Case Report: Complete pathologic response to neoadjuvant selpercatinib in a patient with resectable early-stage RET fusion-positive non-small cell lung cancer (2023)

1 Introduction

Although cytotoxic chemotherapy and immunotherapy remain cornerstones of perioperative therapy in non-small cell lung cancer (NSCLC), many patients experience recurrent disease and limited survival. In trials randomizing epidermal growth factor receptor (EGFR)-mutant NSCLC to targeted therapy versus chemotherapy, neoadjuvant EGFR tyrosine kinase inhibitor (TKI) achieved high objective response rates (42%–62%), major pathologic response (MPR; 8%–24%), and prolonged progression-free survival (1). Neoadjuvant anaplastic lymphoma kinase TKI therapy was likewise found to be active in anaplastic lymphoma kinase fusion-positive NSCLC, including in patients for whom pathologic complete response (pCR) was achieved (2).

We thus prospectively explored the neoadjuvant use of selpercatinib, a highly selective and potent rearrangement during transfection (RET) kinase inhibitor with central nervous system activity approved in multiple countries for the treatment of RET-altered advanced or metastatic lung or thyroid cancers. The LIBRETTO-001 study (NCT03157128; which provided registration data resulting in the aforementioned approvals) was formally amended in 2021 to include neoadjuvant and adjuvant selpercatinib for early-stage RET fusion-positive NSCLC (3) with the primary endpoint of MPR (Figure1).


Figure1 Study design. LIBRETTO-001 trial is a phase 2, open-label, single-arm study of selpercatinib for patients with RET-dependent cancer. The study design of the neoadjuvant-adjuvant cohort (cohort 7) of the trial is summarized in this figure. a Each cycle is 28 days. b Treating physician’s decision. c Up to 3 years of treatment or disease recurrence, patient withdrawal, intolerable toxicity, or death, whichever occurs first. BID, twice daily; NSCLC, non-small cell lung cancer; RET, rearrangement during transfection.

2 Case report

A 76-year-old Caucasian woman with a remote, five pack-year history of former smoking was diagnosed with clinical stage IB (T2aN0M0) adenocarcinoma of the lung at the University of California, Los Angeles, in September 2021. Baseline radiologic tumor assessments identified a left upper lobe tumor (3.1cm, Figure2) and no evidence of lymph node or distant metastasis; no F-fluorodeoxyglucose avidity was observed. A transbronchial tumor biopsy showed adenocarcinoma of the lung (Figure3). DNA- and RNA-based next-generation sequencing of 648 tumor-associated genes (Tempus xT™ Version 4) identified a KIF5B-RET fusion and no other activating genomic aberrations.


Figure2 Radiologic response to neoadjuvant selpercatinib. Computed tomography (CT) imaging of chest before and after neoadjuvant selpercatinib treatment is shown. (A) A baseline CT of the chest before selpercatinib initiation revealed a left lung mass measuring 3.1cm (arrow). (B) A follow-up CT of the chest after 8 weeks of selpercatinib showed disease regression to 2.9cm in the same mass (arrow). This was classified as stable disease by RECIST v1.1 per investigator assessment. RECIST, Response Evaluation Criteria in Solid Tumors.


(Video) RET fusion-positive NSCLC: Delivering targeted treatment | Panel discussion

Figure3 Pathologic response to neoadjuvant selpercatinib. Tumor specimens before and after neoadjuvant selpercatinib treatment are shown. (A) Pathologic assessment of a bronchoscopic biopsy with H&E staining before selpercatinib treatment identified a lung adenocarcinoma (×400). (B) Resected tumor after 8 weeks of selpercatinib treatment showed no evidence of viable tumor cells (×200). Reactive pneumocyte proliferation is denoted by an arrow. Cytogenetic testing of this specimen via RET FISH was negative for a RET fusion. FISH, fluorescence in situ hybridization.

