scholarly journals Phase i trials in melanoma: A framework to translate preclinical findings to the clinic

2015 ◽  
Author(s):  
Eunjung Kim ◽  
Vito W. Rebecca ◽  
Keiran S.M. Smalley ◽  
Alexander R.A. Anderson
Keyword(s):  
Mathematical Model ◽  
Clinical Trial ◽  
Combination Therapy ◽  
Phase I ◽  
Phase 1 ◽  
Cell Populations ◽  
Model Parameters ◽  
Phase I Trials ◽  
Virtual Patients ◽  
Akt Inhibitor

We present a, mathematical model driven, framework to implement virtual or imaginary clinical trials (phase i trials) that can be used to bridge the gap between preclinical studies and the clinic. The trial implementation process includes the development of an experimentally validated mathematical model, generation of a cohort of heterogeneous virtual patients, an assessment of stratification factors, and optimization of treatment strategy. We show the detailed process through application to melanoma treatment, using a combination therapy of chemotherapy and an AKT inhibitor, which was recently tested in a phase 1 clinical trial. We developed a mathematical model, composed of ordinary differential equations, based on experimental data showing that such therapies differentially induce autophagy in melanoma cells. Model parameters were estimated using an optimization algorithm that minimizes differences between predicted cell populations and experimentally measured cell numbers. The calibrated model was validated by comparing predicted cell populations with experimentally measured melanoma cell populations in twelve different treatment scheduling conditions. By using this validated model as the foundation for a genetic algorithm, we generated a cohort of virtual patients that mimics the heterogeneous combination therapy responses observed in a companion clinical trial. Sensitivity analysis of this cohort defined parameters that discriminated virtual patients having more favorable versus less favorable outcomes. Finally, the model predicts optimal therapeutic approaches across all virtual patients.  

Phase I/II clinical trial of NY-ESO-1-specific TCR-engineered T-cell transfer combined with a novel T-cell stimulator CHP:NE1 for patients with refractory soft tissue sarcoma.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. TPS11074-TPS11074 ◽  
Author(s):  
Mikiya Ishihara ◽  
Hiroyoshi Hattori ◽  
Eisuke Arai ◽  
Yoshihiro Nishida ◽  
Kohichi Takada ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Immune Response ◽  
T Cells ◽  
T Cell ◽  
Soft Tissue ◽  
Soft Tissue Sarcoma ◽  
Combination Therapy ◽  
Phase I ◽  
Phase 1 ◽  
Peptide Antigen

TPS11074 Background: Combination therapy to enhance the efficacy of T cell receptor (TCR)-engineered T cells (TCR-T) has received increasing attention. We found that a combination therapy of TCR-T and a long peptide vaccine with CpG adjuvant without lymphodepletion regimen caused regression of immune checkpoint inhibitor-resistant sarcoma in a preclinical mouse model. Based on this finding, we initiated a clinical trial of TBI-1301 combined with CHP:NE1 without lymphodepletion for the patients with NY-ESO-1-expressing advanced soft tissue sarcoma. TBI-1301 is an NY-ESO-1157–165/HLA-A*02:01- or -A*02:06-specific TCR-T engineered to reduce endogenous TCR mRNA expression. CHP:NE1 is a novel T cell stimulator consisting of NY-ESO-1 long peptide antigen, cholesteryl pullulan (CHP) nanogel, and CpG oligoDNA. CHP nanogel is used for efficient delivery of long peptide antigen into the lymph nodes. CpG oligoDNA is a TLR9 agonist and used as an adjuvant. CHP:NE1 is expected to reinforce TBI-1301 T cells in the lymph nodes. Methods: This is an investigator-initiated multi-institutional first-in-human phase I/II clinical trial. TBI-1301 is infused at 5×109 cells one day after subcutaneous injection of CHP:NE1. CHP:NE1 is injected again 7 days after TBI-1301 infusion. This cycle is repeated once more. Lymphodepletion using cyclophosphamide and/or fludarabine is not performed. Key inclusion criteria include: refractory soft tissue sarcoma with NY-ESO-1 antigen expression, HLA-A*02:01- or HLA-A*02:06- positive, ECOG Performance Status 0 or 1, and adequate organ function. The primary objective is to assess the safety and efficacy in the phase 1 and 2 parts, respectively. The secondary objective is to assess the efficacy and immune response (blood concentration, immunophenotype and activity of TBI-1301) in the phase 1 part and the safety and immune response in the phase 2 part. Enrollment in this study is currently ongoing. Clinical trial information: JMA-IIA00346.

