Clinical UM Guideline

This document addresses in vitro chemosensitivity assays and in vitro chemoresistance assays proposed as a means of predicting the in vivo tumor response to various chemotherapies. Several assays have been developed that differ in their processing and in the technique used to measure drug sensitivity. Available test methods typically involve isolation and incubation of tumor cells from biopsy specimens, exposure to drug therapies and assessment of cell survival. Results are reported as drug sensitive, drug resistant or intermediate. Drugs identified as drug sensitive are thought to be a potentially effective in vivo chemotherapy.  

Note: For a high-level overview of this document, please see “Summary for Members and Families” below. 

Not Medically Necessary:

In vitro chemosensitivity assays, as a guide to selection of chemotherapeutic drugs for individuals with cancer, are considered not medically necessary for all indications.

In vitro chemoresistance assays including, but not limited to, extreme drug resistance assays are considered not medically necessary for all indications.

This document describes clinical studies and expert recommendations, and explains why we do not consider chemosensitivity or chemoresistance assays to be clinically appropriate. The following summary does not replace the medical necessity criteria or other information in this document. The summary may not contain all of the relevant criteria or information. This summary is not medical advice. Please check with your healthcare provider for any advice about your health.

Key Information

In vitro chemosensitivity and chemoresistance assays are laboratory tests that use a sample of a person's tumor to see how cancer cells respond to different chemotherapy medicines outside the body. These tests are done by collecting tumor cells from a biopsy or surgery and exposing them to different chemotherapy agents in a laboratory. The results are reported as sensitive, resistant, or somewhere in between. Researchers hope this information will help doctors choose the best chemotherapy for each person. Some newer tests also study cancer stem cells, which are cancer cells that may be more likely to survive treatment and cause the cancer to return.

The goal is to help choose treatments that may work better and avoid medicines that may be less effective. Different tests use different methods, and each has possible advantages and disadvantages. Some studies have shown promising results, but better studies are needed to know whether using these tests to guide treatment improves health.

What the Studies Show

Studies have found that some of these tests can predict how cancer cells respond in the laboratory, and a few studies reported better outcomes when treatment was guided by certain tests. However, many studies included only small numbers of people, ended early, or did not actually use the test results to choose treatment. Some tests are available from only one laboratory or require tumor samples that are difficult to collect.

Professional medical organizations, including the American Society of Clinical Oncology (ASCO) and the National Comprehensive Cancer Network (NCCN), do not recommend routine use of these tests because better studies are needed to know whether they improve health.

Is this clinically appropriate?

In vitro chemosensitivity assays and in vitro chemoresistance assays, including extreme drug resistance assays, are not clinically appropriate because they have not been proven to improve health outcomes.

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The following codes for treatments and procedures applicable to this guideline are included below for informational purposes. Inclusion or exclusion of a procedure, diagnosis or device code(s) does not constitute or imply member coverage or provider reimbursement policy. Please refer to the member's contract benefits in effect at the time of service to determine coverage or non-coverage of these services as it applies to an individual member.

When Services are Not Medically Necessary:
When the code describes a procedure indicated in the Clinical Indications section as not medically necessary.

Summary

In vitro chemosensitivity and chemoresistance assays have been proposed as tools to guide individualized chemotherapy treatment decisions, with the goal of improving clinical outcomes such as response rates, progression-free survival (PFS), and overall survival (OS). These assays aim to measure how an individual’s tumor cells respond to various chemotherapy agents ex vivo, with the assumption that more sensitive tumors in vitro will be more responsive in vivo. While retrospective and observational studies, as well as a few prospective trials, suggest a potential correlation between assay-predicted sensitivity and improved clinical outcomes, the strength of the evidence varies widely. Limitations across studies include small sample sizes, inconsistent assay methodologies, low enrollment due to tissue viability issues, and most importantly, lack of randomization and direct application of assay results to treatment decisions. The ChemoID assay, which tests both cancer stem cells (CSCs) and bulk tumor cells, has shown encouraging results in one randomized trial, but study limitations prevent conclusions about routine clinical use. However, limitations such as early trial termination and single-laboratory availability limit generalizability. Other platforms, such as the ATP-CRA or 3D Predict^™ tests, and combination molecular-sensitivity approaches have shown some predictive and prognostic utility, but no consistent demonstration of improved health outcomes when used to guide treatment. Professional societies including the American Society of Clinical Oncology (ASCO) and National Comprehensive Cancer Network^® (NCCN) currently do not recommend the routine use of these assays in clinical practice, citing insufficient evidence.

