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Incyte Announces Positive Interim Data from Phase 2 Trial of Pemigatinib, Its Selective FGFR Inhibitor, in Patients with Cholangiocarcinoma

On October 21, 2018 Incyte Corporation (Nasdaq:INCY) reported its updated data from its ongoing Phase 2 FIGHT-202 trial evaluating pemigatinib (INCB54828), its selective fibroblast growth factor receptor (FGFR) inhibitor, in patients with advanced/metastatic or surgically unresectable cholangiocarcinoma (bile duct cancer) who failed at least one previous treatment (Press release, Incyte, OCT 21, 2018, View Source [SID1234530010]). In patients with FGFR2 translocations who were followed for at least eight months, interim study results demonstrated an overall response rate (ORR) of 40 percent, the primary endpoint, and a median progression free survival (PFS) of 9.2 months, a key secondary endpoint.

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These results are being presented at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) 2018 Congress in Munich, Germany in a poster presentation on Sunday, October 21 from 12:45 p.m. CEST to 1:45 p.m. CEST (6:45 a.m. ET to 7:45 a.m. ET). (Location: Hall A3 – Poster Area Networking Hub; Abstract #756P)

"We are pleased to share updated interim results from our ongoing FIGHT-202 trial at ESMO (Free ESMO Whitepaper), which underscore the potential of pemigatinib as an effective new treatment option for patients with advanced cholangiocarcinoma who have FGFR2 translocations," said Steven Stein, M.D., Chief Medical Officer, Incyte. "If the full data set warrant it, we look forward to submitting our new drug application to the FDA in 2019, seeking approval of pemigatinib as a first-in-class selective FGFR inhibitor to treat patients with advanced cholangiocarcinoma, a devastating disease."

Cholangiocarcinoma is a cancer that arises from the cells within the bile ducts. It is often diagnosed late (stages III and IV) and the prognosis is poor. It is most common in those over 70 years old and is more common in men than women. FGFR2 fusion genes are drivers of the disease – occurring almost exclusively in patients with intrahepatic cholangiocarcinoma (iCCA), a subset of the disease – and are found in up to 20 percent of iCCA patients. The incidence of cholangiocarcinoma with FGFR2 translocation is increasing and is currently estimated at 2,500-3,000 patients in the U.S., Europe and Japan.

Key Findings from FIGHT-202

Updated, longer-term follow-up data from the interim analysis presented today at ESMO (Free ESMO Whitepaper) (data cut as of July 24, 2018) show that in patients with advanced/metastatic or surgically unresectable iCCA with FGFR2 translocations treated with pemigatinib who had at least eight months of follow up (Cohort A, n=47), the combined overall response rate (ORR) was 40 percent, including 19 (40 percent) patients with confirmed partial responses and 21 (45 percent) patients with stable disease (SD). The combined disease control rate (DCR) was 85 percent (40/47). Additionally, median progression free survival (PFS) was 9.2 months and median overall survival (OS) was 15.8 months.

Pemigatinib was well-tolerated. The most common treatment-emergent adverse events (TEAEs) were hyperphosphatemia (61 percent), alopecia (42 percent), diarrhea (39 percent), decreased appetite (37 percent) and fatigue (36 percent). Grade ≥3 TEAEs (observed >5 percent of patients) were hypophosphatemia (14 percent), hyponatremia (8 percent), abdominal pain (7 percent) and arthralgia (7 percent). Five patients had TEAEs with a fatal outcome, none of which were related to study treatment.

"I am extremely encouraged by the interim results of the FIGHT-202 study, which demonstrated meaningful clinical activity and promising preliminary progression-free survival estimates, and, as a practicing clinician, I am excited about the potential of pemigatinib to provide a new treatment option for my patients suffering from the life-threatening nature of advanced cholangiocarcinoma," said Antoine Hollebecque, M.D., Institut de Cancérologie Gustave Roussy, Villejuif, France.

