Vignette for survAH package

Hajime Uno1, Miki Horiguchi2, Zihan Qian3

December 1, 2025

1 Introduction

An important objective of clinical research investigating the safety and efficacy of a new intervention is to provide quantitative information about the intervention effect on clinical outcomes. Such quantitative information is critical for informed treatment decision making to balance the risks and benefits of the new intervention. In those studies where time-to-event outcomes are clinical endpoints of interest, the traditional Cox’s hazard ratio (HR) has been used for estimating and reporting the treatment effect magnitude for many decades. However, this traditional approach may not have provided the sufficient quantitative information that is needed for informed decision making in clinical practice for the following reasons. First, this approach does not require calculating the absolute hazard in each group in order to calculate the HR, which is a desirable feature from a statistical point of view, but which makes the clinical interpretation difficult. From the clinical point of view, the two numbers from the treatment and control groups are necessary for interpreting a between-group contrast measure (e.g., difference or ratio). Second, if the proportional hazards assumption is not correct, the interpretation of HR is not obvious because it is affected by the underlying study-specific censoring time distribution.[1,2]

The average hazard with survival weight (AHSW), which can be interpreted as the general censoring-free incidence rate (CFIR), is a summary measure of the event time distribution and does not depend on the underlying study-specific censoring time distribution. The approach using AHSW (or CFIR) provides two numbers from the treatment and control groups and allows us to summarize the treatment effect magnitude in both absolute and relative terms, which would enhance the clinical interpretation of the treatment effect on time-to-event outcomes.[3,4,5,6]

This vignette is a supplemental documentation for the survAH package and illustrates how to use the functions in the package to compare two groups with respect to the AHSW (or CFIR). The package was made and tested on R version 4.5.2.

2 Installation

Open the R or RStudio applications. Then, copy and paste either of the following scripts to the command line.

To install the package from the CRAN:

install.packages("survAH")

To install the development version:

install.packages("devtools") #-- if the devtools package has not been installed
devtools::install_github("uno1lab/survAH")

2 Sample Reconstructed Data

We use sample reconstructed data of the CheckMate214 study reported by Motzer et al. [7]. The data consists of 847 patients with previously untreated clear-cell advanced renal-cell carcinoma; 425 for the nivolumab plus ipilimumab group (treatment) and 422 for the sunitinib group (control).

The sample reconstructed data of the CheckMate214 study is available on survAH package as cm214_pfs. To load the data, copy and paste the following scripts to the command line.

library(survAH)

nrow(cm214_pfs)
#> [1] 847

head(cm214_pfs)
#>    time status arm
#> 1 0.451      1   1
#> 2 0.451      1   1
#> 3 0.451      1   1
#> 4 0.451      1   1
#> 5 0.451      1   1
#> 6 0.710      1   1

Here, time is months from the registration to progression-free survival (PFS), status is the indicator of the event (1: event, 0: censor), and arm is the treatment assignment indicator (1: Treatment group, 0: Control group).

Below are the Kaplan-Meier estimates for the PFS for each treatment group.

The two survival curves showed similar trajectories up to six months, but after that, a difference appeared between the two groups. This is the so-called delayed difference pattern often seen in immunotherapy trials. The HR based on the traditional Cox’s method was 0.82 (0.95CI: 0.68 to 0.99, p-value=0.037). Since the validity of the proportional hazards assumption was not clear in this study, there is no clear interpretation on the reported HR. Even if the proportional hazards assumption seemed to be reasonable, the lack of a group-specific absolute value regarding hazard makes the clinical interpretation of the treatment effect difficult. For example, if the baseline absolute hazard is very low, the reported HR (0.82) may indicate a clinically ignorable treatment effect magnitude. If it is high, even an HR that is closer to 1 (e.g., 0.98) may indicate a clinically significant treatment effect magnitude.

3 Average Hazard with Survival Weight (AHSW)

For a given \(\tau,\) a general form of the average hazard (AH) is denoted by \[ \eta(t) = \frac{\int_0^\tau h(u)w(u)du}{\int_0^\tau w(u)du},\] where \(h(t)\) and \(w(t)\) are the hazard function for the event time \(T,\) and a non-negative weight function, respectively. Let \(S(t)\) be the survival function for \(T.\) We use \(S(t)\) as the weight, which gives the AHSW \[ \eta(t) = \frac{\int_0^\tau h(u)S(u)du}{\int_0^\tau S(u)du}.\] The detailed motivation for using \(S(t)\) as \(w(t)\) was discussed in Uno and Horiguchi (2023) [3]. The AHSW has a clear interpretation as the average person-time incidence rate on a given time window \([0,\tau].\) It can also be called as the general censoring-free incidence rate (CFIR) in contrast to the conventional person-time incidence rate that potentially depends on an underlying study-specific censoring time distribution.

