known as KD019) is an orally administered tyrosine kinase Achal S. Achrol, MD inhibitor that has been documented to inhibit multiple molecular drivers of tumor Garni Barkhoudarian, MD growth, including EGFR, HER2, Src, and VEGFR2. Daniel Kelly, MD Tesevatinib effectively penetrates into the brain and has levels in the choroid plex- Santosh Kesari, MD, PhD, us and meninges that are 10 times the plasma levels and may be an effective Steven O’Day, MD treatment for leptomeningeal metastases. Marlon Garzo Saria, PhD, RN Clinical Trial Team KEY Inclusion Criteria Najee Boucher, CRA [email protected] Cohort A: Brain Metastases 310-582-7460 History of NSCLC with EGFR mutation (either exon 19 deletion or L858R muta- Jaya Gill, RN, BSN tion). [email protected] Occurrence or progression of BM while receiving either erlotinib or afatinib or 310-582-7437 gefitinib. Annie Heng, RN, BSN At least one measurable BM by RECIST 1.1 criteria (≥ 10mm in longest diame- [email protected] ter). 310-582-7457 No clinically significant progression outside of the CNS on most recent EGFR Tiffany Juarez, PhD inhibitor therapy. [email protected] 310-449-5225 Cohort B: Leptomeningeal Metastases Anand Moses, CRA History of NSCLC with EGFR mutation (either exon 19 deletion or L858R muta- [email protected] tion). 310-582-7097 Occurrence or progression of LM while receiving either erlotinib or afatinib or Sponsor gefitinib. Presence of at least one CTCAE 4.03 symptom/sign of at least Grade 1 at- Kadmon Corporation, LLC tributed by the investigator to LM Diagnosis of LM by: Cytological evidence in CSF sample of LM due to NSCLC, and/or Findings on gadolinium-enhanced MRI No clinically significant progression outside of the CNS on most recent EGFR inhibitor therapy. .

Copy Link

Recommended publications

Deciphering Molecular Mechanisms and Prioritizing Therapeutic Targets in Cardio-Oncology
Figure 1. This is a pilot view to explore the potential of EpiGraphDB to inform us about proteins that are linked to the pathophysiology of cancer and cardiovascular disease (CVD). For each cancer type (pink diamonds), we searched for cancer related proteins (light blue circles) that interact with other proteins identified as protein quantitative trait loci (pQTLs) for CVD (red diamonds for pathologies, orange triangles for risk factors). These pQTLs can be acting in cis (solid lines) or trans-acting (dotted lines). Proteins can interact either directly, a protein-protein interaction (dotted blue edges), or through the participation in the same pathway (red parallel lines). Shared pathways are represented with blue hexagons. We also queried which of these proteins are targeted by existing drugs. We found that the cancer drug cetuximab (yellow circle) inhibits EGFR. Other potential drugs are depicted in light brown hexagonal meta-nodes that are detailed below. Deciphering molecular mechanisms and prioritizing therapeutic targets in cardio-oncology Pau Erola1,2, Benjamin Elsworth1,2, Yi Liu2, Valeriia Haberland2 and Tom R Gaunt1,2,3 1 CRUK Integrative Cancer Epidemiology Programme; 2 MRC Integrative Epidemiology Unit, University of Bristol; 3 The Alan Turing Institute Cancer and cardiovascular disease (CVD) make by far the immense What is EpiGraphDB? contribution to the totality of human disease burden, and although mortality EpiGraphDB is an analytical platform and graph database that aims to is declining the number of those living with the disease shows little address the necessity of innovative and scalable approaches to harness evidence of change (Bhatnagar et al., Heart, 2016).