About FIGHT-202

The FIGHT-202 open-label, multicenter study (NCT02924376) is evaluating the safety and efficacy of pemigatinib (INCB54828), Incyte’s investigational, selective, potent, oral fibroblast growth factor receptor (FGFR) inhibitor in adult (age ≥ 18 years) patients with advanced/metastatic or surgically unresectable cholangiocarcinoma with known fibroblast growth factor (FGF)/FGFR alterations and who have failed at least one previous treatment.

Patients were enrolled into one of three cohorts – Cohort A (FGFR2 translocations), Cohort B (other FGF/FGFR genetic alterations [GA]) or Cohort C (no FGF/FGFR GAs). All patients received 13.5 mg pemigatinib orally once daily (QD) on a 21-day cycle (two weeks on/one week off) until radiological disease progression or unacceptable toxicity.

The primary endpoint of FIGHT-202 is overall response rate (ORR) in Cohort A, assessed by independent review per RECIST v1.1. Secondary endpoints include ORR in Cohorts B, C and A plus B, progression free survival (PFS), overall survival (OS), duration of response (DOR), disease control rate (DCR) and safety.

The FIGHT-202 study is fully recruited outside of Japan, and updated data are expected to be presented in the second half of 2019. For more information about FIGHT-202, visit View Source

About FIGHT

Phase 2 studies investigating the safety and efficacy of pemigatinib monotherapy across several FGFR-driven malignancies are ongoing—the FIGHT (FIbroblast Growth factor receptor in oncology and Hematology Trials) clinical trial program currently comprises FIGHT-201 in patients with metastatic or surgically unresectable bladder cancer, including with activating FGFR3 alterations; FIGHT-202 in patients with metastatic or surgically unresectable cholangiocarcinoma who have failed previous therapy, including with activating FGFR2 translocations; and FIGHT-203 in patients with myeloproliferative neoplasms with activating FGFR1 translocations. FIGHT-302, a randomized Phase 3 trial in newly-diagnosed patients with cholangiocarcinoma and activating FGFR2 translocations, is expected to be initiated before the end of 2018 (NCT03656536).

About FGFR and Pemigatinib (INCB54828)

Fibroblast growth factor receptors (FGFRs) play an important role in tumor cell proliferation and survival, migration and angiogenesis (the formation of new blood vessels). Activating mutations, translocations and gene amplifications in FGFRs are closely correlated with the development of various cancers.

Pemigatinib is a potent, selective, oral inhibitor of FGFR isoforms 1, 2 and 3 which, in preclinical studies, has demonstrated selective pharmacologic activity against cancer cells with FGFR alterations.

Mirati Therapeutics Announces Updated Data From Ongoing Clinical Trial Of Single Agent Sitravatinib At The 2018 ESMO Congress

On October 21, 2018 Mirati Therapeutics, Inc. (NASDAQ: MRTX), a clinical stage targeted oncology company, reported the completed stage 1 safety and efficacy data from the ongoing Phase 1b clinical trial of single agent sitravatinib in patients with certain classes of oncogenic mutations (Press release, Mirati, OCT 21, 2018, View Source [SID1234530009]). The data for a cohort of patients harboring CBL mutations were presented in a proffered poster session (oral presentation) on Sunday, October 21st, 2018, at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) 2018 Congress in Munich, Germany.

"For patients whose tumors are driven by the CBL mutation, there are limited viable treatment options," said Charles M. Baum, M.D., Ph.D., President and Chief Executive Officer, Mirati Therapeutics, Inc. "Our sitravatinib single agent program will focus on NSCLC and melanoma patients with CBL inactivating mutations, who we believe could benefit most from single agent sitravatinib therapy."

Update from Sitravatinib Single Agent Study with CBL Inactivating Mutations

The presentation provided an update from the pre-planned expansion cohort of the Phase 1b clinical trial of single agent sitravatinib in patients with CBL inactivating mutations. Eight patients were evaluable as of the data cut-off on August 27, 2018.

In the subset of evaluable NSCLC patients, 1/2 confirmed partial responses were observed with 2/2 patients experiencing tumor regression.