Resectability was confirmed by a thoracic surgeon, and the patient consented to LIBRETTO-001 in October 2021, including the consent to publish her study-related information while keeping her identity confidential. In November 2021, neoadjuvant selpercatinib was initiated at the recommended dose of 160 mg twice daily for two 28-day cycles. Treatment was well tolerated; the only treatment-emergent adverse events (TEAEs) were grade 1 fatigue and diarrhea and grade 2 hypertension. During this time, one dose was missed inadvertently, and there was no dose modification planned.

After the completion of neoadjuvant selpercatinib, the tumor decreased from 3.1 to 2.9cm (Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 stable disease, investigator assessment, Figure2). In early January 2022, the patient underwent left upper lobe apical and posterior segmentectomies. The surgery was performed as planned; no surgery-related adverse events were documented. One lymph node in levels 5–6, one lymph node in level 7, and fragments of lymph node(s) from left levels 11, 12, and 13 stations were all negative for carcinoma. The patient declined adjuvant selpercatinib due to low-grade TEAEs during neoadjuvant therapy.

The primary endpoint of the LIBRETTO-001 cohort was MPR. Pathologic assessment of the resected primary tumor in hematoxylin and eosin (H&E) staining was conducted by three independent pathologists including two from the Independent Pathologic Review Committee. On initial assessment, 0%, 10%, and 30% viable tumor cells were found.

To adjudicate the presence or absence of viable tumor cells, dual-color break-apart RET (10q11) fluorescence in situ hybridization (FISH) was performed (University of California, Los Angeles, Clinical Laboratory), which did not detect aberrations in the 200 nuclei examined. Alignment on the pathologic assessment of 0% viable tumor cells (pCR) was then reached among the three pathologists. The consensus was atypical cells represented a reactive pneumocyte proliferation (instead of carcinoma) secondary to treatment effect (Figure3).

Plasma circulating tumor DNA samples were collected. KIF5B-RET was undetectable (Guardant360) in plasma throughout the trial (pre-selpercatinib, pre-operatively, and post-operatively) likely due to the fact that fusions are less well-detected by circulating tumor DNA and early-phase disease may have limited shedding. No other significant alterations were identified; a platelet-derived growth factor receptor alpha V193I variant of uncertain significance was found pre-selpercatinib (0.19% allele frequency) but not thereafter. This mutation was not detected by next-generation sequencing of the pre-selpercatinib lung cancer biopsy.

3 Discussion

In this patient with a KIF5B-RET-positive stage IB lung adenocarcinoma, prospective treatment with neoadjuvant selpercatinib in the LIBRETTO-001 trial achieved pCR. This case provides the first proof of concept of the clinical activity of a RET TKI in the neoadjuvant setting and sets a precedent for ongoing and future investigations in early-stage disease. While this cohort was closed after this patient was treated (for reasons unrelated to safety or activity), a separate trial continues to explore the utility of selpercatinib as adjuvant therapy in RET fusion-positive NSCLC (LIBRETTO-432; NCT04819100) (4).

pCR is an accepted regulatory endpoint that has supported the approval for neoadjuvant systemic therapy in NSCLC. Neoadjuvant nivolumab and chemotherapy were approved based on pCR as a main outcome measure (5). While it remains to be seen if RET inhibition will eventually be approved as perioperative therapy for RET fusion-positive NSCLC, neoadjuvant TKI therapy has already been approved for another fusion-positive subset of non-metastatic cancer (i.e., tropomyosin receptor kinase (TRK) inhibition for NTRK fusion-positive cancer, including NSCLC, one of whose approved indications is the setting where surgical resection likely results in severe morbidity) (6).

Several other factors are notable in this case. The discordance between radiologic (stable disease) and pathologic (pCR) assessments, conducted within a week of each other, highlights the inherent limitations of RECIST and the importance of pathologic evaluation in fully demonstrating the tumor response to effective therapy, especially in the short timelines of neoadjuvant therapy. Pathologic response in the setting of minimal radiologic response may need to be considered in other settings as well where surgical resection is not performed.

