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Research article

Bioinformatics analysis identified MMP14 and COL12A1 as immune-related biomarkers associated with pancreatic adenocarcinoma prognosis


  • Background 

    Pancreatic adenocarcinoma (PAAD) is one of the most common malignant tumors with high mortality rates and a poor prognosis. There is an urgent need to determine the molecular mechanism of PAAD tumorigenesis and identify promising biomarkers for the diagnosis and targeted therapy of the disease.

    Methods 

    Three GEO datasets (GSE62165, GSE15471 and GSE62452) were analyzed to obtain differentially expressed genes (DEGs). The PPI networks and hub genes were identified through the STRING database and MCODE plugin in Cytoscape software. GO and KEGG enrichment pathways were analyzed by the DAVID database. The GEPIA database was utilized to estimate the prognostic value of hub genes. Furthermore, the roles of MMP14 and COL12A1 in immune infiltration and tumor-immune interaction and their biological functions in PAAD were explored by TIMER, TISIDB, GeneMANIA, Metascape and GSEA.

    Results 

    A total of 209 common DEGs in the three datasets were obtained. GO function analysis showed that the 209 DEGs were significantly enriched in calcium ion binding, serine-type endopeptidase activity, integrin binding, extracellular matrix structural constituent and collagen binding. KEGG pathway analysis showed that DEGs were mainly enriched in focal adhesion, protein digestion and absorption and ECM-receptor interaction. The 14 genes with the highest degree of connectivity were defined as the hub genes of PAAD development. GEPIA revealed that PAAD patients with upregulated MMP14 and COL12A1 expression had poor prognoses. In addition, TIMER analysis revealed that MMP14 and COL12A1 were closely associated with the infiltration levels of macrophages, neutrophils and dendritic cells in PAAD. TISIDB revealed that MMP14 was strongly positively correlated with CD276, TNFSF4, CD70 and TNFSF9, while COL12A1 was strongly positively correlated with TNFSF4, CD276, ENTPD1 and CD70. GSEA revealed that MMP14 and COL12A1 were significantly enriched in epithelial mesenchymal transition, extracellular matrix receptor interaction, apical junction, and focal adhesion in PAAD development.

    Conclusions 

    Our study revealed that overexpression of MMP14 and COL12A1 is significantly correlated with PAAD patient poor prognosis. MMP14 and COL12A1 participate in regulating tumor immune interactions and might become promising biomarkers for PAAD.

    Citation: Yuexian Li, Zhou Su, Biwei Wei, Mengbin Qin, Zhihai Liang. Bioinformatics analysis identified MMP14 and COL12A1 as immune-related biomarkers associated with pancreatic adenocarcinoma prognosis[J]. Mathematical Biosciences and Engineering, 2021, 18(5): 5921-5942. doi: 10.3934/mbe.2021296

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  • Background 

    Pancreatic adenocarcinoma (PAAD) is one of the most common malignant tumors with high mortality rates and a poor prognosis. There is an urgent need to determine the molecular mechanism of PAAD tumorigenesis and identify promising biomarkers for the diagnosis and targeted therapy of the disease.

    Methods 

    Three GEO datasets (GSE62165, GSE15471 and GSE62452) were analyzed to obtain differentially expressed genes (DEGs). The PPI networks and hub genes were identified through the STRING database and MCODE plugin in Cytoscape software. GO and KEGG enrichment pathways were analyzed by the DAVID database. The GEPIA database was utilized to estimate the prognostic value of hub genes. Furthermore, the roles of MMP14 and COL12A1 in immune infiltration and tumor-immune interaction and their biological functions in PAAD were explored by TIMER, TISIDB, GeneMANIA, Metascape and GSEA.

    Results 

    A total of 209 common DEGs in the three datasets were obtained. GO function analysis showed that the 209 DEGs were significantly enriched in calcium ion binding, serine-type endopeptidase activity, integrin binding, extracellular matrix structural constituent and collagen binding. KEGG pathway analysis showed that DEGs were mainly enriched in focal adhesion, protein digestion and absorption and ECM-receptor interaction. The 14 genes with the highest degree of connectivity were defined as the hub genes of PAAD development. GEPIA revealed that PAAD patients with upregulated MMP14 and COL12A1 expression had poor prognoses. In addition, TIMER analysis revealed that MMP14 and COL12A1 were closely associated with the infiltration levels of macrophages, neutrophils and dendritic cells in PAAD. TISIDB revealed that MMP14 was strongly positively correlated with CD276, TNFSF4, CD70 and TNFSF9, while COL12A1 was strongly positively correlated with TNFSF4, CD276, ENTPD1 and CD70. GSEA revealed that MMP14 and COL12A1 were significantly enriched in epithelial mesenchymal transition, extracellular matrix receptor interaction, apical junction, and focal adhesion in PAAD development.

    Conclusions 

    Our study revealed that overexpression of MMP14 and COL12A1 is significantly correlated with PAAD patient poor prognosis. MMP14 and COL12A1 participate in regulating tumor immune interactions and might become promising biomarkers for PAAD.



    Kaller and Kamath [1] proposed two-parameter inverse Weibull distribution (IWD) to simulate the degradation of mechanical components of diesel engines. After that, IWD is considered an appropriate model to analyze lifetime data. For example, Abhijit and Anindya [2] found that IWD is superior to the normal distribution when using ultrasonic pulse velocity to measure concrete structures. Elio et al. [3] proposed a new model generated by appropriate mixing of IWD for modeling under extreme wind speed conditions. Langlands et al. [4] observed that breast cancer mortality data can be modeled and analyzed by IWD. Beyond that, IWD is widely used in reliability research. For example, Bi and Gui [5] considered the estimation of stress-strength reliability of IWD. They proposed an approximate maximum likelihood estimation for point and confidence interval estimations. Bayesian estimator and highest posterior density (HPD) confidence interval were derived using Gibbs sampling. Based on adaptive type-Ⅰ progressive hybrid censored scheme, Azm et al. [6] studied the estimation of unknown parameters of IWD when the data were competing risks data. The maximum likelihood estimation and Bayesian estimation were discussed. The asymptotic confidence intervals, the bootstrap confidence intervals and the HPD confidence intervals were derived. Then, two sets of real data were studied to illustrate maximum likelihood estimation and Bayesian estimation. Alslman and Helu [7] assumed that the two components were independent and identically distributed and considered the estimation of stress-strength reliability for IWD. Its estimators were derived by maximum likelihood estimation and maximum product of spacing method and compared using computer simulation. Shawky and Khan [8] assumed that stress and strength both followed IWD, and they focused on the multi-component stress-strength model. The estimation of reliability was obtained by maximum likelihood estimation. Monte Carlo simulation results indicate that the proposed estimating methods are effective.