In the subset of evaluable melanoma patients, 1/2 confirmed partial responses in evaluable patients were observed with 1/2 patients experiencing tumor regression.

In the subset of evaluable patients with other solid tumors, 2/4 had stable disease with 2/4 experiencing tumor regression.
CBL mutations are present in 1.5% of NSCLC, 3.5% of melanoma, and 2% of cancers of unknown origin.

About Sitravatinib

Sitravatinib is a spectrum-selective kinase inhibitor that potently inhibits receptor tyrosine kinases (RTKs), including TAM family receptors (TYRO3, Axl, Mer), split family receptors (VEGFR2, KIT) and RET. As an immuno-oncology agent, sitravatinib is being evaluated in combination with nivolumab (OPDIVO), an anti-PD-1 checkpoint inhibitor, in patients who have experienced documented disease progression following treatment with a checkpoint inhibitor. Sitravatinib’s potent inhibition of TAM and split family RTKs may overcome resistance to checkpoint inhibitor therapy through targeted reversal of an immunosuppressive tumor microenvironment, enhancing antigen-specific T cell response and expanding dendritic cell-dependent antigen presentation.

Sitravatinib is also being evaluated as a single agent in a Phase 1b expansion clinical trial enrolling patients whose tumors harbor specific mutations in the CBL kinase. When CBL is inactivated by mutation, multiple RTKs, including TAM, VEGFR2 and KIT, are dysregulated and may act as oncogenic tumor drivers in NSCLC and melanoma. Sitravatinib potently inhibits these RTKs and is being investigated as a treatment option for cancer patients with CBL mutations.

Genentech’s Investigational Personalized Medicine Entrectinib Shrank Tumors in People with NTRK Fusion-Positive Solid Tumors

On October 21, 2018 Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY), reported results from an integrated analysis of the pivotal Phase II STARTRK-2, Phase I STARTRK-1 and Phase I ALKA-372-001 trials that showed the investigational personalized medicine entrectinib shrank tumors (objective response rate; ORR) in more than half (57.4 percent) of people with neurotrophic tropomyosin receptor kinase (NTRK) fusion-positive solid tumors. Objective responses to entrectinib were seen across 10 different solid tumor types (median duration of response [DoR] = 10.4 months), including in people with and without central nervous system (CNS) metastases at baseline. Importantly, entrectinib shrank tumors that had spread to the brain in over half of people (intracranial response; IC ORR=54.5 percent), with more than a quarter of these people having a complete response (Press release, Genentech, OCT 21, 2018, View Source [SID1234530008]). The safety profile of entrectinib was consistent with that seen in previous analyses.

"These data demonstrate the potential of entrectinib to treat a range of difficult-to-treat and rare cancers regardless of their site of origin," said Sandra Horning, M.D., chief medical officer and head of Global Product Development. "Entrectinib has the potential to redefine personalized medicine, which can utilize tests such as next-generation sequencing to find the right treatment for each individual patient. People with NTRK fusion-positive solid tumors need more options, and we look forward to working with health authorities to bring this potential treatment to patients as soon as possible."

Genentech is leveraging its expertise in developing personalized medicines and advanced diagnostics, in conjunction with Foundation Medicine, to develop a novel diagnostics approach using next-generation sequencing that will help identify people with NTRK gene fusions likely to benefit from entrectinib.

Entrectinib has been granted Breakthrough Therapy Designation (BTD) by the U.S. Food and Drug Administration (FDA) for the treatment of NTRK fusion-positive, locally advanced or metastatic solid tumors in adult and pediatric patients who have either progressed following prior therapies or have no acceptable standard therapies. Breakthrough Therapy Designation is designed to expedite the development and review of medicines intended to treat serious or life-threatening diseases and to help ensure people have access to them through FDA approval as soon as possible.