Discussion

Chemotherapy sensitivity and resistance assays may also be called human tumor stem cell drug sensitivity assays, nonclonogenic or clonogenic cytotoxic drug resistance assays, tumor stem cell assays, or differential staining cytotoxic assays. These assays are intended to provide oncologists with information which assists in the selection of chemotherapy agents, to select potentially more effective chemotherapy regimens and to avoid the toxicity of potentially ineffective chemotherapy agents for an individual.

In vitro chemosensitivity assays are proposed to screen potential anticancer drugs, predict the effect of these drugs on tumors and determine the most appropriate chemotherapeutic regimen. The process assumes that the drugs most effective for treating a particular cancer can be identified. Therefore, in vitro chemosensitivity assays involve tumor cells obtained from an individual that are cultured and exposed to specific drugs in the laboratory setting. This process is done over a set period to evaluate survival and resistance of tumor cells to selected drugs. Drugs that show extreme resistance are considered unlikely to be effective, are eliminated. Examples of in vitro chemosensitivity assays include but are not limited to:

• Histoculture Drug Response Assay
• Afluorescent cytoprint assay
• ChemoFX assay
• CorrectChemo assay (previously known as the Microculture Kinetic [MiCK)] assay)

In vitro chemoresistance assays are reported to provide similar information as in vitro chemosensitivity assays. In addition, they also are said to deselect those drugs that are of no benefit. One of the most widely used techniques is the Extreme Drug Resistance assay (EDR^®). In this assay, cultured cells are exposed to high concentrations of selected chemotherapeutic agents for prolonged periods, far exceeding the exposure anticipated in vivo. Cell lines that survive this exposure are characterized as showing extreme drug resistance. These drugs are then considered potentially ineffective and a physician may be prompted to select another chemotherapeutic agent.

While the current tests utilize tumor tissue samples, there have been some early evaluations using organoids. Organoids are three-dimensional, tissue models generated by culturing freshly resected tumor tissue in order to preserve the architecture, cellular heterogeneity, and the native tumor microenvironment. Originally developed as preclinical models for studying tumor biology, disease mechanisms, and drug discovery, organoids have increasingly been adapted for precision oncology. Recently, these organoids have been used as functional ex vivo platforms to assess tumor sensitivity or resistance to chemotherapy, targeted therapies, and immunotherapies by testing treatment responses before clinical administration, with the goal of predicting individual-specific therapeutic outcomes and informing personalized treatment selection (Logun, 2025; Offi, 2026; Peng, 2025).

In a 2017 meta-analysis, Blom summarized findings from 34 studies on a variety of tests and indications. They evaluated the association between in vitro testing and clinical response (complete or partial remission). Using 70 correlations derived from assay-guided treatment, the predictive value of ex vivo testing had a pooled sensitivity of 92% (95% confidence interval [CI]: 79-98%) and a pooled specificity of 53% (95% CI: 35-71%). The value of the analysis was limited by study design (mainly retrospective) and lack of applicability within the studies; the findings were not used to guide treatment.

A prospective study was published by Kim in 2010. This study attempted to determine the most accurate analytic method to define in vitro chemosensitivity and to assess the accuracy of an ATP-based chemotherapy response assay (ATP-CRA). A total of 48 individuals with chemo-naïve, histologically confirmed, locally advanced or metastatic gastric cancer were enrolled in this study, however only 36 participants were evaluable for both clinical and in vivo responses due to assay failure or loss to follow up. All participants were treated with combination chemotherapy using paclitaxel 175 mg/m² and cisplatin 75 mg/m² for a maximum of six cycles after obtaining specimens for ATP-CRA. Investigators performed receiver operator characteristic curve analysis using individual responses by World Health Organization (WHO) criteria and obtained ATP-CRA results to define the method with the highest accuracy. Median PFS was 4.2 months (95% CI, 3.4-5.0) and median OS was 11.8 months (95% CI, 9.7-13.8) for all those enrolled. The chemosensitivity index method demonstrated highest accuracy of 77.8% by receiver operating characteristic (ROC) curve analysis, and the specificity, sensitivity, positive and negative predictive values were 95.7%, 46.2%, 85.7%, and 75.9% respectively. The in vitro chemosensitive group showed a higher response rate (85.7% vs. 24.1%; p=0.005) compared to the chemoresistant group. The authors concluded that ATP-CRA could predict clinical response to paclitaxel and cisplatin chemotherapy with high accuracy in individuals with advanced gastric cancer and results support the use of ATP-CRA in further validation studies and assay-guided clinical trials. However, there were numerous study limitations noted including, (1) the study took almost 3 years to enroll 36 participants acceptable for evaluation; (2) many samples were not enrolled due to bacterial contamination and an inadequate amount of tissue; (3) the study was terminated early due to a very poor accrual of participants, which resulted in an inadequate power to test the accuracy as originally planned; (4) study results needed validation by an independent cohort; and (5) the study may have been subject to bias because the clinical response was evaluated in participating centers by investigators who were blind to the in vitro chemosensitivity results but there was no independent review of those response evaluations.