From now on, we simply call the AHSW (or CFIR) the average hazard (AH). The AH is denoted by the ratio of cumulative incidence probability and restricted mean survival time at \(\tau < \infty\): \[ \eta(\tau) = \frac{1-S(\tau)}{\int_0^\tau S(t)dt}.\]

Let \(\widehat{S}(t)\) denote the Kaplan-Meier estimator for \(S(t).\) A natural estimator for \(\eta(\tau)\) is then given by
\[ \widehat{\eta}(\tau) = \frac{1-\widehat{S}(\tau)}{\int_0^\tau {\widehat S} (t)dt}.\] The large sample properties and a standard error formula of \(\widehat{\eta}(\tau)\) are given in Uno and Horiguchi (2023) [3].

4 Two-sample comparison using AH and its implementation

Let \(\eta_{1}(\tau)\) and \(\eta_{0}(\tau)\) denote the AH for treatment group 1 and 0, respectively. Now, we compare the two survival curves, using the AH. Specifically, we consider the following two measures to capture the between-group contrast:

  1. Difference in AH (DAH) \[ \eta_{1}(\tau) - \eta_{0}(\tau) \]
  2. Ratio of AH (RAH) \[ \eta_{1}(\tau) / \eta_{0}(\tau) \]

These are estimated by simply replacing \(\eta_{1}(\tau)\) and \(\eta_{0}(\tau)\) by their empirical counterparts (i.e., \(\widehat{\eta_{1}}(\tau)\) and \(\widehat{\eta_{0}}(\tau)\), respectively). For the inference of the ratio type metrics, we use the delta method to calculate the standard error. Specifically, we consider \(\log \{ \widehat{\eta_{1}}(\tau)\}\) and \(\log \{ \widehat{\eta_{0}}(\tau)\}\) and calculate the standard error of log-AH. We then calculate a confidence interval for the log-ratio of AH, and transform it back to the original ratio scale; the detailed formula is given in Uno and Horiguchi (2023) [3].

The procedures below show how to use the function, ah2, to implement these analyses.

time   = cm214_pfs$time
status = cm214_pfs$status
arm    = cm214_pfs$arm
ah2(time=time, status=status, arm=arm, tau=21)

The first argument (time) is the time-to-event vector variable. The second argument (status) is also a vector variable with the same length as time, each of the elements takes either 1 (if event) or 0 (if no event). The third argument (arm) is a vector variable to indicate the assigned treatment of each subject; the elements of this vector take either 1 (if the active treatment arm) or 0 (if the control arm). The fourth argument (tau) is a scalar value to specify the truncation time point \({\tau}\) for the AH calculation.

When \(\tau\) is not specified in ah2, (i.e., when the code looks like below)

ah2(time, status, arm)

the default \(\tau\) (i.e., the maximum time point where the size of risk set for both groups remains at least 10) is used to calculate the AH. It is best to confirm that the size of the risk set is large enough at the specified \(\tau\) in each group to make sure the Kaplan-Meier estimates are stable.

The ah2 function returns AH on each group and the results of the between-group contrast measures listed above. Note that we chose 21 months for \(\tau\) in this example.

obj = ah2(time, status, arm, tau=21)
print(obj, digits=3)
#> 
#> The time window: [eta, tau] = [0, 21] was specified.
#> 
#> Number of observations: 
#>      Total N Event by tau Censor by tau At risk at tau
#> arm0     422          225           163             34
#> arm1     425          219           160             46
#> 
#> 
#> Average Hazard (AH) by arm: 
#>            Est. Lower 0.95 Upper 0.95
#> AH (arm0) 0.066      0.057      0.076
#> AH (arm1) 0.049      0.042      0.057
#> 
#> 
#> Between-group contrast: 
#>                                Est. Lower 0.95 Upper 0.95 P-value
#> Ratio of AH (arm1/arm0)       0.747      0.608      0.917   0.005
#> Difference of AH (arm1-arm0) -0.017     -0.029     -0.005   0.006

The estimated AHs were 0.049 (0.95CI: 0.042 to 0.057) and 0.066 (0.95CI: 0.057 to 0.076) for the treatment group and the control group, respectively. The ratio and difference of AH were 0.747 (0.95CI: 0.608 to 0.917, p-value=0.005) and -0.017 (0.95CI: -0.029 to -0.005, p-value=0.006), respectively.