This case also highlights interobserver variation in the interpretation of pathologic response due to the challenge of using standard H&E staining to determine reactive versus neoplastic epithelium, especially in the setting of lepidic proliferations. To mitigate this challenge, molecular adjudication via FISH was utilized (7). A negative RET FISH result provided evidence of the lack of residual tumor (at least related to the original clone) and helped determine that the initially perceived “viable tumor cells” by two of three pathologists represented a benign reactive proliferation (8). The absence of driver alterations suggests a lack of residual tumor since driver alterations are typically retained during the course of cancer evolution (9). The scenario where the original driver is “lost” likely indicates that an independent clone (not related to the tumor in question) has become dominant. This scenario is unlikely in the present case but cannot be entirely ruled out; however, limited tissue precludes further analysis to address this question.

(Video) ARROW update confirms pralsetinib benefit for RET fusion-positive advanced NSCLC | Stephen Liu

In summary, neoadjuvant selpercatinib was found to be active for a patient with RET fusion-positive NSCLC. Neoadjuvant therapy resulted in low-grade TEAEs but did not preclude or interfere with the performance of definitive surgical therapy. The activity of preoperative selpercatinib in this prospective case establishes proof of concept of the potential utility of selpercatinib in early-stage RET fusion-positive NSCLC.

Data availability statement

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

Ethics statement

The studies involving human participants were reviewed and approved by UCLA Institutional Review Board (UCLA IRB) – Office of the Human Research Protection Program (OHRPP). The patients/participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.

Author contributions

This study was designed jointly by all authors. The sponsor (Loxo Oncology) collected, analyzed, and interpreted the trial data in collaboration with the authors. All authors were involved in the writing of the manuscript and its revisions. All the authors vouch for the completeness and accuracy of the clinical data and analyses and for the adherence of the trial to the protocol. All authors contributed to the article and approved the submitted version.


Preethi Govindarajan and Dana Schamberger from Syneos Health provided medical writing assistance and editorial support.

Conflict of interest

Author JG receives research funding from Eli Lilly and Company. LS consults with Astra Zeneca, Genentech, Eli Lilly and Company, and GV20 Therapeutics. She receives research funding from Bristol Myers Squibb and Genentech. SD is a consultant with Astra Zeneca and receives honoraria from Janssen, Takeda, and Merck. YM-G’s work was supported in part by a National Cancer Institute/ National Institutes of Health Cancer Center Support Grant (P30CA008748) to Memorial Sloan Kettering Cancer Center. YM-G reports travel, accommodation, and expenses from AstraZeneca and Loxo Oncology/Eli Lilly; food/beverages from Endeavor Biomedicines; and honoraria from Virology Education and Projects in Knowledge for a CME program funded by an educational grant from Amgen. She acknowledges associated research funding to the institution from Mirati Therapeutics, Loxo Oncology at Eli Lilly and Company, Elucida Oncology, Taiho Oncology, Hengrui USA, Ltd./Jiangsu Hengrui Pharmaceuticals, Luzsana Biotechnology, and Endeavor Biomedicines. She acknowledges royalties from Rutgers University Press and Wolters Kluwer. YM-G acknowledges receipt of funding from the Andrew Sabin Family Foundation as well as training through an institutional K30 grant from the NIH CTSA UL1TR00457. She has received funding from a Kristina M. Day Young Investigator Award from Conquer Cancer, the ASCO Foundation, endowed by Dr. Charles M. Baum and Carol A. Baum. She is also funded by the Fiona and Stanley Druckenmiller Center for Lung Cancer Research and a Paul Calabresi Career Development Award for Clinical Oncology NIH/NCI K12 CA184746. RR is a consultant with Johnson and Johnson. SS, AS, and BC are employed by Eli Lilly and Company. AD has stocks in TreeLine Bio. He receives honoraria from Medscape, OncLive, PeerVoice, Physicians Education Resources, Targeted Oncology, Research to Practice, Axis, PeerView Institute, Paradigm Medical Communications, WebMD, MJH Life Sciences, Med Learning, Imedex, Answers in CME, Clinical Care Options, EPG Health, JNCC/Harborside, Liberum, and Remedica Ltd. He is in a consulting or advisory role at Ignyta/Genentech/Roche, Loxo/ Bayer/Lilly, Takeda/Ariad/Millenium, TP Therapeutics, AstraZeneca, Pfizer, Blueprint Medicines, Helsinn, BeiGene, BerGenBio, Hengrui Therapeutics, Exelixis, Tyra Biosciences, Verastem, MORE Health, AbbVie, 14ner/Elevation Oncology, ArcherDX, Monopteros, Novartis, EMD Serono, Medendi, Repare RX, Nuvalent, Merus, Chugai Pharmaceutical, Remedica Ltd., mBrace, AXIS, EPG Health, Harborside Nexus, Liberum, RV More, Ology, Amgen, TouchIME, Janssen, Entos, Treeline Bio, Prelude, Applied Pharmaceutical Science, Inc., AiCME, i3 Health, and MonteRosa. He acknowledges research funding from Pfizer, Exelixis, GlaxoSmithKline, Teva, Taiho, and PharmaMar. His patents, royalties, and other intellectual property include Selpercatinib-Osimertinib filed/pending, Wolters Kluwer, Merck, Puma, Merus, and Boehringer Ingelheim. AD is also supported by grants from the National Cancer Institute/National Institutes of Health (P30CA008748, 1R01CA251591001A1, 1R01CA273224-01) and Lungevity.