ProCAID: A phase I clinical trial to combine the AKT inhibitor AZD5363 with docetaxel and prednisolone (DP) chemotherapy for metastatic castration resistant prostate cancer (mCRPC).

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 228-228 ◽  
Author(s):  
Simon J. Crabb ◽  
Alison J. Birtle ◽  
Karen Martin ◽  
Nichola Downs ◽  
Megan Bowers ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Protein Kinase ◽  
Phase I ◽  
Disease Progression ◽  
Phase Ii ◽  
Performance Status ◽  
Research Network ◽  
Castration Resistant Prostate Cancer ◽  
Akt Inhibitor ◽  
Clinical Resistance

228 Background: DP extends survival in mCRPC. However emergent clinical resistance is effectively inevitable. Serine/threonine protein kinase AKT (protein kinase B) pathway activation is highly prevalent in mCRPC contributing to disease progression and DP therapeutic resistance. AZD5363 is a potent oral pan-AKT inhibitor. Pre-clinical data suggest activity in mCRPC and synergy with docetaxel. This phase I trial was to develop a DP/AZD5363 combination in mCRPC. Methods: Eligibility included chemotherapy naive histologically/cytologically proven measurable/evaluable mCRPC, PSA or radiographic disease progression, ECOG performance status 0 or 1, serum testosterone <1.7 nmol/L. Treatment comprised DP up to 10 cycles (75 mg/m2, IV, day 1; prednisolone 5 mg BID, PO, day 1–21) and AZD5363 to disease progression. Planned AZD5363 dose levels were 320 mg (DL1), 400 mg (DL2) and 480 mg (DL3), BID, PO, 4 days on/3 days off, from cycle 1, day 2. We utilised a conventional 3+3 dose escalation to determine a recommended phase II dose (RP2D) for AZD5363 combined with DP according to defined dose limiting toxicity (DLT) using CTCAEv4. Results: 10 patients were recruited (4 DL1, 6 DL2), median age 67.5 (Range: 56-72). A median of 6.5 cycles (Range: 3-10) of DP and 4 cycles (Range: 1-13) of AZD5363 were administered. No DLTs were seen in DL1. 2 patients in DL2 experienced DLTs (G3 rash, G3 diarrhoea). 7 pts (70%) had at least one G3/4 IMP-related AE with neutropenia (n=3) and maculo-papular rash (n=3) the most common. G3/4 AEs considered related to AZD5363 occurred in 3 patients (0 DL1, 3 DL2) including maculo-papular rash, diarrhoea and neutropenia. Transient hyperglycaemia occurred in all patients (Random glucose C1D2 pre dose mean 6.0 mmol/L, 2 hour mean 8.7 mmol/L, 4 hour mean 9.5 mmol/L, 8 hour mean 6.5 mmol/L). Conclusions:The RP2D for AZD5363 is 320 mg bd 4 days on/3 days off in combination with full dose DP for mCRPC. A placebo controlled randomised phase II trial for this approach has commenced recruitment. This work was supported by CRUK [C9317/A16029]. CRUK Reference: CRUK/12/042. This research was conducted with support from the Investigator-Sponsored Study Collaboration between AstraZeneca and the National Cancer Research Network. Clinical trial information: NCT02121639.

Regorafenib and nivolumab combination therapy for advanced and metastatic solid tumors: Phase I clinical trial (EPOC1603).

