Quantitative oncology

Tumor Growth Rate

Turning Tumor Trajectories into Treatment Insight.

We develop tumor growth rate as a dynamic measure of treatment response—transforming serial measurements into clinically useful evidence.

Conceptual kinetic profileserial measures → response
regression, dgrowth, gtimetumor quantity
ggrowth constant
dregression constant
01 / 05

The central idea

A scan is a snapshot. A trajectory tells a story.

Conventional response categories compress a patient's course into a few thresholds. Kinetic modeling instead uses the full longitudinal pattern—separating treatment-sensitive regression from treatment-resistant growth that can occur at the same time.

Model theory

Two processes. One observed trajectory.

The model treats change during therapy as the net result of treatment-sensitive regression and treatment-resistant growth occurring concurrently at constant exponential rates.

A tumor can become smaller even while a resistant component is growing, because regression initially dominates. As the sensitive component diminishes, resistant growth may become visible as a plateau and then regrowth. Serial measurements reveal this trajectory more fully than a single response category.

Tumor quantity may be radiographic burden or a serum marker such as PSA or CA 19-9. Measurements are normalized to baseline and modeled over time. The estimated g-rate describes exponential growth; the d-rate describes exponential regression or decay.

Lower gslower resistant growth
Higher dfaster initial regression
ln(2) / gtumor doubling time

General regression–growth model

f(t) = φe−dt + (1−φ)egt
f(t)
normalized tumor quantity at time t
φ
fraction exhibiting treatment-related decay
d
exponential regression constant
g
exponential growth constant
This is a phenomenologic model of observed tumor quantity; its components should not be interpreted as direct measurement of individual cellular clones.

Broad applicability

One framework across tumors and therapies.

The model uses serial tumor quantity and time—not a specific histology or drug mechanism—so it is tumor-type and therapy agnostic by design.

10+cancer types studied
Multipletherapy classes studied
Agnosticto treatment mechanism

Published tumor-growth kinetics research spans more than 10 cancer types, including prostate, renal cell, colorectal, pancreatic, neuroendocrine, breast, and non-small cell lung cancers. The framework has been applied across chemotherapy, hormonal and androgen-receptor–directed therapy, targeted agents, immunotherapy, anti-angiogenic therapy, PARP inhibition, antibody–drug conjugates, and somatostatin analogs.

The framework is broadly applicable; performance and clinical utility still require validation within each disease and treatment setting. See selected studies.

Methodology

From measurements to a biologic rate.

A reproducible framework for estimating the direction and velocity of tumor change during therapy.

Figure 1 · Simulated regression–growth model

The observed trajectory is the sum of two concurrent processes.

Sum of growth and regressionTreatment-sensitive regression (d)Treatment-resistant growth (g)
+60%+30%0%−30%−60%Sum of growth + regressionGrowth, gRegression, dNadir −45%Days of treatmentChange from baseline
In this simulated example, observed tumor quantity declines to a nadir of −45% as treatment-sensitive disease regresses, then rises as resistant growth becomes dominant. The model estimates these simultaneous exponential rates rather than reducing the trajectory to a single response category.
01

Serial measurements

Assemble repeated tumor burden, PSA, or other quantitative markers with their observed time points.

02

Concurrent kinetics

Model simultaneous treatment-sensitive regression and treatment-resistant growth.

03
g/d

Estimate g and d

Calculate patient-level growth and decay constants, with doubling time as an interpretable derivative.

04

Connect outcomes

Test kinetic estimates against progression, survival, and clinically meaningful treatment benefit.

TUMGr evaluates growth-only, decay-only, combined growth–decay, and φ-weighted combined models. Among fits with significant parameters, the model minimizing Akaike Information Criterion (AIC) is selected.

Open-source software

Download tumgr

The tumgr R package estimates patient-level tumor growth (g), regression (d), and φ from serial tumor measurements. It returns individual and summary results and can plot observed and predicted tumor quantity over time.

R console
# Install from CRAN
install.packages("tumgr")

# Load and estimate rates
library(tumgr)
results <- gdrate(data, 0.10, TRUE)

Current CRAN release · v0.0.4 · MIT License

Tumor kinetics bibliography

From foundational theory to FDA-scale validation.

2026The Oncologist

An FDA analysis of the association of tumor growth rate, overall survival, and progression-free survival in metastatic NSCLC

Malinou JN, Fan J, Cheng J, Gong Y, Shen Y-L, Larkins E

FDA analysis
2025The Oncologist

Cancer interception during treatment: using growth kinetics to create a continuous variable for assessing disease response

Zhou M, Wilkerson J, Bates SE, Fojo AT, et al.

Concept & validation
2025The Oncologist

Correlation between tumor growth rate and survival in patients with metastatic breast cancer treated with trastuzumab deruxtecan

He P, Gambhire D, Zhou H, Fojo AT, Rixe O, et al.