    The probability density function (PDF), the cumulative distribution function (CDF) and the reliability function of IWD are respectively given by

    f(t;η,λ)=ηλtλ1eηtλ,t>0, η>0 , λ>0 (1.1)
    F(t;η,λ)=eηtλ,t>0, η>0 , λ>0 (1.2)

    and

    R(t)=1eηtλ. (1.3)

    Here, η is rate parameter and λ is shape parameter. For convenience, the PDF (1.1) of IWD will be denoted by IW(η,λ).

    The assessment of product reliability often relies on the collection of life data, which can be obtained through a life test. This test involves observing whether a group of test samples fail during the test and recording their corresponding failure time. If the life test continues until all the test samples fail, the failure time can be recorded for all the samples, resulting in complete data. However, if the test stops before all the test samples fail, the data collected are called censored data. With the continuous advancement of science and technology, products are becoming more reliable and have longer lifespans. Collecting complete data in a life test can be expensive, making reliability analysis based on censored data a popular research topic among scholars. A progressive type-Ⅱ censored sample can be expressed as follows: consider an experiment where n units are subjected to a life test at time zero, and the experimenter decides beforehand the number of failures to be observed, denoted by r. Upon observing the first failure time T1, Q1 out of the remaining n1 surviving units are randomly selected and removed. At the second observed failure time T2, Q2 out of the remaining n2Q1 surviving units are randomly selected and removed. This process continues until the r-th failure is observed at time Tr, and the remaining Qr=nrQ1Q2...Qr1 surviving units are all removed. The sample T=(T1,T2,...,Tr) is referred to as a progressively type-Ⅱ censored sample of size r from a sample of size n with censoring scheme Q=(Q1,Q2,...,Qr).

    IWD is one of the commonly used lifetime distributions in reliability estimation [5,6,7,8]. Most of the estimation methods are maximum likelihood estimation and Bayesian estimation, and there is a lack of research on inverse moment estimation. Therefore, this paper aims to provide three methods to compute the point estimations and construct generalized confidence intervals of unknown parameters.

    The rest of this paper is arranged as follows: In Section 2, the maximum likelihood estimators (MLEs) are obtained by Newtown-Raphson method. The Lindley approximation is proposed to derive the Bayesian estimators (BEs) in Section 3. The inverse moment estimators (IMEs) and the construction of the generalized confidence intervals (GCIs) are discussed in Section 4. In Section 5, Monte Carlo simulation is conducted to evaluate the effect of these methods. Section 6 gives a set of real data as a demonstration. Finally, Section 7 gives the conclusions of this paper.

    In this section, we will discuss the MLEs of η, λ and R(t). Due to the nonlinear nature of the likelihood equations, the Newton-Raphson method is considered to solve likelihood equations numerically.

    Let T=(T1,T2,...,Tr) be the collected progressive type-Ⅱ sample under the censoring scheme Q=(Q1,Q2,...,Qr). Denote t=(t1,t2,...,tr) as the observation of T. We can easily get the likelihood function l(η,λ;t) as follows:

    l(η,λ;t)=δηrλrri=1tλ1ieηtλi(1eηtλi)Qi, (2.1)

    where δ=n(nQ11)(nQ1Q22)...(nQ1Q2...Qr1r+1).

    Then the log-likelihood function L(η,λ;t) is

    L(η,λ;t)=lnl(η,λ;t)=lnδ+rlnηλri=1[(λ+1)lnti+ηtλiQiln(1eηtλi)]. (2.2)

    Thus, the partial derivatives of L(η,λ;t) with respect to η and λ are respectively given by

    L(η,λ;t)η=rηri=1[tλiQitλiexp(ηtλi)1exp(ηtλi)], (2.3)
    L(η,λ;t)λ=rλri=1[lntiηtλilnti+ηQitλiexp(ηtλi)lnti1exp(ηtλi)]. (2.4)

    Denote the MLEs of η and λ as ˆηML and ˆλML respectively, and they are the solutions of likelihood equations (2.5). According to the invariance of the maximum likelihood estimation, the MLE ˆRML(t) is obtained by replacing the parameters with ˆηML and ˆλML. Since (2.3) and (2.4) are non-linear, the Newtown-Raphson method is considered to solve likelihood equations numerically. The elements of the Jacobi matrix are given from (2.6) to (2.9).

    {L(η,λ;t)η=0L(η,λ;t)λ=0 (2.5)
    2L(η,λ;t)η2=rη2ri=1Qit2λiexp(ηtλi)[1exp(ηtλi)]2 (2.6)
    2L(η,λ;t)ηλ=ri=1[tλilnti+Qitλieηtλi(lnti)(eηtλi+ηtλi1)(1eηtλi)2] (2.7)
    2L(η,λ;t)λη=ri=1[tλilnti+Qitλieηtλi(lnti)(eηtλi+ηtλi1)(1eηtλi)2] (2.8)
    2L(η,λ;t)λ2=rλ2ηri=1[tλi(lnti)2Qi(lnti)2tλieηtλi(eηtλi+ηtλi1)(1eηtλi)2]. (2.9)

    Define

    H(θ)=[L(η,λ;t)ηL(η,λ;t)λ]

    and

    H(θ)=[2L(η,λ;t)η22L(η,λ;t)ηλ2L(η,λ;t)λη2L(η,λ;t)λ2],

    where θ=(η,λ). The steps involved in Newton-Raphson iteration method for obtaining the MLEs of η and λ are given below.

    Step 1. Pick an arbitrary starting estimate θ0, and desired precision ε=105.

    Step 2. Update θ0 as θnew=θ0[H(θ0)]1H(θ0), where [H(θ0)]1 is the inverse matrix of H(θ0).

    Step 3. If |θnewθ0|ε, then ˆθML=θnew.

    Step 4. If |θnewθ0|>ε, set θ0=θnew and return to Step 2.

    Step 5. Repeat from Step 2 to Step 4 until the condition in Step 3 is achieved.