2018 ◽  
Vol 36 (15_suppl) ◽  
pp. TPS3124-TPS3124
Author(s):  
Shota Fukuoka ◽  
Hiroki Hara ◽  
Satoshi Shimizu ◽  
Hideaki Takahashi ◽  
Masafumi Ikeda ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Combination Therapy ◽  
Phase I ◽  
Solid Tumors ◽  
Phase I Clinical Trial

Clinical outcome and prognosis of metastatic colorectal cancer (mCRC) patients (pts) on phase 1 trials: A single institution experience from 1999 to 2016.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 828-828
Author(s):  
Audrey E. Kam ◽  
Gopichand Pendurti ◽  
Umang H. Shah ◽  
Mohammad Haroon Ghalib ◽  
Imran Chaudhary ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Phase I ◽  
Risk Score ◽  
Phase 1 ◽  
Median Number ◽  
Direct Bilirubin ◽  
P Value ◽  
Phase I Trials ◽  
Phase 1 Trials ◽  
Valuable Treatment

828 Background: Pts with mCRC who progress on all standard therapies have a poor prognosis and limited therapy options. Phase 1 trials represent a valuable treatment option. Herein we report the characteristics and outcomes of mCRC patients treated at our institution. Methods: We reviewed records of pts with mCRC enrolled on phase I trials at our institution from January 1999 to December 2016. Treatment-related response, toxicity, and deaths were recorded. Prognostic factors for overall survival (OS) were calculated using univariate (UVA) and multivariable Cox PH analysis (MVA). Results: We observed 187 enrollments with 152 unique patients accrued on 37 phase I trials. Median age was 59 years (range 29-83) and median number of prior therapies was 3 (range 0-8). 144 patients were evaluable for response. The clinical benefit rate (SD+response, CBR) was 33.2% and the ORR was 4.3%. Grade 3/4 non-hematological and hematological AE were seen in 25.5% and 17.3% of patients, respectively. Treatment-related mortality was 0.5%. Median PFS was 1.7 mos and OS was 8.2 mos. In UVA, the following variables predicted a shorter OS: age (p = 0.049); PS > 1 (p < 0.01); sites of metastases > 2 (p = 0.04); LDH > ULN (p < 0.001); albumin < 3.5 (p < 0.001); direct bilirubin > ULN (p = 0.02); WBC > 5.2 (p = 0.001); anemia (p = 0.046). In MVA, age > 60 (HR 1.63, p < 0.004), albumin < 3.5 (HR 3.69, p < 0.001), direct bilirubin > ULN (HR1.69, p < 0.01), and WBC > 5.2 (HR 1.97, p < 0.001) were negative prognostic factors for OS, adjusted for race and sex. A risk score based on MVA revealed that patients with a score of 0-1 had an improved OS (12.5mos) compared to a score of 2 (9.1mos, p-value < 0.005) and 3 (3.2 mos, p-value < 0.001). Conclusions: Patients with mCRC enrolled on phase 1 trials had a CBR of 33.2% and median OS of 8.2 mos, which exceeds third line therapies including regorafenib and trifluridine/tipiracil. Negative prognostic factors for OS were: age > 60, albumin < 3.5, direct bilirubin > ULN, and WBC > 5.2. A risk score based on these parameters showed that patients with a higher score had a significantly shorter OS, which may be useful in selecting patients for phase 1 trials.

An open label, multicenter, phase I/II study of RP1 as a single agent and in combination with PD1 blockade in patients with solid tumors.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. TPS2671-TPS2671
Author(s):  
Mark R. Middleton ◽  
Joseph J. Sacco ◽  
Jaime R. Merchan ◽  
Brendan D. Curti ◽  
Ari M. Vanderwalde ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Phase I ◽  
Solid Tumors ◽  
Dose Escalation ◽  
Phase 1 ◽  
Single Agent ◽  
Objective Response ◽  
Phase 2 ◽  
Biomarker Analysis ◽  
Tumor Types