The remaining author declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The authors declare that this study received funding from Loxo Oncology, which is now called Loxo@Lilly. The funder had the following involvement in the study: collected, analyzed, and interpreted the trial data in collaboration with the authors.

The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.


EGFR, epidermal growth factor receptor; FISH, fluorescence in situ hybridization; H&E, hematoxylin and eosin; MPR, major pathologic response; NSCLC, non-small cell lung cancer; pCR, pathologic complete response; RET, rearrangement during transfection; TEAEs, treatment-emergent adverse events; TKI, tyrosine kinase inhibitor.


1. Reyes R, Reguart N. Neoadjuvant treatment of stage IIIA-N2 in EGFR-Mutant/ALK-rearranged non-small cell lung cancer. Transl Lung Cancer Res (2021) 10:607–21. doi:10.21037/tlcr-20-780

(Video) Selpercatinib in RET-altered Thyroid Cancers with Dr. Lori Wirth

PubMed Abstract | CrossRef Full Text | Google Scholar

2. Zenke Y, Yoh K, Sakakibara-Konishi J, Daga H, Hosomi Y, Nogami N, et al. P1.18-04 neoadjuvant ceritinib for locally advanced non-small cell lung cancer with ALK rearrangement: SAKULA trial. J Thorac Oncol (2019) 14:S626–7. doi:10.1016/j.jtho.2019.08.1320

CrossRef Full Text | Google Scholar

3. Drilon A, Oxnard GR, Tan DSW, Loong HHF, Johnson M, Gainor J, et al. Efficacy of selpercatinib in RET fusion-positive non-small-cell lung cancer. N Engl J Med (2020) 383:813–24. doi:10.1056/NEJMoa2005653

PubMed Abstract | CrossRef Full Text | Google Scholar

4. Tsuboi M, Goldman JW, Wu YL, Johnson ML, Paz-Ares L, Yang JC, et al. LIBRETTO-432, a phase III study of adjuvant selpercatinib or placebo in stage IB-IIIA RET fusion-positive non-small-cell lung cancer. Future Oncol (2022) 18:3133–41. doi:10.2217/fon-2022-0656

PubMed Abstract | CrossRef Full Text | Google Scholar

5. FDA Approves neoadjuvant nivolumab and platinum-doublet chemotherapy for early-stage non-small cell lung cancer. Available at: (Accessed October 12, 2022).