5 Stratified analysis using the AH and its implementation

Stratified analysis is commonly used in clinical trials to adjust for imbalanced baseline characteristics or known prognostic factors. However, traditional stratified methods (e.g., Stratified Cox or CMH) assume homogeneous effects across strata, which may not hold in practice. To overcome this, we extend the AH framework to stratified settings using standardization [4]. This approach adjusts for stratification while preserving the interpretability of both absolute and relative treatment effects.

In this framework, treatment effects are summarized using the adjusted average hazard (AH), which is defined based on standardized survival curves across strata:

\[ \bar{S}_j(t) = \sum_{k=1}^{K} w_k S_{jk}(t), \]

where \(S_{jk}(t)\) denotes survival function for group \(j\) in stratum \(k\), and \(w_k\) is aset of weights that satisfies \(\sum_{k=1}^{K} w_k = 1\) for \(K\) strata. In this version of the package, \(w_k\) is set to be the proportion of subjects in stratum \(k,\) i.e., \(w_k = (n_{0k}+n_{1k}) / (n_0 + n_1)\), where \(n_{jk}\) is the number of subjects in stratum \(k\) in the group \(j\) and \(n_j\) is the total number of subjects in the group \(j.\)

Using this, the adjusted AH for group \(j\) is defined as

\[ \bar{\eta}_j(\tau) = \frac{1 - \bar{S}_j(\tau)}{\int_{0}^{\tau}\bar{S}_j(t)du} = \frac{1 - \left\{\sum_{k=1}^{K} w_k S_{jk}(\tau)\right\}}{\int_0^\tau \left\{\sum_{k=1}^{K} w_k S_{jk}(u)\right\}du}. \] We estimate \(\bar{\eta}_j(\tau)\) by replacing survival functions with Kaplan–Meier estimators \(\widehat{S}_{jk}(t).\)

\[ \widehat{\bar{\eta}}_j(\tau) = \frac{1 - \left\{\sum_{k=1}^{K} w_k \widehat{S}_{jk}(\tau)\right\}}{\int_0^\tau \left\{\sum_{k=1}^{K} w_k \widehat{S}_{jk}(u)\right\}du}. \]

To compare two groups, we use the following contrast measures: Difference in AH (DAH) is defined as \[ \text{DAH}(\tau) = \bar{\eta}_1(\tau) - \bar{\eta}_0(\tau), \]

and Ratio of AH (RAH) is defined as \[ \text{RAH}(\tau) = \frac{\bar{\eta}_1(\tau)}{\bar{\eta}_0(\tau)}. \]

Their estimators are \[ \widehat{\text{DAH}}(\tau) = \widehat{\bar{\eta}}_1(\tau) - \widehat{\bar{\eta}}_0(\tau), \quad \widehat{\text{RAH}}(\tau) = \frac{\widehat{\bar{\eta}}_1(\tau)}{\widehat{\bar{\eta}}_0(\tau)}. \]

We also illustrate how to perform stratified analysis using the AH with the myeloid dataset from the survival package. This dataset simulates a randomized trial in acute myeloid leukemia and includes a stratification factor based on mutations of the FLT3 gene (levels A, B, C), which is known to affect prognosis [8].

nrow(myeloid)
#> [1] 646
head(myeloid)
#>   id trt sex flt3 futime death txtime crtime rltime
#> 1  1   B   f    C    235     1     NA     44    113
#> 2  2   A   m    B    286     1    200     NA     NA
#> 3  3   A   f    A   1983     0     NA     38     NA
#> 4  4   B   f    A   2137     0    245     25     NA
#> 5  5   B   f    C    326     1    112     56    200
#> 6  6   B   f    C   2041     0    102     NA     NA

# Create new analysis variables:
# - arm_num: binary treatment indicator (1 = arm B [treatment], 0 = arm A [control])
# - time_yr: follow-up time converted from days to years
myeloid$arm_num <- ifelse(myeloid$trt == "B", 1, 0)
myeloid$time_yr <- myeloid$futime / 365.25

This data frame contains 646 observations and 9 variables. For the current analysis, we focus on the following key variables: futime, which represents the time to death or last follow-up; death, a censoring indicator where 1 denotes death and 0 indicates censoring; trt, the treatment variable with two levels, arm A and arm B; and flt3, which represents the mutation burden of the FLT3 gene, categorized as levels A, B, and C, and be used as a stratification factor in our following analysis.