[Show full text]
Therapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities
REVIEW www.jasn.org Therapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities Chelsea C. Estrada,1 Alejandro Maldonado,1 and Sandeep K. Mallipattu1,2 1Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York; and 2Renal Section, Northport Veterans Affairs Medical Center, Northport, New York ABSTRACT Inhibition of vascular endothelial growth factor A (VEGFA)/vascular endothelial with hypertension and proteinuria. Re- growth factor receptor 2 (VEGFR2) signaling is a common therapeutic strategy in ports describe histologic changes in the oncology, with new drugs continuously in development. In this review, we consider kidney primarily as glomerular endothe- the experimental and clinical evidence behind the diverse nephrotoxicities associ- lial injury with thrombotic microangiop- ated with the inhibition of this pathway. We also review the renal effects of VEGF athy (TMA).8 Nephrotic syndrome has inhibition’s mediation of key downstream signaling pathways, specifically MAPK/ also been observed,9 with the clinical ERK1/2, endothelial nitric oxide synthase, and mammalian target of rapamycin manifestations varying according to (mTOR). Direct VEGFA inhibition via antibody binding or VEGF trap (a soluble decoy mechanism and direct target of VEGF receptor) is associated with renal-specific thrombotic microangiopathy (TMA). Re- inhibition. ports also indicate that tyrosine kinase inhibition of the VEGF receptors is prefer- Current VEGF inhibitors can be clas- entially associated with glomerulopathies such as minimal change disease and FSGS. sifiedbytheirtargetofactioninthe Inhibition of the downstream pathway RAF/MAPK/ERK has largely been associated VEGFA-VEGFR2 pathway: drugs that with tubulointerstitial injury. Inhibition of mTOR is most commonly associated with bind to VEGFA, sequester VEGFA, in- albuminuria and podocyte injury, but has also been linked to renal-specificTMA.In hibit receptor tyrosine kinases (RTKs), all, we review the experimentally validated mechanisms by which VEGFA-VEGFR2 or inhibit downstream pathways.
[Show full text]
Leptomeningeal Metastases from Solid Tumors: Recent Advances in Diagnosis and Molecular Approaches
cancers Review Leptomeningeal Metastases from Solid Tumors: Recent Advances in Diagnosis and Molecular Approaches Alessia Pellerino 1,* , Priscilla K. Brastianos 2, Roberta Rudà 1,3 and Riccardo Soffietti 1 1 Department of Neuro-Oncology, University and City of Health and Science Hospital, 10126 Turin, Italy; [email protected] (R.R.); riccardo.soffi[email protected] (R.S.) 2 Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02115, USA; [email protected] 3 Department of Neurology, Castelfranco Veneto and Brain Tumor Board Treviso Hospital, 31100 Treviso, Italy * Correspondence: [email protected]; Tel.: +39-011-633-4904 Simple Summary: Leptomeningeal metastases are a devastating complication of solid tumors with poor survival, regardless of the type of treatments. The limited efficacy of targeted agents is due to the molecular divergence between leptomeningeal recurrences and primary site, as well as the presence of a heterogeneous blood-brain barrier and blood-tumor barrier that interfere with the penetration of drugs into the brain. The diagnosis of leptomeningeal metastases is achieved by neurological examination, and/or brain and spinal magnetic resonance, and/or a positive cerebrospinal fluid cytology. The presence of neoplastic cells in the cerebrospinal fluid examination is the gold-standard for the diagnosis of leptomeningeal metastases; however, novel techniques known as “liquid biopsy” aim to improve the sensitivity and specificity in detecting circulating neoplastic cells or DNA in the cerebrospinal fluid. Targeted therapies and immunotherapies have changed the natural history Citation: Pellerino, A.; Brastianos, of metastatic solid tumors, including lung, breast cancer, and melanoma. Targeting actionable P.K.; Rudà, R.; Soffietti, R.