(Video) Approaches for Optimal Molecular Testing, Treatment, and Management of NSCLC

Google Scholar

6. FDA Approves larotrectinib for solid tumors with NTRK gene fusions . Available at: (Accessed October 12, 2022).

Google Scholar

7. Radonic T, Geurts-Giele WRR, Samsom KG, Roemen GMJM, Von der Thüsen JH, Thunnissen E, et al. RET fluorescence In situ hybridization analysis is a sensitive but highly unspecific screening method for RET fusions in lung cancer. J Thor Onc (2021) 16(5):798–806. doi:10.1016/j.jtho.2021.01.1619

CrossRef Full Text | Google Scholar

8. Baker JA, Sireci AN, Marella N, Cannon HC, Marquart TJ, Holzer TR, et al. Analytical accuracy of RET fusion detection by break-apart fluorescence in situ hybridization. Arch Pathol Lab Med (2022) 146:351–9. doi:10.5858/arpa.2020-0376-OA

PubMed Abstract | CrossRef Full Text | Google Scholar

9. Dressler L, Bortolomeazzi M, Keddar MR, Misetic H, Sartini G, Acha-Sagredo A, et al. Comparative assessment of genes driving cancer and somatic evolution in non-cancer tissues: an update of the network of cancer genes (NCG) resource. Genome Biol (2022) 23(1):35. doi:10.1186/s13059-022-02607-z

(Video) Lung Cancer

PubMed Abstract | CrossRef Full Text | Google Scholar


What is the duration of response for selpercatinib? ›

Moreover, treatment-naïve patients had an ORR of 85% (95% CI, 70-94), with 90% of responses lasting at the 6-month mark.

What is the incidence of RET fusion in nsclc? ›

Abbreviations: AKT, protein kinase B; MAPK, mitogen activated protein kinase; PI3K, phosphoinositide 3 kinases; RET, rearranged during transfection. As noted, RET fusions occur in 1%-2% of patients with NSCLC,7-10,15 and 46% of patients develop brain metastases over their lifetime.

What is the drug for RET fusion lung cancer? ›

Pralsetinib and selpercatinib are approved to treat RET mutation-positive medullary thyroid cancer as well as RET fusion-positive non-small lung cancer and thyroid cancers. However, the FDA has approved selpercatinib to treat any cancer driven by a RET fusion.

What is the mechanism of action of selpercatinib? ›

Mechanism of Action

Upon oral administration, selpercatinib selectively binds to and targets various RET mutants and RET-containing fusion products. This results in an inhibition of cell growth of tumors cells that exhibit increased RET activity.

Does complete response mean remission? ›

(kum-PLEET reh-SPONTS) The disappearance of all signs of cancer in response to treatment. This does not always mean the cancer has been cured. Also called complete remission.

What are the side effects of selpercatinib Retevmo? ›

The most common side effects of RETEVMO are:
  • swelling of your arms, legs, hands, and feet (edema)
  • diarrhea.
  • tiredness.
  • dry mouth.
  • high blood pressure.

What cancers are associated with RET mutation? ›

What is my cancer risk if I have a RET mutation? If you have a mutation in the RET gene, this means you have a condition called Multiple Endocrine Neoplasia type 2 (MEN 2). MEN 2 increases your risk for certain types of cancers, including medullary thyroid cancer (a specific type of thyroid cancer).

What is the prediction of recurrence after complete resection in patients with NSCLC? ›

In fact, many patients with NSCLC have been cured by surgery. However, there are also many cases that fail to achieve a cure following surgery. In fact, 30% to 55% of patients with NSCLC develop recurrence and die of their disease despite curative resection (3-5).

What cancers are associated with RET? ›

RET is altered in 2.61% of all cancers with lung adenocarcinoma, colon adenocarcinoma, thyroid gland medullary carcinoma, cutaneous melanoma, and melanoma having the greatest prevalence of alterations [3].

How effective is Selpercatinib? ›

Selpercatinib had durable efficacy, including intracranial activity, with mainly low-grade toxic effects in patients with RET fusion–positive NSCLC who had previously received platinum-based chemotherapy and those who were previously untreated.

What is the best radiation treatment for lung cancer? ›

External radiation (external beam radiation): A machine outside the body (called a linear accelerator) aims a beam of X-rays directly at the cancer and surrounding tissue. External radiation is the most used radiation treatment for lung cancer.

What is the newest drug for lung cancer? ›

Immunotherapy Approvals

In 2022, one already approved drug received additional use for lung cancer patients. This drug is Libtayo (cemiplimab-rwlc) which is a PD-1 inhibitor.