Another prospective study, reported by Rutherford in 2013, was designed to assess whether the ChemoFX^® assay was predictive of outcomes among women with histologically confirmed epithelial ovarian cancer, fallopian tube cancer, or primary peritoneal cancer. Physicians were blinded to the assay results and treatment was selected from 1 of 15 prospectively specified protocols based on the oncologist’s medical judgment. A total of 262 participants (78.2% of total) had both clinical follow-up data and a ChemoFX result. Cancer cells were classified based on the ChemoFX result as sensitive, intermediate, or resistant to each of several chemotherapeutic agents. Those treated with an assay-sensitive regimen had a PFS median of 8.8 months, compared with 5.9 months for those with assay-intermediate or -resistant regimens (hazard ratio [HR], 0.67, p=0.009). Mean OS was 37.5 months for women treated with an assay-sensitive regimen, compared with 23.9 months for those with assay-intermediate or -resistant regimens (HR, 0.67, p=0.010). Although study results showed potential, the selection of a chemotherapeutic agent was not based on assay results but based on physician judgment and the impact of chemosensitivity testing on health outcomes could be determined.

Herzog (2010) evaluated in vitro tumor responses to platinum therapy by performing chemosensitivity testing on tumors from 192 women with primary ovarian cancer. Tumors were categorized as responsive, intermediately responsive, and nonresponsive to chemotherapy. Median OS was 72.5 months for women with tumors classified as responsive, 48.6 months for intermediately responsive, and 28.2 months for nonresponsive (p=0.03; HR, 0.70; 95% CI, 0.50-0.97). The authors concluded that the prediction of response to platinum agents by the chemosensitivity testing was consistent with expected population response rates. Limitations of this series included restriction of the survival analysis to only platinum agents in the primary setting, lack of information on subsequent chemotherapy, and a lack of reported assessments of clinical tumor response or disease status at death.

A prospective study by Howard (2017) correlated results of the ChemoID test to health outcomes but did not use the test results to guide treatment. A total of 41 individuals with glioblastoma (GBM) underwent standard-of-care treatment with temozolomide (TMZ)/radiotherapy and optimal surgical resection. Surgical biopsy samples were tested with ChemoID. The primary endpoint of the study was the 12-month response to TMZ therapy, defined as lack of tumor recurrence. Tumor recurrence was significantly correlated with ChemoID assay results. That is, for every 5% increase in TMZ cancer stem cell percent kill as identified by the test, there was a two-fold increase in 12-month nonrecurrence of cancer (odds ratio [OR], 2.2; 95% CI, 1.16-4.17; p=0.016). This cohort study was intended as a preliminary study to inform design of a randomized controlled trial (RCT). A subsequent RCT could provide data on whether individuals prospectively managed with the ChemoID test would have improved outcomes.

In 2023, Ranjan reported the results of a randomized trial to assess the effectiveness of chemotherapy regimens guided by the ChemoID assay compared to those chosen by physicians for individuals with recurrent glioblastoma. The primary efficacy point was OS and PFS. Following surgical resection and biopsy, 78 individuals were randomly assigned either to a group receiving chemotherapy guided by the ChemoID assay or to a group for whom the chemotherapy regimen was chosen by physicians. An interim analysis was planned after 35 deaths. At that time, the median OS was 12.5 months in the ChemoID guided group compared to 9 months in the physician choice group. In an intention-to-treat analysis, the OS in the ChemoID guided group was 12 months compared to 7.5 months in the physician choice group. While treatments for both groups were chosen from a list of standard treatments, treatment options did not include newer targeted therapies. The functional assay's utility was also limited by its dependence on the availability of viable tumor tissue samples, the study’s inclusion of only individuals with rGBM who underwent surgical resection or biopsy, and lack of use of available targeted therapies.