[Show full text]
Cell-Cycle and DNA-Damage Response Pathway Is Involved In
Published OnlineFirst October 13, 2017; DOI: 10.1158/1078-0432.CCR-17-1582 Biology of Human Tumors Clinical Cancer Research Cell-Cycle and DNA-Damage Response Pathway Is Involved in Leptomeningeal Metastasis of Non–Small Cell Lung Cancer Yun Fan1, Xuehua Zhu2, Yan Xu3, Xuesong Lu4, Yanjun Xu1, Mengzhao Wang3, Haiyan Xu4, Jingyan Ding2, Xin Ye2, Luo Fang5, Zhiyu Huang5, Lei Gong5, Hongyang Lu1, Weimin Mao1, and Min Hu2 Abstract Purpose: Leptomeningeal metastasis (LM) is a detrimental risk. Intriguingly, low overlapping of somatic protein-changing complication of non–small cell lung cancer (NSCLC) and asso- variants was observed between paired CSF and primary lesions, ciated with poor prognosis. However, the underlying mechanisms exhibiting tumor heterogeneity and genetic divergence. Moreover, of the metastasis process are still poorly understood. genes with CSF-recurrent genomic alterations were predominant- Experimental Design: We performed next-generation panel ly involved in cell-cycle regulation and DNA-damage response sequencing of primary tumor tissue, cerebrospinal ﬂuid (CSF), (DDR), suggesting a role of the pathway in LM development. and matched normal controls from epidermal growth factor Conclusions: Our study has shed light on the genomic varia- receptor (EGFR) mutation-positive NSCLC patients with LM. tions of NSCLC-LM, demonstrated genetic heterogeneity and Results: The status of EGFR-activating mutations was highly divergence, uncovered involvement of cell-cycle and DDR path- concordant between primary tumor and CSF. PIK3CA aberrations way, and paved the way for potential therapeutic approaches to were high in these patients, implicating an association with LM this unmet medical need. Clin Cancer Res; 24(1); 209–16.
[Show full text]
Patent Application Publication ( 10 ) Pub . No . : US 2019 / 0192440 A1
US 20190192440A1 (19 ) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2019 /0192440 A1 LI (43 ) Pub . Date : Jun . 27 , 2019 ( 54 ) ORAL DRUG DOSAGE FORM COMPRISING Publication Classification DRUG IN THE FORM OF NANOPARTICLES (51 ) Int . CI. A61K 9 / 20 (2006 .01 ) ( 71 ) Applicant: Triastek , Inc. , Nanjing ( CN ) A61K 9 /00 ( 2006 . 01) A61K 31/ 192 ( 2006 .01 ) (72 ) Inventor : Xiaoling LI , Dublin , CA (US ) A61K 9 / 24 ( 2006 .01 ) ( 52 ) U . S . CI. ( 21 ) Appl. No. : 16 /289 ,499 CPC . .. .. A61K 9 /2031 (2013 . 01 ) ; A61K 9 /0065 ( 22 ) Filed : Feb . 28 , 2019 (2013 .01 ) ; A61K 9 / 209 ( 2013 .01 ) ; A61K 9 /2027 ( 2013 .01 ) ; A61K 31/ 192 ( 2013. 01 ) ; Related U . S . Application Data A61K 9 /2072 ( 2013 .01 ) (63 ) Continuation of application No. 16 /028 ,305 , filed on Jul. 5 , 2018 , now Pat . No . 10 , 258 ,575 , which is a (57 ) ABSTRACT continuation of application No . 15 / 173 ,596 , filed on The present disclosure provides a stable solid pharmaceuti Jun . 3 , 2016 . cal dosage form for oral administration . The dosage form (60 ) Provisional application No . 62 /313 ,092 , filed on Mar. includes a substrate that forms at least one compartment and 24 , 2016 , provisional application No . 62 / 296 , 087 , a drug content loaded into the compartment. The dosage filed on Feb . 17 , 2016 , provisional application No . form is so designed that the active pharmaceutical ingredient 62 / 170, 645 , filed on Jun . 3 , 2015 . of the drug content is released in a controlled manner. Patent Application Publication Jun . 27 , 2019 Sheet 1 of 20 US 2019 /0192440 A1 FIG .