    Statistical inference requires three kinds of information: overall information, sample information and prior information. The statistical inference based on the first two kinds of information is called classical statistics, and the statistical inference based on comprehensive consideration of the three kinds of information is called Bayes statistics. Prior information already exists before sampling, which mostly comes from experience and historical data. The distribution obtained by processing prior information is called a prior distribution. We all know that a random variable can be described by a certain distribution. Bayesian scholars believe that an unknown parameter can be regarded as a random variable. In other words, an unknown parameter can also be described by a certain distribution, that is, a prior distribution. Kundu and Howlader [9] considered the estimation of parameters of IWD using the Bayesian approach under the squared error loss function when the sample is a type-Ⅱ censoring sample. Akgul et al. [10] discussed Bayes estimation of the step-stress partially accelerated life test model with type-Ⅰ censored sample for the IWD. The point estimators were obtained using the Lindley approximation and Tierney–Kadane approximation. The credible intervals were constructed using the Gibbs sampling method. Helu and Samawi [11] considered the Bayesian inferences based on IWD based on progressive first-failure censored data. The point estimators were derived under three loss functions. Additionally, the estimators were calculated by Lindley approximation. Based on generalized adaptive progressively hybrid censored sample, Lee [12] considered the estimation of uncertainty measure for IWD. For the BE and HPD confidence interval, the Tierney-Kadane approximation and importance sampling technique were proposed.

    In this section, the BEs of η, λ and R(t) are derived under the symmetric entropy (SE) loss function, scale squared error (SSE) loss function and LINEX loss function. Since there is a complex ratio of two integrals in BEs, Lindley approximation is proposed to solve this problem.

    (i) The SE loss function is defined as (Xu et al. [13]):

    S1(θ,ˆθ)=θˆθ+ˆθθ2. (3.1)

    (ii) The SSE loss function is defined as (Song et al. [14]):

    S2(θ,ˆθ)=(θˆθ)2θd. (3.2)

    (iii) The LINEX loss function is defined as (Varian [15]):

    S3(θ,ˆθ)=ea(ˆθθ)a(ˆθθ)1 , a>0, (3.3)

    where ˆθ is the estimator of unknown parameter θ and d is a nonnegative integer.

    As an important part of Bayesian estimation, the selection of prior distribution will directly affect the final Bayesian estimation. It usually follows two rules making full use of prior information, such as empirical and historical data and being convenient for computational use. The most widely used prior distributions are mainly non-informative prior distribution, conjugate prior distribution and hierarchical prior distribution. The gamma prior belongs to the conjugate prior, which makes the computation process of estimation results easier.

    Assume the prior distributions of η and λ are gamma prior. η follows Gamma(a1,b1) and λ follows Gamma(a2,b2).

    π(η)ηb11ea1η a1>0, b1>0. (3.4)
    π(λ)λb21ea2λ a2>0, b2>0. (3.5)

    Based on (3.4) and (3.5), the joint prior distribution is

    π(η,λ)ηb11λb21ea1ηa2λ. (3.6)

    Using (2.1) and (3.6), the posterior distribution is

    π(η,λ|T)=Kηr+b11λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qi, (3.7)

    where K=[+0+0ηr+b11λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ]1.

    Based on (3.7), the margin posterior distribution of η is

    π(η|T)=Kηr+b11ea1η+0[λr+b21ea2λri=1tλ1ieηtλi(1eηtλi)Qi]dλ. (3.8)

    The margin posterior distribution of λ is

    π(λ|T)=Kλr+b21ea2λ+0[ηr+b11ea1ηri=1tλ1ieηtλi(1eηtλi)Qi]dη. (3.9)

    Lindley [16] proposed an approximation algorithm to calculate the ratio of two integrals in the form:

    I(t)=E[W(η,λ)|T]=W(η,λ)eL(η,λ;t)+J(η,λ)d(η,λ)eL(η,λ;t)+J(η,λ)d(η,λ). (3.10)

    Here is a continuous function in η and λ, L(η,λ;t) as shown in (2.2) and J(η,λ) is the logarithm of joint prior distribution (3.6). This ratio usually occurs in BE, which is why the Lindley approximation is often used to calculate the Bayesian estimator.

    The expression (3.10) can be approximated by (3.11) under regularity conditions or with a large sample size. Here A, B and C are given by (3.12). Lηηη denotes the third derivative of log-likelihood function (2.2) for η, and ˆLηηη represents the value of Lηηη at η=ˆηML. ψij is the element of inverse matrix of Lij (i,j=η,λ), and ˆψij represents the value of ψij at η=ˆηML and λ=ˆλML. Other terms are defined as the same as the above rules. The detailed expressions are presented in (3.13) to (3.18).

    I(t)=W(ˆηML,ˆλML)+12(A+B+C) (3.11)
    A=(ˆWηη+2ˆWηˆJη)ˆψηη+(ˆWλη+2ˆWλˆJη)ˆψλη+(ˆWηλ+2ˆWηˆJλ)ˆψηλ+(ˆWλλ+2ˆWλˆJλ)ˆψλλB=(ˆWηˆψηη+ˆWλˆψηλ)(ˆLηηηˆψηη+ˆLηληˆψηλ+ˆLληηˆψλη+ˆLλληˆψλλ)C=(ˆWηˆψλη+ˆWλˆψλλ)(ˆLηηλˆψηη + ˆLηλλˆψηλ+ˆLληλˆψλη+ˆLλλλˆψλλ) (3.12)
    Lηηη=2rη3+ri=1Qit3λieηtλi(1+eηtλi)(1eηtλi)3 (3.13)
    Lηηλ=2ri=1Qit2λieηtλilnti(1eηtλi)2ηri=1Qit3λieηtλi(lnti)(1+eηtλi)(1eηtλi)3 (3.14)
    Lληλ=ri=1tλi(lnti)2+η2ri=1Qit3λieηtλi(lnti)2(1+eηtλi)(1eηtλi)33ηri=1Qit2λieηtλi(lnti)2(1eηtλi)2+ri=1Qitλieηtλi(lnti)21eηtλi (3.15)
    Lλλλ=2rλ3+ηri=1tλi(lnti)3η3ri=1Qit3λieηtλi(lnti)3(1+eηtλi)(1eηtλi)3+η2ri=1Qit2λieηtλi(lnti)3(1eηtλi)2+ηri=1Qitλieηtλi(lnti)3(1+eηtλi)(1eηtλi)2 (3.16)
    Lηλη=Lληη=Lηηλ , Lλλη=Lηλλ=Lληλ (3.17)
    Jη=b11ηa1 , Jλ=b21λa2. (3.18)

    Lemma 1. Suppose that T is a random sample. The BE ˆθSE of unknown parameter θ under the SE loss function (3.1) for any prior distribution π(θ) is

    ˆθSE=[E(θ|T)E(θ1|T)]12, (3.19)

    where E(θ|T) and E(θ1|T) denote the posterior expectations of θ and θ1.

    Proof. Based on the SE loss function (3.1), the Bayesian risk of ˆθSE is

    R(ˆθSE)=Eθ(E(S1(θ,ˆθSE)|T)).

    To minimize R(ˆθSE), only need to minimize E(S1(θ,ˆθSE)|T). Denote h1(ˆθSE)=E(S1(θ,ˆθSE)|T) for convenience.