Breast cancer
2024EBioMedicine

Assessing olaparib efficacy in U.S. Veterans with metastatic prostate cancer utilizing a time-indifferent g-rate method

Leuva H, Bates SE, Fojo AT, et al.

Prostate cancer
2024Seminars in Oncology

Assessment of PSA responses and changes in the rate of tumor growth with immune checkpoint inhibitors in U.S. Veterans

Leuva H, Bose A, Bates SE, et al.

Prostate cancer
2024Breast Cancer Research and Treatment

Analysis of data from the PALOMA-3 trial confirms the efficacy of palbociclib and offers alternatives for novel assessment of clinical trials

Yeh C, Zhou M, Bapodra N, Fojo AT, Bates SE, et al.

Breast cancer
2023The Oncologist

Tumor Growth Rate Informs Treatment Efficacy in Metastatic Pancreatic Adenocarcinoma

Yeh C, Zhou M, Bates SE, Fojo AT, et al.

Pancreatic cancer
2021The Oncologist

Novel Tumor Growth Rate Analysis in the Randomized CLARINET Study Establishes the Efficacy of Lanreotide Depot/Autogel

Dromain C, Loaiza-Bonilla A, Mirakhur B, Fojo AT, et al.

Neuroendocrine tumors
2020Clinical Cancer Research

Enhanced Detection of Treatment Effects on Metastatic Colorectal Cancer with Volumetric CT Measurements for Tumor Burden Growth Rate Evaluation

Maitland ML, Wilkerson J, Zhou M, Fojo AT, et al.

Colorectal cancer
2019Seminars in Oncology

A novel approach to assess real-world efficacy of cancer therapy in metastatic prostate cancer

Leuva H, Wilkerson J, Bates SE, Fojo AT, et al.

Real-world methods
2017The Lancet Oncology

Estimation of tumour regression and growth rates during treatment in patients with advanced prostate cancer

Wilkerson J, Abdallah K, Fojo AT, et al.

Prostate cancer
2014The Oncologist

Continuing a cancer treatment despite tumor growth may be valuable: sunitinib in renal cell carcinoma as example

Burotto M, Wilkerson J, Stein WD, Bates SE, Fojo AT, et al.

Renal cell carcinoma
2012The Oncologist

Analyzing the pivotal trial that compared sunitinib and IFN-α in renal cell carcinoma using a method that assesses tumor regression and growth

Stein WD, Wilkerson J, Bates SE, Fojo AT, et al.

Renal cell carcinoma
2011The Oncologist

Tumor regression and growth rates determined in five intramural NCI prostate cancer trials: the growth rate constant as an indicator of therapeutic efficacy

Stein WD, Gulley JL, Schlom J, Bates SE, Fojo AT, et al.

Prostate cancer
2009The Cancer Journal

Other paradigms: growth rate constants and tumor burden determined using computed tomography data correlate strongly with overall survival

Stein WD, Yang J, Bates SE, Fojo AT

Foundational methods
2009Cancer

Progression-free survival is simply a measure of a drug’s effect on tumor growth while administered

Wilkerson J, Fojo AT

Endpoint theory
2008The Oncologist

Tumor growth rates derived from clinical-trial data correlate strongly with patient survival

Stein WD, Yang J, Bates SE, Fojo AT

Foundational methods
2008The Oncologist

Bevacizumab reduces the growth rate constants of renal carcinomas

Stein WD, Yang J, Bates SE, Fojo AT

Renal cell carcinoma

Ongoing work

Research portfolio

Four connected lines of inquiry move the method from measurement to decision-making.

01Clinical validation

Prospective validation in clinical trials

Testing whether early kinetic changes provide an actionable signal of treatment benefit before conventional progression endpoints mature.

02Methods development

Dynamic survival models

Comparing growth rate at three, six, and later months to determine when kinetic estimates become stable and prognostically useful.

03Real-world evidence

Therapy comparison at scale

Applying time-indifferent growth-rate methods to longitudinal clinical data, including irregularly spaced measurements.

04Translational research

Biology × kinetics

Linking tumor-growth phenotypes with genomic and circulating biomarkers to understand resistance and treatment sensitivity.

Next-generation tools

Built to translate.

Planned tools will make tumor kinetics more accessible to researchers, clinicians, and trainees.

In development01

Interactive growth-rate calculator

Enter serial measurements and dates to explore patient-level growth estimates and doubling time.

Planned02

Educational resource hub

Methods primers, worked examples, implementation notes, and teaching materials for quantitative oncology.

Contact us

Let’s study tumor kinetics together.

For research collaborations, data partnerships, or implementation questions, contact the Tumor Growth Rate Research Program.

Send an inquiry

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