[Show full text]
Kadmon Holdings, Inc. Annual Report 2018
Kadmon Holdings, Inc. Annual Report 2018 Form 10-K (NYSE:KDMN) Published: March 6th, 2018 PDF generated by stocklight.com UNITED STATES SECURITIES AND EXCHANGE COMMISSION Washington, D.C. 20549 _______________________________ FORM 10-K _______________________________ (Mark One) ☒ ANNUAL REPORT PURSUANT TO SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934 For the fiscal year ended December 31, 2017 or ☐ TRANSITION REPORT PURSUANT TO SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934 For transition period from to . Commission File Number: 001-37841 Kadmon Holdings, Inc. (Exact name of registrant as specified in its charter) _______________________________ Delaware 27‑3576929 (State or other jurisdiction of (I.R.S. Employer incorporation or organization) Identification No.) 450 East 29th Street, New York, 10016 NY (Zip Code) (Address of principal executive offices) (212) 308‑6000 (Registrant’s telephone number, including area code) Securities registered pursuant to Section 12(b) of the Act: Title of each class Name of exchange on which registered Common Stock, par value $0.001 per share The New York Stock Exchange Securities registered pursuant to Section 12(g) of the Act: None _______________________________ Indicate by check mark if the Registrant is a well-known seasoned issuer, as defined in Rule 405 of the Securities Act. YES ☐ NO ☒ Indicate by check mark if the Registrant is not required to file reports pursuant to Section 13 or 15(d) of the Act. YES ☐ NO ☒ Indicate by check mark whether the Registrant: (1) has filed all reports required to be filed by Section 13 or 15(d) of the Securities Exchange Act of 1934 during the preceding 12 months (or for such shorter period that the Registrant was required to file such reports), and (2) has been subject to such filing requirements for the past 90 days.
[Show full text]
Management of Her2+ Brain and Leptomeningeal Disease
Please note, these are the actual video-recorded proceedings from the live CME event and may include the use of trade names and other raw, unedited content. MANAGEMENT OF HER2+ BRAIN AND LEPTOMENINGEAL DISEASE Kathy D. Miller, M.D. Ballvé-Lantero Professor Indiana University Melvin and Bren Simon Cancer Center DISCLOSURES AbbVie Inc, Astellas Pharma Global Development Contracted Research Inc, Medivation Inc, a Pfizer Company, Merrimack Pharmaceuticals Inc, Novartis, Pfizer Inc Case presentation: Dr Brooks 69-year-old morbidly obese woman (350 pounds) with a history of DM • 2016: Metastatic ER/PR-negative, HER2- positive BC: 8-cm breast mass, 5-cm axillary mass, 3 liver lesions (9 cm, 7 cm and 2.5 cm) and 2 small lung lesions – Trastuzumab/pertuzumab/paclitaxel x 2 cycles • Mucositis, oral candida, diarrhea • Decreased paclitaxel dose - hypersensitivity reaction – Nab paclitaxel at 30% dose reduction à oral candida, umbilical candida, diarrhea, tachycardia – Currently on pertuzumab/trastuzumab and faring well Case presentation: Dr Hart 58-year-old woman • 2011: Metastatic ER/PR-positive, HER2- positive BC with symptomatic brain mets à surgical resection of brain lesion à XRT to brain à chemotherapy/trastuzumab à trastuzumab + AI • 2016: Lapatinib + capecitabine – Further resection of cerebellar lesions • 2017: Fulvestrant + lapatinib + capecitabine • Currently on fulvestrant + palbociclib + trastuzumab ROADMAP • Incidence • Guidelines for management • Systemic therapy • New directions BRAIN METASTASES IN BREAST CANCER Median Survival • Brain metastases ER-HER2+ 17.9 months common in breast TNBC 24% ER-HER2+ 31% ER+HER2+ 20.7 cancer months • Incidence and ER+HER2- 20% ER+HER2- 9.7 months outcome varies with ER+HER2+ 26% different breast TNBC cancer subtypes 6.4 months Brain Met Distribution n = 400 Sperduto, Int J Radiat Oncol Biol Phys.
[Show full text]
Targeted Therapies for Brain Metastases from Breast Cancer
International Journal of Molecular Sciences Review Targeted Therapies for Brain Metastases from Breast Cancer Vyshak Alva Venur and José Pablo Leone * Division of Hematology, Oncology, Blood and Bone Marrow Transplantation, Department of Internal Medicine, University of Iowa Hospitals and Clinics, Iowa City, IA 52242, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-319-356-7839 Academic Editor: Dario Marchetti Received: 24 July 2016; Accepted: 8 September 2016; Published: 13 September 2016 Abstract: The discovery of various driver pathways and targeted small molecule agents/antibodies have revolutionized the management of metastatic breast cancer. Currently, the major targets of clinical utility in breast cancer include the human epidermal growth factor receptor 2 (HER2) and epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF) receptor, mechanistic target of rapamycin (mTOR) pathway, and the cyclin-dependent kinase 4/6 (CDK-4/6) pathway. Brain metastasis, however, remains a thorn in the ﬂesh, leading to morbidity, neuro-cognitive decline, and interruptions in the management of systemic disease. Approximately 20%–30% of patients with metastatic breast cancer develop brain metastases. Surgery, whole brain radiation therapy, and stereotactic radiosurgery are the traditional treatment options for patients with brain metastases. The therapeutic paradigm is changing due to better understanding of the blood brain barrier and the advent of tyrosine kinase inhibitors and monoclonal antibodies. Several of these agents are in clinical practice and several others are in early stage clinical trials. In this article, we will review the common targetable pathways in the management of breast cancer patients with brain metastases, and the current state of the clinical development of drugs against these pathways.