    Because

    h1(ˆθSE)=ˆθSE1E(θ|T)+ˆθSEE(θ1|T)2,

    and the derivative is

    h1(ˆθSE)=ˆθSE2E(θ|T)+E(θ1|T).

    The BE ˆθSE can be obtained by solving the equation h1(ˆθSE)=0.

    According to Lemma 1, the BEs ˆηSE, ˆλSE and ˆRSE(t) under the SE loss function can be written as:

    ˆηSE=[E(η|T)E(η1|T)]12, (3.20)
    ˆλSE=[E(λ|T)E(λ1|T)]12, (3.21)

    and

    ˆRSE(t)=[E(R(t)|T)E(R1(t)|T)]12. (3.22)

    From the marginal posterior distribution (3.8), the BE (3.20) may be written as

    ˆηSE=[+0ηπ(η|T)dη+0η1π(η|T)dη]12=[+0+0ηr+b1λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidλdη+0+0ηr+b12λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidλdη]12. (3.23)

    From the marginal posterior distribution (3.9), the BE (3.21) may be written as

    ˆλSE=[+0λπ(λ|T)dλ+0λ1π(λ|T)dλ]12=[+0+0λr+b2ηr+b11ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ+0+0λr+b22ηr+b11ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ]12. (3.24)

    From the posterior distribution (3.7), the BE (3.22) may be written as

    ˆRSE(t)=[+0+0(1eηtλ)π(η,λ|T)dηdλ+0+0(1eηtλ)1π(η,λ|T)dηdλ]12=[+0+0(1eηtλ)ηr+b11λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ+0+0(1eηtλ)1ηr+b11λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ]12. (3.25)

    It is obvious that (3.23)–(3.25) cannot be evaluated explicitly. Thus, the Lindley approximation is used to approximate them.

    (i) When W(η,λ)=η, there are

    Wη=1 , Wλ=Wηη=Wηλ=Wλη=Wλλ=0. (3.26)

    Submitting W(η,λ)=η and (3.26) in the expression (3.11), the posterior expectation E(η|T) may be written as

    E(η|T)=ˆηML+ˆJηˆψηη+ˆJλˆψηλ+12[ˆψηη(ˆLηηηˆψηη+ˆLηληˆψηλ+ˆLληηˆψλη+ˆLλληˆψλλ)+ˆψλη(ˆLηηλˆψηη + ˆLηλλˆψηλ+ˆLληλˆψλη+ˆLλλλˆψλλ)]. (3.27)

    (ii) When W(η,λ)=η1, there are

    Wη=1η2 , Wηη=2η3 , Wλ=Wηλ=Wλη=Wλλ=0. (3.28)

    Submitting W(η,λ)=η1 and (3.28) in the expression (3.11), the posterior expectation E(η1|T) may be written as

    E(η1|T)=12ˆη2ML[ˆψηη(ˆLηηηˆψηη+ˆLηληˆψηλ+ˆLληηˆψλη+ˆLλληˆψλλ)ˆψλη(ˆLηηλˆψηη + ˆLηλλˆψηλ+ˆLληλˆψλη+ˆLλλλˆψλλ)]+ˆη1ML+(ˆη3MLˆη2MLˆJη)ˆψηηˆη2MLˆJλˆψηλ. (3.29)

    The BE ˆηSE of rate parameter η under the SE loss function can be obtained by submitting (3.27) and (3.29) in the expression (3.20).

    Using Lindley approximation, the BEs ˆλSE and ˆRSE(t) under SE loss function are obtained as similar to the above steps.

    Lemma2. Suppose that T is a set of simple random samples. The BE ˆθSSE of unknown parameter θ under the SSE loss function (3.2) for any prior distribution π(θ) is

    ˆθSSE=E(θ1d|T)E(θd|T). (3.30)

    Proof. The Bayesian risk of ˆθSSE based on SSE loss function (3.2) is

    R(ˆθSSE)=Eθ(E(S2(θ,ˆθSSE)|T)).

    Denote h2(ˆθSSE)=E(S2(θ,ˆθSSE)|T), and

    h2(ˆθSSE)=E(θ2d|T)2ˆθSSEE(θ1d|T)+ˆθ2SSEE(θd|T).

    The derivative of h2(ˆθSSE) is

    h2(ˆθSSE)=2ˆθSSEE(θd|T)2E(θ1d|T).

    Therefore, the BE ˆθSSE under the SSE loss function is derived by solving equation h2(ˆθSSE)=0.

    According to Lemma 2, the BEs ˆηSSE, ˆλSSE and ˆRSSE(t) under SSE loss function are presented in (3.31) and (3.33) respectively.

    ˆηSSE=E(η1d|T)E(ηd|T), (3.31)
    ˆλSSE=E(λ1d|T)E(λd|T), (3.32)

    and

    ˆRSSE(t)=E[R1d(t)|T]E[Rd(t)|T]. (3.33)

    From the marginal posterior distribution (3.8), the BE (3.31) may be written as

    ˆηSSE=+0η1dπ(η|T)dη+0ηdπ(η|T)dη=+0+0ηr+b1dλr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidλdη+0+0ηr+b1d1λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidλdη. (3.34)

    From the marginal posterior distribution (3.9), the BE (3.32) can be written as

    ˆλSSE=+0λ1dπ(λ|T)dλ+0λdπ(λ|T)dλ=+0+0λr+b2dηr+b11ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ+0+0λr+b21dηr+b11ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ. (3.35)

    From the posterior distribution (3.7), the BE (3.33) can be written as

    ˆRSSE(t)=+0+0R1d(t)π(η,λ|T)dηdλ+0+0Rd(t)π(η,λ|T)dηdλ=+0+0(1eηtλ)1dηr+b11λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ+0+0(1eηtλ)dηr+b11λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ. (3.36)

    Then, Lindley approximation is used to approximate (3.34) to (3.36).