Is selpercatinib targeted therapy? ›

Targeted therapy options are selpercatinib or pralsetinib (Gavreto). Chemotherapy with or without immunotherapy, bevacizumab, or both may also be recommended.

Is selpercatinib a chemotherapy drug? ›

Selpercatinib belongs to the group of medicines called antineoplastics (cancer medicines). It works by interfering with the growth of cancer cells, which are eventually destroyed.

What is another name for selpercatinib? ›

Selpercatinib, sold under the brand name Retevmo among others, is a medication for the treatment of cancers in people whose tumors have an alteration (mutation or fusion) in a specific gene (RET which is short for "rearranged during transfection").

What is the prognosis after a complete pathological response? ›

Pathological complete response appears as a strong prognostic factor in the TNBC subgroup. The initial general poor prognosis of this subtype is altered for patients achieving pCR (5 years-OS 93% versus 47%), as it has been initially reported by Liedtke et al.

What does pathologic complete response mean? ›

Listen to pronunciation. (PA-thuh-LAH-jik kum-PLEET reh-SPONTS) The lack of all signs of cancer in tissue samples removed during surgery or biopsy after treatment with radiation or chemotherapy.

Is complete remission good? ›

In a complete remission, all signs and symptoms of cancer have disappeared. If you remain in complete remission for 5 years or more, some doctors may say that you are cured. Still, some cancer cells can remain in your body for many years after treatment. These cells may cause the cancer to come back one day.

What is the success rate of TABRECTA? ›

Close to 7 out of 10 (68%) people had their tumors shrink or disappear, which is the overall response rate. Of the responders, 5% had a complete response and 63% had a partial response.

What is the success rate of Retevmo? ›

The full approval in NSCLC was based on Retevmo showing tumor shrinkage in 84% of patients compared to 61% on platinum-based chemotherapy.

How long is TABRECTA effective? ›

In the GEOMETRY mono-1 pivotal trial, TABRECTA® (capmatinib) tablets delivered an overall response rate (ORR) of 68% and a median duration of response (mDOR) of over 1 year (16.6 months) in treatment-naive patients (n=60). CR, complete response; PR, partial response.

What does RET mutation lead to? ›

Mutations in the RET gene are the most common genetic cause of Hirschsprung disease, a disorder that causes severe constipation or blockage of the intestine. More than 200 RET gene mutations are known to cause this condition.

Which mutation is responsible for most of the cancers are called? ›

Most human cancers are thought to be caused by acquired (somatic) mutations. Germline mutations are involved in a small portion of cases. Tumors form when cell growth gets out of control.

What does RET positive mean? ›

A positive test for the RET biomarker means that you are eligible for targeted therapy. Targeted therapy drugs keep cancer from growing and spreading. These drugs may have fewer side effects than chemotherapy. The U.S. Food and Drug Administration has approved. two drugs to treat RET+ cancers.

How long after chemo does SCLC return? ›

An important distinction recognized widely is the time from completion of initial chemotherapy to relapse: relapse ≤ 6 months versus relapse > 6 months, where reinitiation of the previously administered first-line chemotherapy regimen is recommended for SCLC relapse > 6 months.

Does recurrence mean metastasis? ›

Regional recurrence means that the tumor has grown into lymph nodes or tissues near the original cancer. Distant recurrence means the cancer has spread to organs or tissues far from the original cancer. When cancer spreads to a distant place in the body, it is called metastasis or metastatic cancer.

What is recurrence after complete remission? ›

When cancer returns after a period of remission, it's considered a recurrence. A cancer recurrence happens because, in spite of the best efforts to rid you of your cancer, some cells from your cancer remained. These cells can grow and may cause symptoms.

What diseases are associated with RET gene? ›

RET gene mutation is associated with thyroid disease. The RET proto-oncogene is considered the major candidate gene for causing Hirschsprung's disease. Germ-line mutations in axons 10 and 11 of RET are responsible for the development and cytopathology of familial medullary thyroid carcinomas.