[Show full text]
Supplementary Material For
Wang et al. Supplemental: Acquired resistance mutation in BRAF. Supplementary Material for: A secondary mutation in BRAF confers resistance to RAF inhibition in a BRAF V600E-mutant brain tumor Jiawan Wang, Zhan Yao, Philip Jonsson, Amy N. Allen, Alice Can Ran Qin, Sharmeen Uddin, Ira J. Dunkel, Mary Petriccione, Katia Manova, Sofia Haque, Marc K. Rosenblum, David J. Pisapia, Neal Rosen, Barry S. Taylor, Christine A. Pratilas Supplementary Figures ⚫ Supplementary Figure S1: Representative H&E, phospho-ERK and FISH images of pre-dabrafenib (3) and post-dabrafenib (4) tumors. ⚫ Supplementary Figure S2: WES analysis of copy number variation in pre- and post- dabrafenib tumors. ⚫ Supplementary Figure S3: Whole copy number profiles from WES of pre- and post- treatment tumors. ⚫ Supplementary Figure S4: Homology alignment of BRAF p. L514 with residues in other tyrosine kinases. ⚫ Supplementary Figure S5: Relative frequency of BRAF variant alleles in SK-BT-DR cells determined by individual clone sequencing. ⚫ Supplementary Figure S6: BRAF V600E/L514V reduces dabrafenib sensitivity in NIH- 3T3 cells, related to Figure 2. ⚫ Supplementary Figure S7: BRAF V600E/L514V confers biochemical resistance to dabrafenib over a time course, related to Figure 2G. ⚫ Supplementary Figure S8: Comparison of IC50, IC75 and IC90 of dabrafenib against A375 cells expressing BRAF V600E and BRAF V600E/L514V, related to Figure 2H. ⚫ Supplementary Figure S9: The BRAF V600E/L514V double mutant promotes homodimerization, related to Figure 3A and B. ⚫ Supplementary Figure S10: BRAF L514V alone is hypoactive and associated with decreased ERK signaling that is not sensitive to dabrafenib. ⚫ Supplementary Figure S11: BRAF V600E/L514V is inhibited by dabrafenib in a purified kinase assay, indicating that it is not a gatekeeper mutation.
[Show full text]
Figure S1. Effect of 4NQO, A-1155463 Or Their Combination on General Transcription, Translation, and Specific Apoptotic Proteins
Supplementary figures and tables Figure S1. Effect of 4NQO, A-1155463 or their combination on general transcription, translation, and specific apoptotic proteins. (a) RPE cells were treated with 1 M 4NQO, 1 M A-1155463 or their combination. Control cells were treated with 0.1% DMSO. [alpha-P32]UTP was added to cell culture medium to label newly transcribed cellular RNA. Total RNA was isolated and subjected to agarose gel electrophoresis followed by radioautography. (b) RPE cells were treated as for (a). [35S] methionine and cysteine were added to methionine- and cysteine-free culture medium to label newly synthetized cellular proteins. Cells were lysed and proteins were separated on SDS-polyacrylamide gel. 35S-labelled proteins were detected using radioautography. (c) RPE cells were treated as for (a). Relative levels of apoptosis- related proteins were determined using proteome profiler human apoptosis kit (n=2). Figure S2. Chemical structures of monomeric MB2Py(Ac) and dimeric DB2Py(n) bisbenzimidazole-pyrroles, as well as dimeric bisbenzimidazoles DBA(n). Table S1. The active compounds of 48 commonly prescribed drugs in Norway, their suppliers and catalogue numbers. Purity, Drug CAS MW Formula Cat N % Supplier 17α- E4876- Ethynylestradiol 57-63-6 296 C20H24O2 100MG ≥98 Sigma Aldrich 4- Acetamidophenol 103-90-2 151 C8H9NO2 102330050 98 Acros Organics Acetylsalicylic acid 50-78-2 180 C9H8O4 AC158180500 99 Acros Organics Amlodipine 88150-42-9 409 C26H31ClN2O8S CAYM14838 ≥98 Cayman Chemicals 134523-03- Atorvastatin 8 559 C33H35FN2O5 CAYM10493
[Show full text]