These NTRK fusion-positive results will be presented at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) 2018 Congress in Munich, Germany on Sunday, October 21, 2018 from 11:24–11:36 a.m. CEST (Abstract LBA17; Hall B3 – Room 22). Follow Genentech on Twitter via @Genentech and keep up to date with ESMO (Free ESMO Whitepaper) 2018 Congress news and updates by using the hashtag #ESMO2018.

Genentech also recently presented positive results at the International Association for the Study of Lung Cancer (IASLC) 19th World Conference on Lung Cancer (WCLC) that showed entrectinib shrank tumors (ORR) in 77.4 percent of people with locally advanced or metastatic ROS1-positive non-small cell lung cancer (NSCLC). In addition, entrectinib demonstrated a durable response of more than two years (DoR = 24.6 months). Importantly, entrectinib was shown to shrink tumors in more than half of people with cancer in the CNS (IC ORR: 55.0 percent). The safety profile of entrectinib was consistent with that seen in previous analyses.

Genentech plans to submit results from these integrated analyses to global health authorities for the treatment of NTRK fusion-positive solid tumors and ROS1-positive NSCLC.

About the integrated analysis

The integrated analysis included data from 54 people with locally advanced or metastatic NTRK fusion-positive solid tumors (10 tumor types, >19 histopathologies) from the Phase II STARTRK-2, Phase I STARTRK-1 and Phase I ALKA-372-001 trials. The studies enrolled people across 15 countries and more than 150 clinical trial sites. Tumor types evaluated in the studies to date included breast, cholangiocarcinoma, colorectal, gynecological, neuroendocrine, non-small cell lung, salivary gland, pancreatic, sarcoma and thyroid cancers.

STARTRK-2 is a Phase II, global, multicenter, open-label basket study in people with solid tumors that harbor an NTRK1/2/3, ROS1 or ALK-positive gene fusion. The primary endpoint is ORR, and DoR is a secondary endpoint. Other secondary outcome measures include time to response, clinical benefit rate, intracranial tumor response, progression-free survival (PFS), CNS PFS and overall survival (OS).
STARTRK-1 is a Phase I, multicenter, open-label dose escalation study of a daily continuous dosing schedule in people with solid tumors with NTRK1/2/3, ROS1 or ALK gene fusions in the U.S. and South Korea. The trial assessed the safety and tolerability of entrectinib via a standard dose escalation scheme and determined the recommended Phase II dose.
ALKA-372-001 is Phase I, multicenter, open-label dose escalation study of an intermittent and continuous entrectinib dosing schedule in people with advanced or metastatic solid tumors with TRKA/B/C, ROS1 or ALK gene fusions in Italy.
Overall, entrectinib was well tolerated and the majority of adverse events were Grade 1-2, reversible, and managed with treatment interruption or dose reduction. Treatment-related adverse events leading to discontinuation occurred in 3.9 percent of patients. The most common treatment-related adverse events were altered sense of taste (dysgeusia), fatigue and dizziness.

About entrectinib

Entrectinib (RXDX-101) is an investigational, oral medicine in development for the treatment of locally advanced or metastatic solid tumors that harbor NTRK1/2/3 or ROS1 gene fusions. It is a selective tyrosine kinase inhibitor designed to inhibit the kinase activity of the TRK A/B/C and ROS1 proteins, whose activating fusions drive proliferation in certain types of cancer. Entrectinib can block ROS1 and NTRK kinase activity and may result in the death of cancer cells with ROS1 or NTRK gene fusions. Entrectinib is being investigated across a range of solid tumor types, including breast, cholangiocarcinoma, colorectal, gynecological, neuroendocrine, non-small cell lung, salivary gland, pancreatic, sarcoma and thyroid cancers.

About NTRK gene fusions

Neurotrophic tyrosine receptor kinase (NTRK) fusion-positive cancer occurs when the NTRK1/2/3 genes fuse with other genes, resulting in altered TRK proteins (TRKA/TRKB/TRKC) that can activate signaling pathways involved in proliferation of certain types of cancer. NTRK gene fusions are tumor-agnostic, meaning they are present in tumors irrespective of site of origin. These fusions have been identified in a broad range of solid tumor types, including breast, cholangiocarcinoma, colorectal, gynecological, neuroendocrine, non-small cell lung, salivary gland, pancreatic, sarcoma and thyroid cancers. There is a high unmet medical need for treatments for people with life-threatening and hard-to-treat NTRK fusion-positive tumors.