Below are Kaplan-Meier plots of survival stratified by FLT3 mutation levels (A, B, C). These curves suggest potential heterogeneity in treatment effects across strata.

We now apply the ah2() function from the survAH package to conduct a stratified AH analysis with FLT3 mutation levels as the stratification factor.

myel_time   = myeloid$time_yr
myel_status = myeloid$death
myel_arm <- ifelse(myeloid$trt == "B", 1, 0) # Convert treatment variable to binary: 1 = treatment (arm B), 0 = control (arm A)
myel_strata = myeloid$flt3
ah2(time = myel_time,
    status = myel_status,
    arm = myel_arm,
    tau = 3,
    strata = myel_strata)

We set \(\tau\) to 3 (years). Compared to the previous sections, the other arguments remain the same, but we now introduce a new argument strata to perform a stratified analysis. The strata argument allows us to specify a categorical variable that defines the strata for the analysis. In this case, we use the FLT3 mutation levels as the stratification factor. The function will then report results from both unstratified and stratified analyses.


myel_obj <- ah2(time = myel_time,
                status = myel_status,
                arm = myel_arm,
                tau = 3,
                strata = myel_strata)

print(myel_obj,digit = 3)
#> 
#> The time window: [eta, tau] = [0, 3] was specified.
#> 
#> Number of observations: 
#>         total arm0 arm1
#> strata1   149   74   75
#> strata2   319  154  165
#> strata3   178   89   89
#> total     646  317  329
#> 
#> 
#>      Total N Event by tau Censor by tau At risk at tau
#> arm0     317          160            28            129
#> arm1     329          142            18            169
#> 
#> 
#> <Unstratified analysis> Average Hazard (AH) by arm: 
#>            Est. Lower 0.95 Upper 0.95
#> AH (arm0) 0.290      0.245      0.343
#> AH (arm1) 0.207      0.175      0.246
#> 
#> 
#> <Unstratified analysis> Between-group contrast: 
#>                                Est. Lower 0.95 Upper 0.95 P-value
#> Ratio of AH (arm1/arm0)       0.715      0.563      0.910   0.006
#> Difference of AH (arm1-arm0) -0.082     -0.143     -0.022   0.007
#> 
#> 
#> <Stratified analysis> Average Hazard (AH) by arm: 
#>            Est. Lower 0.95 (orginal scale) Upper 0.95 (orginal scale)
#> AH (arm0) 0.286                      0.235                      0.337
#> AH (arm1) 0.207                      0.170                      0.243
#>           Lower 0.95 (based on log scale) Upper 0.95 (based on log scale)
#> AH (arm0)                           0.239                           0.342
#> AH (arm1)                           0.173                           0.247
#> 
#> 
#> <Stratified analysis> Between-group contrast: 
#>                                Est. Lower 0.95 Upper 0.95 P-value
#> Ratio of AH (arm1/arm0)       0.723      0.562      0.930   0.011
#> Difference of AH (arm1-arm0) -0.079     -0.142     -0.016   0.013

As shown in the ah2 results above, in the unstratified analysis, the estimated AHs were 0.290 (95% CI: 0.245 to 0.343) for the control group and 0.207 (95% CI: 0.175 to 0.246) for the treatment group. The estimated RAH was 0.715 (95% CI: 0.563 to 0.910, p = 0.006), and the DAH was -0.082 (95% CI: -0.143 to -0.022, p = 0.007). In the stratified analysis, which adjusts for FLT3 mutation subgroups, the AHs were 0.286 (95% CI: 0.235 to 0.337) for the control group and 0.207 (95% CI: 0.170 to 0.243) for the treatment group. The RAH was 0.723 (95% CI: 0.562 to 0.930, p = 0.011), and the DAH was -0.079 (95% CI: -0.142 to -0.016, p = 0.013).