Is RET mutation hereditary? ›

Your close relatives (like your parents, brothers, sisters, children) have a 50/50 random chance of inheriting the RET mutation that you carry, and other family members (like your aunts, uncles, cousins) may also inherit it. Your relatives can be tested for this same mutation.

Is RET a tumor suppressor? ›

These findings suggest RET is a tumor suppressor gene in the colon that is inactivated by both epigenetic and genetic mechanisms.

What is the duration of response for Pralsetinib? ›

Median duration of response, progression-free survival and overall survival were 12 months, 7 months and 14 months, respectively.

What category is selpercatinib? ›

Selpercatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.

Will dostarlimab work on all cancers? ›

“Because it's an immunotherapy drug, it's not specific for tumor types,” she said. This means the drug could technically be used to treat a range of cancers.

What is the hardest lung cancer to treat? ›

Large-cell undifferentiated carcinoma tends to grow and spread quickly. Other key facts about large-cell undifferentiated carcinoma include: This type of lung cancer may grow and spread quickly, making it difficult to treat.

Which lung cancer responds best to chemotherapy? ›

Chemotherapy is the main treatment for small cell lung cancer. Doctors use it because this type of cancer responds very well to chemotherapy. And small cell lung cancer tends to have spread beyond the lung when it is diagnosed.

What is the best cancer facility for lung cancer? ›

Cleveland Clinic is consistently ranked as one of the best hospitals for lung cancer treatment in the United States. The hospital's team of specialists uses the most advanced techniques and technologies to provide comprehensive care for patients with all types of lung cancer, including stage IV.

What is the new lung cancer treatment for 2023? ›

On January 26, 2023, the FDA approved the use of adjuvant pembrolizumab (Keytruda) after the resection and platinum-based chemotherapy for stage IB (T2a ≥4 cm), II, or IIIA NSCLC.

What is the new cancer drug in 2023? ›

On April 19, 2023, the Food and Drug Administration approved polatuzumab vedotin-piiq (Polivy, Genentech, Inc.)

What is the newest treatment for small cell lung cancer? ›

Immunotherapy for Extensive-Stage Small Cell Lung Cancer

This is based on research showing that adding immunotherapy resulted in longer survival times compared to those treated with chemotherapy alone.

What is the success rate of targeted therapy? ›

Cancer in its initial stages can be detected and diagnosed during annual health check-ups. Targeted therapy can be up to 80% effective, but traditional courses of chemotherapy only offer an approximately 30% chance of success.

Is targeted therapy better than chemotherapy? ›

Both chemotherapy and targeted therapy are two effective methods for cancer therapy. The difference is that chemotherapy can also kill the normal cells when eliminating the cancer cells. On the other side, the normals cells can survive the targeted therapy, when the growth of cancer cells was limited.

Why is targeted therapy better than chemotherapy? ›

How does targeted therapy work against cancer? Most types of targeted therapy help treat cancer by interfering with specific proteins that help tumors grow and spread throughout the body. This is different from chemotherapy, which often kills all cells that grow and divide quickly.

What is the duration of treatment for selpercatinib? ›

In the full safety population (n = 796), the median treatment duration was 36.1 months.

What are the ingredients in selpercatinib? ›

Active ingredient: selpercatinib Inactive ingredients: microcrystalline cellulose, colloidal silicon dioxide. The 40 mg capsule shell contains: gelatin, titanium dioxide, ferric oxide black and black ink.

What class of chemotherapy is taxol? ›

Taxol belongs to a class of chemotherapy drugs called plant alkaloids. Plant alkaloids are made from plants. The vinca alkaloids are made from the periwinkle plant (catharanthus rosea). The taxanes are made from the bark of the Pacific Yew tree (taxus).

What is the mode of action of selpercatinib? ›

The mechanism of action of selpercatinib is as a Rearranged during Transfection (RET) Inhibitor, and Cytochrome P450 2C8 Inhibitor, and Cytochrome P450 3A Inhibitor, and P-Glycoprotein Inhibitor, and Breast Cancer Resistance Protein Inhibitor, and Multidrug and Toxin Extrusion Transporter 1 Inhibitor.