Loxo Oncology Announces Larotrectinib Clinical Update in Patients with TRK Fusion Cancers at the European Society for Medical Oncology 2018 Congress

On October 21, 2018 Loxo Oncology, Inc. (Nasdaq: LOXO), a biopharmaceutical company developing highly selective medicines for patients with genomically defined cancers, and Bayer AG, Germany, reported updated clinical data for larotrectinib, an investigational oral, selective, and CNS-active TRK inhibitor, in adult and pediatric patients with TRK fusion cancers (Press release, Loxo Oncology, OCT 21, 2018, View Source [SID1234529995]). The update included approximately one year of additional follow-up for the 55 patients described in the larotrectinib New England Journal of Medicine publication from February 2018. In addition, the update included data for an additional 67 patients who were subsequently enrolled across the larotrectinib development program. As of a data cut-off date of July 30, 2018, median duration of response (DOR) had not been reached in either dataset. These data are being presented today at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) 2018 Congress.

"It is exciting to see larotrectinib deliver durable responses to patients in these studies with TRK fusion cancer, regardless of age, tumor site of origin, or CNS involvement," said Ulrik Lassen, M.D., Ph.D., Department of Oncology, Rigshospitalet, Copenhagen. "The sixty-seven new patients have nearly the same overall response rate as the first fifty-five, and duration of response has actually improved with longer patient follow-up. It is interesting to note that once again, depth of response, indicated by a complete response or deep partial response, is a good predictor of duration of response. Additionally, we observed a safety profile with larotrectinib that is conducive to such chronic therapy. The larotrectinib experience provides strong clinical evidence supporting the development of single-purpose drugs against oncogenic driver targets, and underscores the importance of tumor genomic profiling capable of identifying NTRK gene fusions alongside other activating alterations."

Loxo Oncology and Bayer are engaged in a collaboration for the development and commercialization of larotrectinib. The U.S. Food and Drug Administration (FDA) has accepted the New Drug Application (NDA) submitted by Loxo Oncology, and granted Priority Review for larotrectinib for the treatment of adult and pediatric patients with locally advanced or metastatic solid tumors harboring a neurotrophic tyrosine receptor kinase (NTRK) gene fusion. The FDA has set a target action date of November 26, 2018, under the Prescription Drug User Fee Act (PDUFA). Bayer has submitted a Marketing Authorization Application (MAA) in the European Union (EU) and additional filings in other markets are underway.

Key Data Presented

The ESMO (Free ESMO Whitepaper) presentation included additional follow-up for the first 55 consecutively enrolled adult and pediatric patients with TRK fusion cancers treated across Loxo Oncology’s Phase 1 adult trial, Phase 2 trial (NAVIGATE), and Phase 1/2 pediatric trial (SCOUT). These patients were the subject of the New England Journal of Medicine publication from February 2018, and constitute the primary analysis population supporting larotrectinib’s NDA filing. The presentation also included data for the 67 TRK fusion patients subsequently enrolled. Presented data were based on a July 30, 2018 data cut-off date, providing approximately one year of additional follow up for the primary analysis population.

The datasets adhered to the intent to treat (ITT) principle and included patients with RECIST-evaluable disease enrolled to the three clinical trials, regardless of prior therapy or tumor tissue diagnostic method used to establish their TRK fusion diagnosis. In the ESMO (Free ESMO Whitepaper) presentation, response evaluations were based on investigator assessment.