TPS2671 Background: RP1 is an attenuated oncolytic HSV-1 that expresses a fusogenic glycoprotein from gibbon ape leukemia virus (GALV-GP R-) and GM-CSF. RP1 induces potent GALV-GP R- enhanced immunogenic cell death and host anti-tumor immunity in murine tumor models and increases PD-L1 expression. This clinical trial (NCT03767348) was designed to test the hypotheses that RP1 is safe when given alone and together with nivolumab (phase 1) and has efficacy together with nivolumab in four tumor types (phase 2). Methods: The primary goals of this clinical trial in a total of ~150 patients are to define the safety profile of RP1 alone and together with nivolumab, determine the recommended phase 2 dose (phase 1), and then in four phase 2 cohorts, to determine objective response rate in patients with melanoma, non-melanoma skin cancer, urothelial carcinoma and MSI-H solid tumors. Secondary objectives include duration of response, CR rate, PFS, viral shedding, and immune biomarker analysis. Patients with advanced cancer who failed prior therapy were eligible for the phase I component. In Phase 2 patients with histologic diagnoses of the four tumor types (N=30 for each) and who meet safety criteria for nivolumab treatment are eligible. Prior treatment with checkpoint blockade is not allowed except for the melanoma cohort. In the phase 1 portion patients are treated by intra-patient dose escalation of virus (range, 104 - 108 PFU) by intratumoral injection every two weeks for 5 total doses followed by 12 patients dosed 8 times at the RP2D in combination with nivolumab. Phase 1 patients were divided into two groups based on presence of clinically accessible lesions amenable to direct injection or those with visceral/deep lesions requiring image guidance for injection. In the phase 2 portion patients will receive the RP2D for eight injections and nivolumab will be given starting with the second RP1 injection. For the phase 1 portion, a modified 3+3 dose escalation design is used to assess safety and in the phase 2 portion, statistical analysis will be performed using a two-stage three-outcome optimum design with objective responses determined by RECIST criteria. As of February 11, 2019, 27 patients have been enrolled. Clinical trial information: NCT03767348.

scholarly journals Evaluation of Safety and Efficacy of Cell Therapy Based on Osteoblast Derived from Umbilical Cord Mesenchymal Stem Cell for Osteonecrosis of the Femoral Head: Study Protocol for a Single-Center, Open-Label, Phase I Clinical Trial

2021 ◽  
Author(s):  
Heejae Won ◽  
Shin-Yoon Kim ◽  
Sunray Lee ◽  
Hyun Sook Park ◽  
Seung-Hoon Baek
Keyword(s):  
Clinical Trial ◽  
Femoral Head ◽  
Phase I ◽  
Umbilical Cord ◽  
Early Stage ◽  
Phase 1 ◽  
High Dose ◽  
Human Umbilical Cord ◽  
Single Center ◽  
Safety And Efficacy

Abstract BackgroundVarious techniques for joint preservation have been attempted in early stage of osteonecrosis of femoral head (ONFH), but the effects are still controversial. Recently, a combination therapy of core decompression (CD) and MSCs collected from bone marrow, adipocytes or human umbilical cord has been introduced, and satisfactory results have been reported. However, there is no study in which human umbilical cord-derived osteoblasts (hUC-O) were administered directly to the lesion in early ONFH. We have classified the location and size of lesions in early-stage ONFH, and will evaluate the hypothesis that the application of hUC-O is a safe and effective treatment.MethodsThis is a prospective, single-center, phase I and open-labeled clinical trial. Nine patients with Association Research Circulation Osseous (ARCO) stage 1 or 2 ONFH will be assigned to a low-dose (n = 3, 1 ´ 107 hUC-O cells), medium-dose (n = 3, 2 ´ 107 cells), and high-dose group (n = 3, 4 ´ 107 cells) in the order of their arrival at the facility, and up to 18 patients will be enrolled depending on whether dose limiting toxicity occurs. We will perform CD on the participants, administer hUC-O according to the assigned group, and followed up for 12 weeks, including a total of 5 visits. This study will have 3 aims; first, to evaluate the safety of hUC-O through adverse events assessment, laboratory tests, vital sign assessment, physical examination, and electrocardiogram (ECG) test.; and second, to assess the clinical outcomes after hUC-O application by comparing pain visual analog scale (VAS), Harris Hip scores (HHS), and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) before and after surgery; and third, to evaluate the radiographic results after hUC-O application by comparing extent of necrotic lesions according to the ARCO and Japanese Investigation Committee (JIC) classification on magnetic resonance imaging.DiscussionThis clinical trial is a pilot phase 1 study evaluating the safety and efficacy of hUC-O local application combined with CD in early-stage ONFH patients. This study will provide the useful information on the treatment with hUC-O for those suffering from ONFH.Trial registration: Clinical Research Information Center (CRIS) established at the Korea Centers for Disease Control and Prevention (KDCA), KCT0006627. Registered 30 September 2021, https://cris.nih.go.kr/cris/search/detailSearch.do/20332