6 Regression analysis for AH and its implementation

Sections 4 and 5 focused on two-sample comparisons of AH, with or without stratification. In clinical research, however, regression models are frequently used to adjust for confounding factors, investigate prognostic variables, and develop risk prediction models for patient outcomes. Motivated by these needs, Uno et al. (2024) [6] proposed a regression analysis framework for AH at a pre-specified truncation time \(\tau\).

The AH regression framework is a general regression modeling approach for assessing the association between model covariates and the outcome. In the two-group setting considered previously, it can be used to perform between-group comparisons while adjusting for multiple covariates that may be associated with the outcome. This framework allows the treatment effect to be summarized in both absolute (difference in AH) and relative (ratio of AH) terms, along with the group-specific AH values, while simultaneously adjusting for important baseline characteristics, thereby improving the likelihood that the magnitude of the treatment effect is correctly interpreted in clinical settings.

The ahreg function can handle three kinds of censoring mechanisms:

  1. Independent censoring
  2. Group-specific censoring
  3. Covariate-dependent censoring

Let \(\eta(\tau \mid \mathbf{X})\) denote the AH at time \(\tau\) for an individual with covariate vector \(\mathbf{X} = (X_1,\ldots,X_p)^\top\). The ahreg function fits a regression model of the form \[ g\{\eta(\tau \mid \mathbf{X})\} = \beta_0 + \beta_1 X_1 + \cdots + \beta_p X_p, \] where \(g(\cdot)\) is a link function.

The current implementation supports the following link functions:

Under the log link, \(\exp(\beta_j)\) represents the ratio of AH (RAH) associated with a one-unit increase in covariate \(X_j\), adjusted for other covariates. Under the identity link, \(\beta_j\) represents the difference in AH associated with a one-unit increase in \(X_j\), adjusted for other covariates. Further methodological details and the large-sample properties of the estimator are described in Uno et al. (2024) [6].

6.1 Example data

We illustrate the use of ahreg with a subset of the pbc dataset from the survival package. The original dataset includes 418 patients, comprising both randomized and non-randomized cases. For this vignette, we use the 312 patients who participated in the randomized clinical trial (158 assigned to D-penicillamine and 154 to placebo). The survAH package provides the helper function ahreg.sample.data(), which extracts and prepares the analysis dataset for illustrating examples of AH regression analysis.

D = ahreg.sample.data()
nrow(D)
#> [1] 312
head(D)
#>        time status arm      age edema bili albumin protime
#> 1  1.095140      1   1 58.76523   1.0 14.5    2.60    12.2
#> 2 12.320329      0   1 56.44627   0.0  1.1    4.14    10.6
#> 3  2.770705      1   1 70.07255   0.5  1.4    3.48    12.0
#> 4  5.270363      1   1 54.74059   0.5  1.8    2.54    10.3
#> 5  4.117728      0   0 38.10541   0.0  3.4    3.53    10.9
#> 6  6.852841      1   0 66.25873   0.0  0.8    3.98    11.0

Here, time is years from registration to death or last known alive; status is the event indicator (1 = death, 0 = censored); and arm is the treatment assignment indicator (1 = D-penicillamine, 0 = placebo).

For baseline covariates, the dataset includes age (years), edema (0 = no edema, 0.5 = untreated or successfully treated, 1 = edema despite diuretic therapy), bili (serum bilirubin in mg/dl), albumin (serum albumin in g/dl), and protime (standardized blood clotting time).

Below is the KM estimate of time to death by treatment group.

In the following subsections (6.2, 6.3, and 6.4), we illustrate how to implement AH regression for each of the three censoring mechanisms, using the log link, \(g(x) = \log(x)\) as the link function. Section 6.5 illustrates the case of using the identity link \(g(x) = x\).

6.2 AH regression under independent censoring

The first example is the application of ahreg under independent censoring assumption. Because the default values of cens_strata and cens_covs are NULL, the AH regression can be implemented in the following simple specification:

a1 <- ahreg(Surv(time, status) ~ arm + edema + bili, 
            tau  = 7, 
            data = D)

The key arguments are:

The output provides coefficient estimates, standard errors, confidence intervals, \(z\)-values, and two-sided p-values for each predictor.