The 122-patient integrated dataset included both adult and pediatric patients, who ranged in age from one month to 80 years and carried 24 unique TRK fusion-positive tumor diagnoses. Tumor types included 10 distinct soft tissue sarcomas, salivary gland, infantile fibrosarcoma, thyroid, lung, melanoma, colon, gastrointestinal stromal tumor (GIST), breast, bone sarcoma, cholangiocarcinoma, carcinoma of unknown primary, congenital mesoblastic nephroma, appendiceal, and pancreas cancers.

In the primary dataset, the overall response rate (ORR) was 80% (44/55) (95% CI: 67-90%), with a 62% partial response rate and an 18% complete response rate. In the supplementary dataset, the ORR was 81% (44/54) (95% CI: 69-91%), with a 65% partial response rate and a 17% complete response rate. Across both datasets, the ORR was 81% (88/109) (95% CI: 72-88%), with a 63% partial response rate and 17% complete response rate. The ORR analyses for the supplementary and integrated datasets included nine patients with unconfirmed partial responses awaiting confirmatory response assessments, but did not include 13 patients who were awaiting an initial response assessment and continuing on study.

Median duration of response (DOR) had not been reached in either the primary dataset or supplementary dataset, with median follow-up of 17.6 months and 7.4 months, respectively. In the primary dataset, Kaplan-Meier landmark analyses improved since the July 2017 data cut-off date. At 6 months, 88% of responses were ongoing (83% based on the July 2017 data cut-off date). At 12 months, 75% of responses were ongoing (71% based on the July 2017 data cut-off date). Kaplan-Meier landmark analyses of the supplementary dataset were highly concordant with the primary dataset. At 6 months, 93% of responses were ongoing and at 12 months, 81% of responses were ongoing. Across the integrated dataset, as of the July 2018 data cut-off date, 84% of responding patients remained on treatment or had undergone surgery with curative intent. Of 8 TRK fusion patients treated in the Phase 1 trial, 6 remained in response and on therapy at 22, 30, 33, 34, 37, and 41 months of follow up. With median follow-up for progression-free survival (PFS) of 19.6 months in the primary dataset, median PFS had been reached, at 28.3 months (95% CI: 9.9 months – Not estimable). This estimate is not statistically stable due to a low number of progression events, as evidenced by the wide confidence interval.

The safety data presented at ESMO (Free ESMO Whitepaper) encompassed the entire larotrectinib safety database in cancer patients (n=207), which includes 70 patients without a TRK fusion diagnosis. Larotrectinib was well tolerated, with the majority of adverse events recorded as grade 1 or 2. No treatment-related grade 3 or 4 adverse events occurred in more than 5% of patients. Eleven patients (9%) required larotrectinib dose reductions. In all cases, patients whose doses were reduced maintained their best response at the lower dose. One patient (<1%) discontinued larotrectinib due to an adverse event.

The ESMO (Free ESMO Whitepaper) presentation will be available online at View Source

Larotrectinib Program Update

As of September 30, 2018, the larotrectinib program had treated 179 patients with TRK fusion cancer, which includes the 122 patients reported at ESMO (Free ESMO Whitepaper), an additional 15 treated since the ESMO (Free ESMO Whitepaper) data cut-off date, 24 treated under expanded access protocols, and 18 who had either non-measurable disease or primary central nervous system tumors. By comparison, the program had treated 133 patients with TRK fusion cancer as of March 31, 2018 and 98 as of September 30, 2017.

About Larotrectinib
Larotrectinib is an oral, selective, and CNS-active investigational tropomyosin receptor kinase (TRK) inhibitor in clinical development for the treatment of patients with cancers that harbor a neurotrophic tyrosine receptor kinase (NTRK) gene fusion. Growing research suggests that the NTRK genes, which encode for TRKs, can become abnormally fused to other genes, resulting in growth signals that can lead to cancer in many sites of the body. In clinical trials, larotrectinib demonstrated anti-tumor activity in patients with tumors harboring NTRK gene fusions, regardless of patient age or tumor type. In an analysis of 55 RECIST-evaluable adult and pediatric patients with NTRK gene fusions, using a July 17, 2017 data cutoff, larotrectinib demonstrated a 75 percent centrally-assessed confirmed overall response rate (ORR) and an 80 percent investigator-assessed confirmed ORR, across many different types of solid tumors. The majority (93 percent) of all adverse events were grade 1 or 2.