Herzog (2025) evaluated the efficacy of ChemoID-guided chemotherapy in individuals with recurrent platinum-resistant ovarian cancer, a population known to be more likely to have poor clinical outcomes due to therapy-resistant CSCs. This multicenter RCT was designed to evaluate 220 participants who would be randomized 1:1 to receive either physician-choice chemotherapy or treatment guided by the ChemoID assay. Enrollment was stopped after the results for the first 75 participants met a predetermined efficacy outcome threshold. The final report reflects results for 81 participants. The interim result showed that the objective response rate (ORR) at 6 months was significantly better for the ChemoID group (50%) compared to the control group (5%) (p<0.0001). The ChemoID-guided therapy arm experienced longer progression-free survival (11.0 vs. 3.0 months) (p<0.001), improved duration of response (8 vs. 5.5 months) (p<0.0001), and higher clinical benefit rate (83% vs. 24%). Although these results are promising, several factors limit the generalizability of the findings. Early termination of the trial, while statistically justifiable, may overestimate treatment effects and limit understanding of long-term outcomes. This study only assessed outcomes for platinum-resistant ovarian cancer and results may not apply to other tumor types. This test depends on collection of viable CSCs for analysis. Testing is only available from one proprietary laboratory and the median assay turnaround in this study was 14 days.

Several non-randomized studies used the microculture kinetic (MiCK) assay (Ballard 2010; Kravtsov, 1998; Liminga, 2000; Salom 2012; Strickland, 2013). The MiCK assay, also known as CorrectChemo test does not appear to be commercially available.

An RCT   by Cree (2007) compared individuals managed with and without in vitro chemosensitivity or chemoresistance assays. This study examined tumor chemosensitivity assay-directed chemotherapy versus physician’s choice in recurrent platinum-resistant ovarian cancer. The primary aim of this trial was to determine response rate and PFS following chemotherapy in individuals with platinum-resistant recurrent ovarian cancer who had received treatment according to an adenosine triphosphate (ATP) based tumor chemosensitivity assay in comparison with physician’s choice. A total of 180 participants were randomized into two groups with median ages of 59 and 61 years. Ninety-four individuals received assay-directed chemotherapy and 86 received physician’s choice therapy. The two primary end points studied were response rate and PFS. Response could only be assessed in 147 participants, and 40.5% achieved a partial or complete response in the assay-directed group compared with a 31.5% response in the physician’s choice group (p<0.3; not significant). In an intention-to-treat analysis, response rates were 31% in the assay-directed group vs. 26% in the physician choice group. Intention-to-treat analysis showed a median PFS of 93 days in the physician’s choice group and 104 days in the assay-directed group (HR, 0.8; not significant). No difference was seen in OS between the two groups. The study did not demonstrate that use of the ATP-based tumor chemosensitivity assay improved progression-free survival, overall survival, or other clinically meaningful health outcomes compared with physician-directed treatment.

Acanda De La Rocha (2024) reported the results of a feasibility and proof-of-concept study in which a combination of genomic profiling and drug sensitivity testing was used on 25 pediatric tissue samples from relapsed or refractory cancer. Recommendations were developed based on tissue samples tested against 120 FDA approved drugs. A total of 14 individuals received the therapy and 6 of those individuals received therapy consistent with the tissue testing combination. The authors reported significantly improved clinical outcomes compared to both response to previous therapies and to those 8 children who received treatment not guided by testing. This study’s observational design does not allow improved clinical outcomes to be attributed to testing guided treatments.

In 2021, Shuford evaluated the 3D-Predict’s ability to predict drug response in 33 prospectively enrolled adults (≥ 18 years) with suspected or known high-grade glioma who received standard of care treatment; both enrollees and their practitioners were blinded to the assay results. The predicted ‘responders’ had a median OS of 11.6 months (4.2-30.4) compared to 5.9 months (3.3-11.7) for predicted ‘nonresponders’ (HR, 0.35; 95% CI, 0.13 to 0.90; p=0.04). Given the limited sample size, marginal significance and lack of demonstrated clinical utility beyond case series, the results of this study are performed on tumor cells removed from the body identify not sufficient to establish the approach as a standard part of a treatment plan.

Ledford (2024) published the results of a prospective observational study evaluating the 3D Predict^™ Glioma test in individuals with newly diagnosed high-grade glioma to predict response to temozolomide. Among 59 participants for whom tissue specimens were analyzed, those predicted to respond showed significantly longer progression-free and overall survival. The findings suggest the test may provide prognostic insight that could support more personalized treatment approaches beyond standard biomarkers. However, the test was not directly applied to   guide treatment decisions during the study. All individuals received standard therapy regardless of test predictions.