Patients involved in clinical research are more concerned about intrinsic and traditional research (“publish or perish”) conflicts of interests (COI) than potential financial conflicts: Results of interviews with advanced cancer patients enrolling in phase I trials

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 6008-6008
Author(s):  
C. K. Daugherty ◽  
F. J. Hlubocky ◽  
S. Gray ◽  
M. J. Ratain
Keyword(s):  
Clinical Trial ◽  
Phase I ◽  
Cancer Patients ◽  
Career Advancement ◽  
Trial Participation ◽  
Phase I Trials ◽  
Financial Benefit ◽  
Advanced Cancer Patients ◽  
Traditional Research ◽  
Financial Benefits

6008 Background: Concerns exist about the potential for financial COI to bias the design, conduct, analysis, and reporting of clinical trials. However, information is lacking about the perceptions of these COI among actual research subjects—both in general and relative to more intrinsic and traditional research COI. Methods: Using a standardized survey, cancer patients (pts) were asked closed-ended and semi-qualitative questions regarding their concerns about extrinsic, e.g., financial, and intrinsic, e.g. career advancement, COI. Results: To date, 120 pts either enrolled, or being evaluated for participation, in phase I trials have been approached for an interview with 96 completing the interview (80% response rate). Median age of respondents is 61 y (33–82); 55% male; 83% Ca, 10% AA, 2% AsA or HA; 38% college educated. 91%, 100%, and 94% thought that the involved investigators (MDs), drug companies, and hospitals benefited from a clinical trial respectively. The benefits cited for MDs was improvement in knowledge/ability to treat pts. The benefits cited for the hospital and drug company were described as prestige and financial. 38% would be concerned if an MD involved in a clinical trial receives financial benefit from the research, e.g., being a paid consultant or owning stock in company involved in a trial, and 43% thought that they should be informed of these potential benefits. 64% thought they should be concerned if an MD receives career advancement benefits from trial participation, and 69% thought they should be informed of this benefit. 45% thought that investigators might feel institutional pressure to enroll pts. Qualitative data revealed that pts’ lack of concern about financial COI related to their assumption that MDs already receive financial benefits-believing this to be acceptable-with some even encouraging it. Conclusions: Cancer pts were more concerned about intrinsic and traditional research COI than potential financial COI. As well, many assume that MDs receive financial benefits from research. These results may be helpful when considering COI management policies. No significant financial relationships to disclose.

A phase I trial with cohort expansion of BYL719 in combination with gemcitabine and nab-paclitaxel in locally advanced and metastatic pancreatic cancer.

2016 ◽  
Vol 34 (4_suppl) ◽  
pp. TPS467-TPS467
Author(s):  
Heloisa P. Soares ◽  
Danny Nguyen ◽  
Gregory M. Springett ◽  
Richard D. Kim ◽  
Irene Williams-Elson ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Clinical Trial ◽  
Phase I ◽  
Phase 1 ◽  
Locally Advanced ◽  
Class I ◽  
Therapeutic Window ◽  
Pharmacokinetic Data ◽  
Open Label ◽  
Clinical Trial Information