Who makes selpercatinib? ›

21, 2022 /PRNewswire/ -- Eli Lilly and Company (NYSE: LLY) today announced the U.S. Food and Drug Administration (FDA) has granted approval to Retevmo® (selpercatinib, 40 mg & 80 mg capsules) for adult patients with locally advanced or metastatic solid tumors with a rearranged during transfection (RET) gene fusion that ...

What is the duration of action of cisplatin? ›

[20] Theoretically, cisplatin may not be as useful for slow-growing tumors. The drug is primarily excreted in the urine, with 10% in the bile. Its initial half-life is approximately 20 to 30 minutes, with a terminal half-life of 24 hours.

What is the response rate for cisplatin? ›

For a number of years, cisplatin has been considered the most active drug for the treatment of cervical cancer, with initial response rates as high as 50%.

What is duration of response chemotherapy? ›

Duration of response (DoR) is defined as the time from randomization to disease progression or death in patients who achieve complete or partial response [32].

What is the longest period of chemotherapy? ›

A course of chemotherapy usually takes between 3 to 6 months, although it can be more or less than that. The treatment will include one or more chemotherapy drugs. You may have the chemotherapy into a vein (intravenous drugs), or as tablets or capsules.

What is the longest chemo cycle? ›

A chemotherapy cycle can last anywhere from two to six weeks. Individual sessions can be over quickly or last hours to days. This can depend on whether you receive chemotherapy orally, through an injection, or intravenously.

Why does transplatin not work? ›

As you saw previously, transplatin is not active. The distance between the two chlorine leaving groups is longer than in cisplatin (Figure 24), resulting in transplatin being unable to form 1,2-intrastrand DNA adducts similar to cisplatin.

How effective is selpercatinib? ›

Selpercatinib had durable efficacy, including intracranial activity, with mainly low-grade toxic effects in patients with RET fusion–positive NSCLC who had previously received platinum-based chemotherapy and those who were previously untreated.

What is complete response in recist? ›

* Complete Response (CR): Disappearance of all non-target lesions and normalization of tumor marker level. * Incomplete Response/ Stable Disease (SD): Persistence of one or more non-target lesion(s) or/and maintenance of tumor marker level above the normal limits.

What is the response rate for Axitinib? ›

In one study of Western patients with cytokine-refractory mRCC, an objective response rate (ORR) of 44.2% (95% CI 30.5, 58.7) was achieved. The median time to progression was 15.7 months (95% CI 8.4, 23.4) and the median overall survival (OS) was 29.9 months (95% CI 20.3, not estimable).

What is the response rate to platinum chemotherapy? ›

Of the 38 patients with platinum-sensitive disease, 92% responded to therapy with a median survival of 26 months, 91% of the patients with platinum-intermediate disease (a platinum free interval of 4–12 months) responded with a median survival of 16 months.

What should I monitor with cisplatin? ›

Cisplatin may cause serious kidney problems. Tell you doctor right away if you have blood in urine, change in frequency of urination or amount of urine, difficulty in breathing, drowsiness, increased thirst, loss of appetite, nausea or vomiting, swelling of the feet or lower legs, or weakness.

What is the difference between partial and complete response to chemotherapy? ›

A complete response is the disappearance of all target lesions, and a partial response (PR) is defined as at least a 30% decrease in the sum of the target lesions. Stable disease is defined as fitting the criteria neither for progressive disease nor a PR.

What is the 7 day rule in chemotherapy? ›

Short, planned delays in chemotherapy for good-risk GCT patients (less than or equal to 7 days per cycle) appear to be acceptable since they may prevent serious toxicity in this curable patient population. Delays of longer than 7 days are strongly discouraged except in extraordinary life-threatening circumstances.

Is a partial response to chemo good? ›

Partial response (PR) implies that further treatment will probably be required to attempt a cure. In some slow-growing tumors (including low-grade lymphomas) no further treatment may be immediately necessary until the disease starts increasing in size again.


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