Society Guidelines

The ASCO clinical practice guideline update on the use of chemotherapy sensitivity and resistance assays (2011) does not recommend the use of chemotherapy sensitivity and resistance assays to select chemotherapeutic agents for individuals outside of the clinical trial setting. ASCO cited an insufficient evidence base to support the use in oncology practice. ASCO indicates that a review of the literature did not identify any chemotherapy sensitivity and resistance assays for which the evidence was sufficient to support the use in oncology practice. This recommendation is similar to the current NCCN recommendation.

The NCCN Clinical Practice Guideline (CPG) for ovarian cancer (V4.2026) indicates that the current level of evidence for chemosensitivity/resistance assays is not sufficient to supplant generally accepted standards of chemotherapy. The NCCN CPG for central nervous system cancers (V2.2026) does not address chemosensitivity/resistance assays.

Apoptosis: The innate ability of a cell to undergo programmed death due to detrimental or incompatible derangements in its DNA.

Chemoresistance assay: Laboratory test performed on tumor cells removed from the body to identify anticancer drugs to which the tumor is unlikely to respond. The results may help identify the chemotherapy agents that are not likely to be effective for an individual.

Chemosensitivity assay: Laboratory test performed on tumor cells removed from the body to identify anticancer drugs to which the tumor is likely to respond. The results may help identify the chemotherapy agents most likely to be effective for an individual.

Cytotoxic drug: Drugs that possess a destructive action on specific cells; often refers to drugs used to fight cancer, such as chemotherapy.

In vitro (Latin: “in glass”): A process conducted outside of a living body, typically within a glass petri dish or test tube.

In vivo (Latin: “within the living”): A process, such as a treatment, conducted within a living body.

Peer Reviewed Publications:

1. Acanda De La Rocha AM, Berlow NE, Fader M, et al. Feasibility of functional precision medicine for guiding treatment of relapsed or refractory pediatric cancers. Nat Med. 2024; 30(4):990-1000.
2. Ballard KS, Homesley HD, Hodson C, et al. Endometrial carcinoma in vitro chemosensitivity testing of single and combination chemotherapy regimens using the novel microculture kinetic apoptosis assay: implications for endometrial cancer treatment. J Gynecol Oncol. 2010; 21(1):45-49.
3. Blom K, Nygren P, Larsson R, Andersson CR. Predictive value of ex vivo chemosensitivity assays for individualized cancer chemotherapy: a meta-analysis. SLAS Technol 2017; 22(3):306-314.
4. Cree IA, Kurbacher CM, Lamont A, et al. TCA Ovarian Cancer Trial Group. A prospective randomized controlled trial of tumour chemosensitivity assay directed chemotherapy versus physician's choice in patients with recurrent platinum-resistant ovarian cancer. Anticancer Drugs. 2007; 18(9):1093-1101.
5. Herzog TJ, Krivak TC, Bush S 2nd, et al. ChemoID-guided therapy improves objective response rate in recurrent platinum-resistant ovarian cancer randomized clinical trial. NPJ Precis Oncol. 2025; 9(1):86.
6. Herzog TJ, Krivak TC, Fader AN, Coleman RL. Chemosensitivity testing with ChemoFx and overall survival in primary ovarian cancer. Am J Obstet Gynecol. 2010; 203(1):68.e1-6.
7. Howard CM, Valluri J, Alberico A, et al. Analysis of chemopredictive assay for targeting cancer stem cells in glioblastoma patients. Transl Oncol. 2017; 10(2):241-254.
8. Kim JH, Lee KW, Kim YH, et al. Individualized tumor response testing for prediction of response to Paclitaxel and Cisplatin chemotherapy in patients with advanced gastric cancer. J Korean Med Sci. 2010; 25(5):684-690.
9. Kravtsov VD, Greer JP, Whitlock JA, Koury MJ. Use of the microculture kinetic assay of apoptosis to determine chemosensitivities of leukemias. Blood. 1998; 92(3):968-980.
10. Ledford A, Rodriguez A, Lipinski L, et al. Functional prediction of response to therapy prior to therapeutic intervention is associated with improved survival in patients with high-grade glioma. Sci Rep. 2024; 14(1):19474.
11. Liminga G, Martinsson P, Jonsson B, et al. Apoptosis induced by calcein acetoxymethyl ester in the human histiocytic lymphoma cell line U-937 GTB. Biochem Pharmacol. 2000; 60(12):1751-1759.
12. Logun M, Wang X, Sun Y, et al. Patient-derived glioblastoma organoids as real-time avatars for assessing responses to clinical CAR-T cell therapy. Cell Stem Cell. 2025; 32(2):181-190.e4.
13. Offi M, Buccarelli M, Chiesa S, et al. In vitro assays as a tool to personalize treatment in central nervous system tumors: a systematic literature review. Clin Exp Med. 2026; 26(1):140.
14. Peng T, Ma X, Hua W, et al. Individualized patient tumor organoids faithfully preserve human brain tumor ecosystems and predict patient response to therapy. Cell Stem Cell. 2025; 32(4):652-669.e11.
15. Ranjan T, Howard CM, Yu A, et al. Cancer stem cell chemotherapeutics assay for prospective treatment of recurrent glioblastoma and progressive anaplastic glioma: a single-institution case series. Transl Oncol. 2020; 13(4):100755.
16. Ranjan T, Sengupta S, Glantz MJ, et al. Cancer stem cell assay-guided chemotherapy improves survival of patients with recurrent glioblastoma in a randomized trial. Cell Rep Med. 2023; 4(5):101025.
17. Rutherford T, Orr J Jr, Grendys E Jr, et al. A prospective study evaluating the clinical relevance of a chemoresponse assay for treatment of patients with persistent or recurrent ovarian cancer. Gynecol Oncol. 2013; 131(2):362-367.
18. Salom E, Penalver M, Homesley H, et al. Correlation of pretreatment drug induced apoptosis in ovarian cancer cells with patient survival and clinical response. J Transl Med. 2012; 10:162.
19. Shuford S, Lipinski L, Abad A, et al. Prospective prediction of clinical drug response in high-grade gliomas using an ex vivo 3D cell culture assay. Neurooncol Adv. 2021; 3(1):vdab065.
20. Shuford S, Wilhelm C, Rayner M, et al. Prospective validation of an ex vivo, patient-derived 3D spheroid model for response predictions in newly diagnosed ovarian cancer. Sci Rep. 2019; 9(1):11153.
21. Strickland SA, Raptis A, Hallquist A, et al. Correlation of the microculture-kinetic drug-induced apoptosis assay with patient outcomes in initial treatment of adult acute myelocytic leukemia. Leuk Lymphoma. 2013; 54(3):528-534.