    (i) When W(η,λ)=η1d, there are

    Wη=(1d)ηd , Wηη=d(1d)ηd1 , Wλ=Wηλ=Wλη=Wλλ=0. (3.37)

    Putting W(η,λ)=η1d and (3.37) into (3.11), the posterior expectation E(η1d|T) can be written as

    E(η1d|T)=ˆη1dML+(1d)ˆηdMLˆJηˆψηη+(1d)ˆηdMLˆJλˆψηλ+12[d(1d)ˆηd1MLˆψηη+(1d)ˆηdMLˆψηη(ˆLηηηˆψηη+ˆLηληˆψηλ+ˆLληηˆψλη+ˆLλλαˆψλλ)+(1d)ˆηdMLˆψλη(ˆLηηλˆψηη + ˆLηλλˆψηλ+ˆLληλˆψλη+ˆLλλλˆψλλ)]. (3.38)

    (ii) When W(η,λ)=ηd, there are

    Wη=dηd1 , Wηη=d(d+1)ηd2 , Wλ=Wηλ=Wλη=Wλλ=0. (3.39)

    Putting W(η,λ)=ηd and (3.39) into (3.11), the posterior expectation E(ηd|T) can be written as

    E(ηd|T)=ˆηdMLdˆηd1MLˆJηˆψηηdˆηd1MLˆJλˆψηλ+12[d(d+1)ˆηd2MLˆψηηdˆηd1MLˆψηη(ˆLηηηˆψηη+ˆLηληˆψηλ+ˆLληηˆψλη+ˆLλληˆψλλ)dˆηd1MLˆψλη(ˆLηηλˆψηη + ˆLηλλˆψηλ+ˆLληλˆψλη+ˆLλλλˆψλλ)]. (3.40)

    Hence the BE ˆηSSE under the SSE loss function are obtained by submitting (3.38) and (3.40) in (3.31).

    Using Lindley approximation, the BEs ˆλSSE and ˆRSSE(t) under SSE loss function can be obtained by the similar steps.

    Lemma 3. Suppose that T is a set of simple random samples. The BE ˆθL of unknown parameter θ under the LINEX loss function (3.3) for any prior distribution π(θ) is

    ˆθL=1aln[E(eaθ|T)]. (3.41)

    Proof. The Bayesian risk of ˆθL based on LINEX loss function (3.3) is

    R(ˆθL)=Eθ(E(S3(θ,ˆθL)|T)).

    Denote h3(ˆθL)=E(S3(θ,ˆθL)|T), and

    h3(ˆθL)=E[ea(ˆθLθ)|T]aˆθL+aE(θ|T).

    The derivative of h3(ˆθL) is

    h3(ˆθL)=aea(ˆθLθ)E[ea(ˆθLθ)|T]a.

    Therefore, the BE ˆθL under the LINEX loss function is derived by solving equation h3(ˆθL)=0.

    It follows from Lemma 3 that the BEs under LINEX loss function are

    ˆηL=1aln[E(eaη|T)] (3.42)
    ˆλL=1aln[E(eaλ|T)] (3.43)
    ˆRL(t)=1aln[E(exp(aeηtλ)|T)]. (3.44)

    Subsequently, (3.42)–(3.44) can be written as

    ˆηL=1aln[+0eaηπ(η|T)dη]=1aln[K+0+0ηr+b11λr+b21ea1ηa2λaηri=1tλ1ieηtλi(1eηtλi)Qidηdλ] (3.45)
    ˆλL=1aln[+0eaλπ(λ|T)dλ]=1aln[K+0+0λr+b21ηr+b11ea1ηa2λaλri=1tλ1ieηtλi(1eηtλi)Qidηdλ] (3.46)
    ˆRL(t)=1aln[+0+0exp(aeηtλ)π(η,λ|T)dηdλ]=1aln[K+0+0exp(aeηtλ)ηr+b11λr+b21ea1ηa2λri=1tλ1ieηtλi(1eηtλi)Qidηdλ]. (3.47)

    Next, the explicit expressions of these BEs are obtained by using the Lindley approximation. When W(η,λ)=eaη, there are

    Wη=aeaη, Wηη=a2eaη, Wλ=Wηλ=Wλη=Wλλ=0. (3.48)

    According to Lindley's formula (3.11), the posterior expectation E(eaη|T) can be written as

    E(eaη|T)=eaˆηML+12[(a2eaˆηML2aeaˆηMLˆJη)ˆψηη2aeaˆηMLˆJλˆψηλaeaˆηMLˆψηη(ˆLηηηˆψηη+ˆLηληˆψηλ+ˆLληηˆψλη+ˆLλληˆψλλ)aeaˆηMLˆψλη(ˆLηηλˆψηη + ˆLηλλˆψηλ+ˆLληλˆψλη+ˆLλλλˆψλλ)]. (3.49)

    The BE ˆηL under LINEX loss function is derived by substituting (3.49) into (3.42). The BEs ˆλL and ˆRL(t) can be acquired using a comparable method to the aforementioned steps, and therefore will not be reiterated here.

    In Sections 2 and 3, the MLEs and BEs have been derived. However, we cannot obtain the explicit forms of MLEs and BEs easily by using both methods. In addition, it is necessary to select the appropriate initial values when using the Newtown-Raphson iteration method. Therefore, the generalized pivot quantity is constructed for deriving IMEs and GCIs in this Section. Compared with the maximum likelihood estimation and Bayes estimation, the inverse moment estimation is much simpler in calculation. It only needs some mathematical transformations and finally solves the equations. Wang [17] proposed a new method and named it as inverse moment estimation method in 1992. Additionally, the method was applied to parameter estimation of Weibull distribution. After that, inverse moment estimation has been widely used and studied. For example, Luo et al. [18] used the inverse third-moment method when forecasting a single time series using a large number of predictors in the presence of a possible nonlinear forecast function. Qin and Yuan [19] proposed an ensemble of IMEs to explore the central subspace. Based on progressive censored data, Gao et al. [20] proposed the pivotal inference for inverse exponentiated Rayleigh distribution. The point estimators were derived using the method that combined pivotal quantity with inverse moment estimation.

    In this section, the IMEs and GCIs of η, λ and R(t) are obtained by constructing the generalized pivot quantity.

    Definition 1. Assume that T is a random variable and t is the observation of T, and θ1 is an interest parameter and θ2 is a nuisance parameter. A function G(T;t,θ1,θ2) is called a generalized pivotal quantity if it satisfies the following conditions:

    (1) Given t, the distribution of G(T;t,θ1,θ2) is unrelated to both θ1 and θ2.

    (2) Given t, the observation G(t;t,θ1,θ2) of generalized pivotal quantity G(T;t,θ1,θ2) is unrelated to θ2.