Larotrectinib has been granted Priority Review, Breakthrough Therapy Designation, Rare Pediatric Disease Designation and Orphan Drug Designation by the U.S. FDA.

In November 2017, Loxo Oncology and Bayer entered into an exclusive global collaboration for the development and commercialization of larotrectinib and LOXO-195, a next-generation TRK inhibitor. Bayer and Loxo Oncology are jointly developing the two products with Loxo Oncology leading the ongoing clinical studies as well as the filing in the U.S., and Bayer leading ex-U.S. regulatory activities and worldwide commercial activities. In the U.S., Loxo Oncology and Bayer will co-promote the products.

For additional information about the larotrectinib clinical trials, please refer to www.clinicaltrials.gov. Interested patients and physicians can contact the Loxo Oncology Physician and Patient Clinical Trial Hotline at 1-855-NTRK-123 or visit www.loxooncologytrials.com/trk-trials.

About TRK Fusion Cancer
TRK fusion cancer occurs when a neurotrophic tyrosine receptor kinase (NTRK) gene fuses with another unrelated gene, producing an altered tropomyosin receptor kinase (TRK) protein. The altered protein, or TRK fusion protein, is constantly active, triggering a permanent signal cascade. These proteins become the primary driver of the spread and growth of tumors in patients with TRK fusion cancer. TRK fusion cancer is not limited to certain types of cells or tissues and can occur in any part of the body. NTRK gene fusions occur in various adult and pediatric solid tumors with varying prevalence, including appendiceal cancer, breast cancer, cholangiocarcinoma, colorectal cancer, GIST, infantile fibrosarcoma, lung cancer, mammary analogue secretory carcinoma of the salivary gland, melanoma, pancreatic cancer, thyroid cancer, and various sarcomas. Only sensitive and specific tests can reliably detect TRK fusion cancer. Next-generation sequencing (NGS) can provide a comprehensive view of genomic alterations across a large number of genes. Fluorescence in situ hybridization (FISH) can also be used to test for TRK fusion cancer, and immunohistochemistry (IHC) can be used to detect the presence of TRK protein.

IntegraGen presents new data expanding application of miR-31 to stage III colon cancer during ESMO 2018

On October 21, 2018 IntegraGen reported that it presented data on the company’s proprietary miR-31 microRNA biomarkers during the European Society of Medical Oncology (ESMO) (Free ESMO Whitepaper) 2018 Annual Congress being held in Munich, Germany (link) (Press release, Integragen, OCT 21, 2018, View Source [SID1234529994]). The study, entitled "miR-31 as a prognostic and predictive marker of disease-free survival (DFS) in resected stage III colon cancer: a retrospective analysis of the PETACC-8 trial," was based on an analysis of tumor samples from over 1,400 patients enrolled in the PETACC-8 Phase III Clinical Trial.

Key findings from the study included:

miR‐31‐3p and miR‐31‐5p levels were prognostic of disease-free survival (DFS) and overall survival (OS) in several subpopulations of patients with resected stage III colon cancer.

Low miR‐31‐3p and miR‐31‐5p expression levels identified patients who benefited from the additional of cetuximab to FOLFOX adjuvant therapy.

miR‐31‐5p expression level was predictive of cetuximab efficacy in three separate subpopulations which were studied.

"The present study provides additional evidence of the ability of miR-31 to predict response to cetuximab therapy in patients with colorectal cancer," stated Severine Martin-Lannerée, PhD, R&D project leader at IntegraGen and co-author of the study. "While our previous studies with these biomarkers focused on patients with advanced stage metastatic colorectal cancer, this new data demonstrates that low miR-31 expression can identify the potential benefits of adding cetuximab to adjuvant therapy during an earlier stage of colorectal cancer for several subpopulations of patients, potentially expanding the clinical application of this marker."