print(a1, digits=3)
#> Call: ahreg() 
#> 
#> [1] "Link: log"
#> Surv(time, status) ~ arm + edema + bili
#> 
#>              Est    SE low_0.95 upp_0.95       Z     p
#> Intercept -3.413 0.203   -3.811   -3.015 -16.805 0.000
#> arm        0.297 0.217   -0.129    0.723   1.366 0.172
#> edema      1.389 0.357    0.690    2.087   3.895 0.000
#> bili       0.115 0.016    0.083    0.147   7.055 0.000

In this example, the estimated coefficient for arm is \(\hat{\beta}_{\text{arm}} = 0.297\). Under the log link, exponentiating this value yields the ratio of AH:

\[ \exp({\hat{\beta}}_{\text{arm}}) \approx 1.34. \] This result can be summarized as:

The adjusted ratio of AH was 1.34 (95% CI: 0.88, 2.06; p-value=0.172).

This indicates that, on average, the treatment group experienced a 34% higher incidence rate of death than the placebo group over 7 years of follow-up, after adjusting for edema and bili.

6.3 AH regression with group-specific censoring

Next, we consider the AH regression under a group-specific censoring scenario. Suppose the underlying censoring distribution differs across treatment groups. This situation may arise, for example, when follow-up schedules or discontinuation patterns vary by treatment arm.

We use the cens_strata argument to specify the variable that is associated with censoring time. This option instructs ahreg to estimate the censoring distribution separately within each specified group, enabling valid AH estimation and regression even when censoring behavior differs across treatment groups. In the present case, the code is as follows:

a2 = ahreg(Surv(time, status) ~ arm + edema + bili,
           tau         = 7,
           data        = D,
           cens_strata = "arm")

While we used the treatment group (i.e., arm) in this example, any variable that defines groups with potentially different censoring distributions can be assigned to cens_strata. Note that cens_strata accepts only one variable. Thus, if several variables (e.g., arm and sex) are thought to influence censoring, one needs to create a new variable combining them and then specify this combined variable in cens_strata. When many variables are associated with censoring, or when a continuous variable is involved, a different approach is preferable (see Section 6.4).

As before, exponentiated coefficients under the log link yield the ratio of AH, now adjusted for group-specific censoring mechanisms.

print(a2, digits = 3)
#> Call: ahreg() 
#> 
#> [1] "Link: log"
#> Surv(time, status) ~ arm + edema + bili
#> 
#>              Est    SE low_0.95 upp_0.95       Z     p
#> Intercept -3.406 0.207   -3.813   -3.000 -16.443 0.000
#> arm        0.278 0.229   -0.171    0.728   1.214 0.225
#> edema      1.392 0.358    0.690    2.093   3.890 0.000
#> bili       0.115 0.016    0.083    0.147   7.044 0.000

6.4 AH regression with covariate-dependent censoring

Lastly, we consider AH regression under a covariate-dependent censoring scenario. In this setting, a Cox model is fitted to the censoring time to estimate the censoring distribution as a function of the variables specified in cens_covs. This argument accepts a vector of variable names (default = NULL). The resulting regression estimates account for covariate-dependent censoring, providing a more flexible approach when the censoring mechanism is complex.

Suppose both arm and edema are associated with the censoring time. In this case, the code is as follows:

a3 <- ahreg(Surv(time, status) ~ arm + edema + bili,
            tau       = 7,
            data      = D,
            cens_covs = c("arm", "edema"))
print(a3, digits = 3)
#> Call: ahreg() 
#> 
#> [1] "Link: log"
#> Surv(time, status) ~ arm + edema + bili
#> 
#>              Est    SE low_0.95 upp_0.95       Z     p
#> Intercept -3.407 0.214   -3.827   -2.987 -15.893 0.000
#> arm        0.300 0.234   -0.158    0.758   1.283 0.199
#> edema      1.470 0.398    0.689    2.250   3.692 0.000
#> bili       0.113 0.017    0.079    0.147   6.488 0.000

Note that only one of cens_strata or cens_covs can be specified in the ahreg function.

7 Conclusions

As illustrated in this vignette, AH-based methods provide more robust and reliable quantitative summaries of time-to-event outcomes than the traditional Cox hazard ratio approach. We anticipate that the procedures implemented in the survAH package will help clinical researchers quantify treatment effects in a more transparent and interpretable manner, thereby supporting more informed decision making in clinical practice.

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  1. Dana-Farber Cancer Institute, ↩︎

  2. Dana-Farber Cancer Institute, ↩︎

  3. Massachusetts General Hospital, ↩︎