    First, let

    Xi=ηTλi, i=1,2,...,r. (4.1)

    The distribution of Xi is

    FX(xi)=P(Xixi)=P(ηTλixi)=1exi. (4.2)

    Let Exp(1) be the standard exponential distribution. It is obvious that XiExp(1), and Xr<Xr1<...<X1. Let

    {S1=rXrS2=(r1)(Xr1Xr)S3=(r2)(Xr2Xr1)...Sr=X1X2. (4.3)

    Then, S1,S2,...,Sr are independent of each other and SiExp(1). Denote U=2ri=1Si and V=2S1, so U follows {{\mathtt{χ}}^{\text{2}}} distribution with 2r - 2 degrees of freedom and V follows {{\mathtt{χ}}^{\text{2}}} distribution with 2 degrees of freedom. Finally, let

    {G_1} = {{\frac{V}{2}} \mathord{\left/ {\vphantom {{\frac{V}{2}} {\frac{U}{{2r - 2}}}}} \right. } {\frac{U}{{2r - 2}}}} = \frac{{r(r - 1)T_r^{ - \lambda }}}{{\sum\limits_{i = 1}^r {T_i^{ - \lambda }} - rT_r^{ - \lambda }}} (4.4)
    {G_2} = U + V = 2\eta \sum\limits_{i = 1}^r {T_i^{ - \lambda }} . (4.5)

    Therefore, {G_1} and {G_2} are independent, {G_1} follows {\text{F}} distribution with 2 and 2r - 2 degrees of freedom and {G_2} follows {{\mathtt{χ}}^{\text{2}}} distribution with 2r degrees of freedom. According to Definition 1, {G_1} is the generalized pivotal quantity of \lambda , but {G_2} is neither a generalized pivotal quantity of \eta nor \lambda . Since (r - 1){(r - 2)^{ - 1}} is the mean of {\text{F}}(2, 2r - 2) and 2r is the mean of {{\mathtt{χ}}^{\text{2}}}(2r), Theorem 1 can be derived.

    Theorem 1. Let T = ({T_1}, {T_2}, ..., {T_r}) be a progressive type-Ⅱ censored sample following {\text{IW(}}\eta {\text{, }}\lambda {\text{)}}, and let Q = ({Q_1}, {Q_2}, ..., {Q_r}) be the censoring scheme. Denote t = ({t_1}, {t_2}, ..., {t_r}) as the observation of T. The IME {\hat \eta _G} of \eta and the IME {\hat \lambda _G} of \lambda are determined by the following expressions. The IME {\hat R_G}(t) is obtained by replacing the parameters with {\hat \eta _G} and {\hat \lambda _G}.

    \left\{ \begin{array}{l} {G_1} = \frac{{r(r - 1)t_r^{ - \lambda }}}{{\sum\limits_{i = 1}^r {t_i^{ - \lambda }} - rt_r^{ - \lambda }}} = \frac{{r - 1}}{{r - 2}} \hfill \\ {G_2} = 2\eta \sum\limits_{i = 1}^r {t_i^{ - {{\hat \lambda }_G}}} = 2r \hfill \\ \end{array} \right.. (4.6)

    This section will discuss the GCIs by generalized pivotal quantity.

    Lemma 3. Suppose that a set of constants {k_i} (i = 1, 2, ..., r) satisfy 0 < {k_1} < {k_2} < ... < {k_r} and denote G(\lambda) = \frac{{r(r - 1)k_r^{ - \lambda }}}{{\sum\limits_{i = 1}^r {k_i^{ - \lambda }} - rk_r^{ - \lambda }}}.

    (i) G(\lambda) decreases monotonically when \lambda > 0;

    (ii) The equation G(\lambda) = k has only one solution, which k > 0 and k is a constant.

    Proof. (i) The derivative of G(\lambda) is

    \begin{array}{l} G'(\lambda ) = r(r - 1)k_r^{ - \lambda }[\sum\limits_{i = 1}^r {k_i^{ - \lambda }\ln {k_i}} - (\ln {k_r})\sum\limits_{i = 1}^r {k_i^{ - \lambda }} ] \\ = r(r - 1)k_r^{ - \lambda }({k_1}\ln {k_1} + {k_2}\ln {k_2} + ... + {k_r}\ln {k_r} - {k_1}\ln {k_r} - {k_2}\ln {k_r} - ... - {k_r}\ln {k_r}) \\ = r(r - 1)k_r^{ - \lambda }[{k_1}(\ln {k_1} - \ln {k_r}) + {k_2}(\ln {k_2} - \ln {k_r}) + ... + {k_{r - 1}}(\ln {k_{r - 1}} - \ln {k_r})] \\ \end{array} .

    According to 0 < {k_1} < {k_2} < ... < {k_r}, it can be derived 0 < \ln {k_1} < \ln {k_2} < ... < \ln {k_r}. That is \ln {k_i} - \ln {k_r} < 0 (i = 1, 2, ..., r - 1). Therefore, G(\lambda) decreases monotonically when \lambda > 0.

    (ii) Suppose that the equation G(\lambda) = k has two unequal solutions, {\lambda _1} and {\lambda _2} respectively. Based on G({\lambda _1}) = G({\lambda _2}), there is

    \frac{{r(r - 1)k_r^{ - {\lambda _1}}}}{{\sum\limits_{i = 1}^r {k_i^{ - {\lambda _1}}} - rk_r^{ - {\lambda _1}}}} = \frac{{r(r - 1)k_r^{ - {\lambda _2}}}}{{\sum\limits_{i = 1}^r {k_i^{ - {\lambda _2}}} - rk_r^{ - {\lambda _2}}}}.

    That is

    \frac{1}{{\sum\limits_{i = 1}^r {{{(\frac{{{k_i}}}{{{k_r}}})}^{ - {\lambda _1}}}} - r}} = \frac{1}{{\sum\limits_{i = 1}^r {{{(\frac{{{k_i}}}{{{k_r}}})}^{ - {\lambda _2}}}} - r}} .

    Here, {(\frac{{{k_i}}}{{{k_r}}})^{ - \lambda }} is monotone because of \frac{{{k_i}}}{{{k_r}}} \geqslant 1. Hence the above expression is inconsistent with the supposition, and the equation G(\lambda) = k has only one solution.

    Theorem 2. Let T = ({T_1}, {T_2}, ..., {T_r}) with observation t = ({t_1}, {t_2}, ..., {t_r}) be a progressive type-Ⅱ censored sample following {\text{IW(}}\eta {\text{, }}\lambda {\text{)}}, and let Q = ({Q_1}, {Q_2}, ..., {Q_r}) be the censoring scheme. {{\text{F}}_\omega }(2, 2r - 2) and {\mathtt{χ}}_\omega ^2(2r) denote the upper quantile of {\text{F}}(2, 2r - 2) and {{\mathtt{χ}}^2}(2r) respectively with \omega = \frac{{1 - \sqrt {1 - \gamma } }}{2}. The 100(1 - \gamma)\% GCIs of \eta and \lambda are given as follows:

    \left\{ \begin{array}{l} \varphi ({t_1},...,{t_r},{{\text{F}}_{1 - \omega }}(2,2r - 2)) < \lambda < \varphi ({t_1},...,{t_r},{{\text{F}}_\omega }(2,2r - 2)) \hfill \\ {(2\sum\limits_{i = 1}^r {t_i^{ - {{\hat \lambda }_G}}} )^{ - 1}}{\mathtt{χ}}_\omega ^2(2r) < \eta < {(2\sum\limits_{i = 1}^r {t_i^{ - {{\hat \lambda }_G}}} )^{ - 1}}{\mathtt{χ}}_{1 - \omega }^2(2r) \hfill \\ \end{array} \right. (4.7)

    where \varphi ({t_1}, ..., {t_r}, {{\text{F}}_{1 - \omega }}(2, 2r - 2)) is the solution of equation (4.8) and \varphi ({t_1}, ..., {t_r}, {{\text{F}}_\omega }(2, 2r - 2)) is the solution of Eq (4.9).