Government Agency, Medical Society, and Other Authoritative Publications:

1. Burstein HJ, Mangu PB, Somerfield MR, et al.; American Society of Clinical Oncology (ASCO). American Society of Clinical Oncology clinical practice guideline update on the use of chemotherapy sensitivity and resistance assays. J Clin Oncol. 2011; 29(24):3328-3330.
2. Centers for Medicare and Medicaid Services. National Coverage Decision for human tumor stem cell drug sensitivity assays (190.7). Available at: https://www.cms.gov/medicare-coverage-database/search.aspx. Accessed on July 6, 2026.
3. National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology. 2026^®. For additional information visit the NCCN website: http://www.nccn.org. Accessed on July 6, 2026.
   • Central Nervous System Cancers. (V2.2026). Revised June 10, 2026.
   • Ovarian Cancer Including Fallopian Tube Cancer and Primary Peritoneal Cancer. (V4.2026). Revised April 10, 2026.
4. Schrag, D, Garewal HS, Burstein HJ, et al. American Society of Clinical Oncology technology assessment: chemotherapy sensitivity and resistance assays. J Clin Oncol. 2004; 22(17):3631-3638.

3D Predict Glioma
3D Predict Ovarian Doublet Panel
3D Predict Ovarian PARP Panel
ATP Assay
Chemo Fx
ChemoFX Assay
ChemoID Assay
Chemotherapy Sensitivity and Resistance Assays
Clonogenic Cytotoxic Drug Resistance Assays
Cytoprint
Differential Staining Cytotoxic Assays
Extreme Drug Resistance Assay (EDR or EDRA)
Ex-vivo analysis of programmed cell death (EVA/PCD^™) assay
Human Tumor Stem Cell Drug Sensitivity Assays
MICK Assay
Microculture Kinetics (MiCK) assay (Correct Chemo^™)
MTT Assay
Nonclonogenic Clonogenic Cytotoxic Drug Resistance Assays
Tumor Stem Cell Assays

The use of specific product names is illustrative only. It is not intended to be a recommendation of one product over another, and is not intended to represent a complete listing of all products available.

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