Receptor Tyrosine Kinase-Targeted Cancer Therapy
International Journal of Molecular Sciences Review Receptor Tyrosine Kinase-Targeted Cancer Therapy Toshimitsu Yamaoka 1,* , Sojiro Kusumoto 2, Koichi Ando 2, Motoi Ohba 1 and Tohru Ohmori 2 1 Advanced Cancer Translational Research Institute (Formerly, Institute of Molecular Oncology), Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan; [email protected] 2 Division of Allergology and Respiratory Medicine, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan; [email protected] (S.K.); [email protected] (K.A.); [email protected] (T.O.) * Correspondence: [email protected]; Tel.: +81-3-3784-8146 Received: 25 September 2018; Accepted: 2 November 2018; Published: 6 November 2018 Abstract: In the past two decades, several molecular targeted inhibitors have been developed and evaluated clinically to improve the survival of patients with cancer. Molecular targeted inhibitors inhibit the activities of pathogenic tyrosine kinases. Particularly, aberrant receptor tyrosine kinase (RTK) activation is a potential therapeutic target. An increased understanding of genetics, cellular biology and structural biology has led to the development of numerous important therapeutics. Pathogenic RTK mutations, deletions, translocations and ampliﬁcation/over-expressions have been identiﬁed and are currently being examined for their roles in cancers. Therapies targeting RTKs are categorized as small-molecule inhibitors and monoclonal antibodies. Studies are underway to explore abnormalities in 20 types of RTK subfamilies in patients with cancer or other diseases. In this review, we describe representative RTKs important for developing cancer therapeutics and predicting or evaluated resistance mechanisms.
[Show full text]
Dual Targeting of the Epidermal Growth Factor Receptor Using
OncoTargets and Therapy Dovepress open access to scientific and medical research Open Access Full Text Article CASE SERIES Dual Targeting of the Epidermal Growth Factor Receptor Using Combination of Nimotuzumab and Erlotinib in Advanced Non-Small-Cell Lung Cancer with Leptomeningeal Metastases: A Report of Three Cases This article was published in the following Dove Press journal: OncoTargets and Therapy Hongyu Xu1 Abstract: Leptomeningeal metastases (LM) occur in 3–5% of patients with advanced non- Lin Zhou2 small-cell lung cancer (NSCLC) and are associated with a dismal prognosis. We report three Yo u L u 2 cases of NSCLC with LM who were treated with the combination of nimotuzumab and fi Xiaomei Su1 erlotinib. Magnetic Resonance Imaging (MRI) evaluation during follow-up showed signi - Peng Cheng1 cant improvement in cancer symptoms and decreased tumor size in all three patients. Grade 3 and 4 toxicities were rarely seen. Based on apparent efficacy of the regimen and fewer side Dong Li1 effects, we suggest that nimotuzumab in combination with erlotinib may be a promising Hui Gao1 1 option for the treatment of NSCLC with LM. Hua Li Keywords: leptomeningeal metastases, non-small cell lung cancer, nimotuzumab, erlotinib Weiwei Yuan1 Ling Zhang1 1 Tao Zhang Introduction 1 Department of Oncology, The General Leptomeningeal metastases (LM) occur in 3–5% of patients with non-small-cell Hospital of Western Theater Command, Chengdu, People’s Republic of China; lung caner (NSCLC) and are a detrimental complication associated with poor 2 Department of Thoracic Oncology, prognosis.1,2 Patients with LM are usually unable to accept systematic chemother- West China Hospital, Sichuan University, Chengdu, People’s Republic of China apy and present devastating headache.
[Show full text]