    \frac{{r(r - 1)t_r^{ - \lambda }}}{{\sum\limits_{i = 1}^r {t_i^{ - \lambda }} - rt_r^{ - \lambda }}} = {{\text{F}}_{1 - \omega }}(2,2r - 2) (4.8)
    \frac{{r(r - 1)t_r^{ - \lambda }}}{{\sum\limits_{i = 1}^r {t_i^{ - \lambda }} - rt_r^{ - \lambda }}} = {{\text{F}}_\omega }(2,2r - 2). (4.9)

    Proof. From Section 4.1, there are {G}_{1}~\text{F}(2, 2r-2) and {G_2} \sim {{\mathtt{χ}}^2}(2r). {G_1} and {G_2} are independent, so

    \begin{array}{l} P({{\text{F}}_{1 - \omega }}(2,2r - 2) < {G_1} < {{\text{F}}_\omega }(2,2r - 2),{\mathtt{χ}}_\omega ^2(2r) < {G_2} < {\mathtt{χ}}_{1 - \omega }^2(2r)) \hfill \\ = P({{\text{F}}_{1 - \omega }}(2,2r - 2) < {G_1} < {{\text{F}}_\omega }(2,2r - 2)) \cdot P({\mathtt{χ}}_\omega ^2(2r) < {G_2} < {\mathtt{χ}}_{1 - \omega }^2(2r)) \hfill \\ = \sqrt {1 - \gamma } \cdot \sqrt {1 - \gamma } \hfill \\ = 1 - \gamma \hfill \\ \end{array} .

    The {{\text{F}}_{1 - \omega }}(2, 2r - 2) < {G_1} < {{\text{F}}_\omega }(2, 2r - 2) may be written as

    {{\text{F}}_{1 - \omega }}(2,2r - 2) < \frac{{r(r - 1)t_r^{ - \lambda }}}{{\sum\limits_{i = 1}^r {t_i^{ - \lambda }} - rt_r^{ - \lambda }}} < {{\text{F}}_\omega }(2,2r - 2) .

    According to Lemma 3, {{\text{F}}_{1 - \omega }}(2, 2r - 2) and {{\text{F}}_\omega }(2, 2r - 2) are positive constants, the above inequation is equivalent to

    \varphi ({t_1},...,{t_r},{{\text{F}}_{1 - \omega }}(2,2r - 2)) < \lambda < \varphi ({t_1},...,{t_r},{{\text{F}}_\omega }(2,2r - 2)) .

    {\mathtt{χ}}_\omega ^2(2r) < {G_2} < {\mathtt{χ}}_{1 - \omega }^2(2r) is equivalent to

    {(2\sum\limits_{i = 1}^r {t_i^{ - {{\hat \lambda }_G}}} )^{ - 1}}{\mathtt{χ}}_\omega ^2(2r) < \eta < {(2\sum\limits_{i = 1}^r {t_i^{ - {{\hat \lambda }_G}}} )^{ - 1}}{\mathtt{χ}}_{1 - \omega }^2(2r) .

    In this Section, the proposed estimation methods are compared using MATLAB. For point estimates, the mean squared errors (MSEs) are calculated by Eq (5.1). For interval estimates, coverage probability (CP) is used to reflect the performance of GCIs. The simulation is carried out under true value ({\eta _{real}}, {\lambda _{real}}) = (2, 2) and different n, r and Q, and the trials are N at 1000 times. The hyper-parameter of the prior distribution is ({a_1}, {b_1}) = (2, 1.8) and ({a_2}, {b_2}) = (1.5, 2), and the parameters of SSE loss function and LINEX loss function are d = 4 and a = 4 respectively. The MSEs of \eta , and \lambda are shown in Tables 1 and 2 respectively, and the MSEs of R(t) are shown in Table 3 with t = 3. The CP values is shown in Table 4.

    Table 1.  The MSEs of \eta .
    n r Q MSE
    {\hat \eta _{ML}} {\hat \eta _{SE}} {\hat \eta _{SSE}} {\hat \eta _L} {\hat \eta _G}
    20 10 (3*1, 0*4, 7*1, 0*4) 0.4045 0.1702 0.2618 0.3882 0.4207
    (10*1, 0*9) 0.6676 0.1367 0.3823 0.4630 0.5111
    (2*5, 0*5) 0.5663 0.1397 0.4627 0.2966 0.3729
    20 (0*20) 0.3788 0.1225 0.2355 0.2871 0.2957
    30 10 (5*3, 0*2, 5*1, 0*4) 0.3418 0.1099 0.2446 0.2133 0.5184
    (20*1, 0*9) 0.3413 0.1399 0.3037 0.2509 0.2788
    (4*5, 0*5) 0.6002 0.1364 0.3790 0.2189 0.5100
    20 (0*10, 2*5, 0*5) 0.2588 0.0913 0.1663 0.1542 0.3119
    (10*1, 0*19) 0.2918 0.1106 0.2028 0.2170 0.1997
    (1*10, 0*10) 0.2529 0.1004 0.1790 0.1629 0.2052
    30 (0*30) 0.1962 0.0944 0.1454 0.1435 0.1687
    50 15 (2*4, 1*6, 0*5) 0.1479 0.0860 0.1356 0.1850 0.3282
    (35*1, 0*14) 0.2021 0.1098 0.1999 0.1703 0.1994
    (7*5, 0*10) 0.1516 0.0886 0.1450 0.1474 0.4038
    20 (5*6, 0*10, 0*4) 0.1304 0.0784 0.1153 0.1297 0.2861
    (30*1, 0*19) 0.1854 0.0969 0.1595 0.1506 0.1690
    (6*5, 0*15) 0.1316 0.0858 0.1324 0.1273 0.2458
    30 (3*4, 0*7, 1*8, 0*11) 0.1121 0.0689 0.0919 0.0975 0.2010
    (4*5, 0*25) 0.1270 0.0811 0.1137 0.1012 0.1412
    (20*1, 0*29) 0.1578 0.0916 0.1315 0.1108 0.1525
    50 (0*50) 0.1038 0.0667 0.0844 0.0903 0.1042