TPS467 Background: The phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR pathway which is aberrantly stimulated in many tumors has emerged as a potential target for anticancer therapy. Although several class I PI3K inhibitors are under development, there is considerable evidence suggesting that targeting a single isoform of PI3K (p110α) would have sufficient antitumor activity and improved therapeutic window. The PI3K pathway is frequently activated and plays an important role in pancreatic cancer. Further, PI3KCA mutations, the gene encoding isoform p110α, are observed in this disease. BYL719 is an oral class I α-specific PI3K inhibitor that showed anti-tumor activity in different preclinical models. Recently, the first in human phase 1 trial of BYL719 defined the maximum tolerated dose (MTD) at 400 mg once daily. Methods: This is a single institution, open label, single group, phase I study with cohort expansion that utilizes the standard 3+3 design for dose. The primary objective is to determine the MTD of BYL719 in combination with gemcitabine and nab-paclitaxel as frontline therapy in patients with locally advanced, recurrent or metastatic pancreatic adenocarcinoma. Up to 24 patients will be enrolled in 4 dose escalation levels. The MTD is defined as the highest dose level at which 1 or less of 6 patients experience a dose limiting toxicity (DLT). Once the MTD is reached and/or the recommended dose for expansion is determined, an additional dose expansion cohort of 15 patients will be included. Secondary endpoints include characterizing the safety profile at the MTD and DLTs associated with it as well as obtaining pharmacokinetic data. Peripheral blood and pre-treatment tumor samples will be collected for evaluation of biomarkers that could predict treatment response, including levels of pAKT, p4EBP1 and pS6. BYL719 will be administered daily. Standard doses of gemcitabine and nab-paclitaxel will be given on days 1, 8 and 15 of the 28 days cycle. Patients will get restaging scans every 2 cycles. As per September 2015, twelve patients have been included in this study which is currently enrolling patients on cohort 3. Clinical trial information: NCT02155088 Clinical trial information: NCT02155088.

A phase I clinical trial of AZD1775 in combination with neoadjuvant weekly cisplatin and docetaxel in borderline resectable head and neck squamous cell carcinoma (HNSCC).

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 6034-6034 ◽  
Author(s):  
Eduardo Mendez ◽  
Cristina P. Rodriguez ◽  
Michael Kao ◽  
Richard A. Harbison ◽  
Renato G. Martins ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Phase I ◽  
Phase 1 ◽  
Phase I Clinical Trial ◽  
Cancer Genes ◽  
Borderline Resectable ◽  
Hpv Status ◽  
Common Grade ◽  
Grade 3 ◽  
Recommended Phase Ii Dose

6034 Background: The WEE1 tyrosine kinase regulates G2/M transition and maintains genomic stability. In TP53-deficient tumors (via mutation or HPV inactivation), inhibiting WEE1 with AZD1775 can lead to unrestrained mitosis and cell death. We conducted a Phase I clinical trial of AZD1775 in combination with chemotherapy to define the toxicity profile, establish the maximal tolerated dose (MTD) and assess preliminary efficacy in borderline resectable HNSCC. Methods: Stage III/IVB HNSCC deemed borderline resectable by a multidisciplinary team were enrolled in a phase 1, 3 + 3 design to evaluate escalating doses of AZD1775 starting at 125 mg PO BID x 2.5 days alone as lead-in and in combination with cisplatin (25mg/m2) and docetaxel (35 mg/m2) for three additional weeks. Tumors were sequenced with UWOncoPlex (262 cancer genes); HPV status assessed via p16 IHC; toxicities graded with CTCAE v. 4.04; responses measured via RECIST 1.1 and through pathologic assessment when available. Trial is open but primary endpoints were met. Results: Eleven patients were screened; 10 enrolled and were evaluable for toxicities. The most common Grade ≥ 2 toxicities were diarrhea (4), fatigue (4), neutropenia (3) and nausea (3). The drug-limiting toxicity was Grade 3 diarrhea (2). The MTD was established at 150mg PO BID x 2.5 days, alone and in combination with neoadjuvant cisplatin and docetaxel. Two patients were HPV+/TP53wt, 1 was HPV+/ TP53 mut; 6 were TP53mut/HPV-; 1 was TP53 wt/HPV-. Seven out 10 patients had a response. Two patients dropped out after the first week with AZD1775, one due to an allergic reaction to docetaxel and another due to non-compliance. Eight completed neoadjuvant therapy and 7 of those converted to surgery: 2 had pathologic CRs (both HPV+/TP53wt); 4 had PR (all TP53 mutants); 1 (TP53wt/HPV-) had a PR by RECIST, but SD by pathology and 1 had PD. Conclusions: AZD1775 is safe and tolerable in combination with neoadjuvant cisplatin and docetaxel. Results show this combination to have promising anti-tumor efficacy in borderline resectable HNSCC with TP53 deficiency, and merits further investigation with the established MTD as the recommended Phase II dose. Clinical trial information: NCT02508246.

Sign in / Sign up

Export Citation Format

Share Document