     | Show Table
    DownLoad: CSV
    Table 2.  The MSEs of \lambda .
    n r Q MSE
    {\hat \lambda _{ML}} {\hat \lambda _{SE}} {\hat \lambda _{SSE}} {\hat \lambda _L} {\hat \lambda _G}
    20 10 (3*1, 0*4, 7*1, 0*4) 0.4838 0.2817 0.2544 0.2704 0.5386
    (10*1, 0*9) 0.5354 0.1750 0.2800 0.3230 0.4666
    (2*5, 0*5) 0.4809 0.1760 0.2538 0.3093 0.5099
    20 (0*20) 0.1701 0.0966 0.1241 0.1230 0.3621
    30 10 (5*3, 0*2, 5*1, 0*4) 0.4990 0.1847 0.2592 0.2567 0.5616
    (20*1, 0*9) 0.4024 0.1763 0.2308 0.2739 0.4615
    (4*5, 0*5) 0.5383 0.1622 0.2823 0.2722 0.5173
    20 (0*10, 2*5, 0*5) 0.1760 0.0967 0.1166 0.1277 0.4387
    (10*1, 0*19) 0.1746 0.0979 0.1198 0.1160 0.3448
    (1*10, 0*10) 0.1874 0.1099 0.1303 0.1148 0.3156
    30 (0*30) 0.0982 0.0670 0.0800 0.0774 0.2799
    50 15 (2*4, 1*6, 0*5) 0.2545 0.1383 0.1596 0.1655 0.4156
    (35*1, 0*14) 0.1876 0.1183 0.1280 0.1448 0.3584
    (7*5, 0*10) 0.2201 0.1309 0.1416 0.1609 0.3567
    20 (5*6, 0*10, 0*4) 0.1587 0.1010 0.1093 0.1194 0.3233
    (30*1, 0*19) 0.1461 0.1004 0.1067 0.0938 0.3066
    (6*5, 0*15) 0.1500 0.1023 0.1121 0.1058 0.2882
    30 (3*4, 0*7, 1*8, 0*11) 0.1099 0.0760 0.0825 0.0848 0.2882
    (4*5, 0*25) 0.0946 0.0700 0.0761 0.0719 0.2754
    (20*1, 0*29) 0.0904 0.0672 0.0735 0.0728 0.2723
    50 (0*50) 0.0575 0.0447 0.0476 0.0488 0.2112

     | Show Table
    DownLoad: CSV
    Table 3.  The MSEs of R(t).
    n r Q MSE
    {\hat R_{ML}}(t) {\hat R_{SE}}(t) {\hat R_{SSE}}(t) {\hat R_L}(t) {\hat R_G}(t)
    20 10 (3*1, 0*4, 7*1, 0*4) 0.0088 0.0061 0.0113 0.0110 0.0129
    (10*1, 0*9) 0.0107 0.0069 0.0121 0.0129 0.0166
    (2*5, 0*5) 0.0090 0.0021 0.0111 0.0108 0.0142
    20 (0*20) 0.0052 0.0040 0.0096 0.0913 0.0128
    30 10 (5*3, 0*2, 5*1, 0*4) 0.0092 0.0064 0.0103 0.0129 0.0131
    (20*1, 0*9) 0.0091 0.0064 0.0123 0.0180 0.0166
    (4*5, 0*5) 0.0112 0.0080 0.0096 0.0129 0.0120
    20 (0*10, 2*5, 0*5) 0.0047 0.0037 0.0061 0.0119 0.0082
    (10*1, 0*19) 0.0049 0.0039 0.0058 0.0152 0.0122
    (1*10, 0*10) 0.0048 0.0038 0.0057 0.0081 0.0095
    30 (0*30) 0.0036 0.0030 0.0041 0.0068 0.0101
    50 15 (2*4, 1*6, 0*5) 0.0059 0.0045 0.0070 0.0066 0.0099
    (35*1, 0*14) 0.0063 0.0050 0.0078 0.0104 0.0127
    (7*5, 0*10) 0.0064 0.0051 0.0083 0.0083 0.0100
    20 (5*6, 0*10, 0*4) 0.0044 0.0036 0.0056 0.0079 0.0092
    (30*1, 0*19) 0.0053 0.0043 0.0062 0.0070 0.0111
    (6*5, 0*15) 0.0053 0.0044 0.0064 0.0088 0.0096
    30 (3*4, 0*7, 1*8, 0*11) 0.0034 0.0029 0.0039 0.0042 0.0072
    (4*5, 0*25) 0.0033 0.0029 0.0039 0.0045 0.0087
    (20*1, 0*29) 0.0032 0.0027 0.0037 0.0062 0.0091
    50 (0*50) 0.0019 0.0017 0.0021 0.0039 0.0085

     | Show Table
    DownLoad: CSV
    Table 4.  The CP values with confidence level 95%.
    n r Q \eta \lambda
    20 10 (3*1, 0*4, 7*1, 0*4) 0.897 0.970
    (10*1, 0*9) 0.976 0.987
    (2*5, 0*5) 0.937 0.974
    20 (0*20) 0.960 0.977
    30 10 (5*3, 0*2, 5*1, 0*4) 0.842 0.974
    (20*1, 0*9) 0.980 0.981
    (4*5, 0*5) 0.854 0.979
    20 (0*10, 2*5, 0*5) 0.826 0.958
    (10*1, 0*19) 0.977 0.978
    (1*10, 0*10) 0.930 0.977
    30 (0*30) 0.963 0.975
    50 15 (2*4, 1*6, 0*5) 0.889 0.974
    (35*1, 0*14) 0.976 0.982
    (7*5, 0*10) 0.832 0.986
    20 (5*6, 0*10, 0*4) 0.866 0.977
    (30*1, 0*19) 0.978 0.982
    (6*5, 0*15) 0.901 0.985
    30 (3*4, 0*7, 1*8, 0*11) 0.868 0.974
    (4*5, 0*25) 0.942 0.978
    (20*1, 0*29) 0.968 0.977
    50 (0*50) 0.957 0.977

     | Show Table
    DownLoad: CSV

    Balakrishnan and Sandhu [21] proposed an algorithm to produce progressive type-Ⅱ censored sample from any continuous distribution. The specific steps applied to the IWD are as follows:

    Step 1. Generate samples {w_1}, {w_2}, ..., {w_r} from U(0, 1), where {w_1}, {w_2}, ..., {w_r} are independent.

    Step 2. Let {v_i} = w_i^{{{(i + {Q_r} + {Q_{r - 1}} +... + {Q_{r - i + 1}})}^{ - 1}}} and {u_i} = 1 - {v_r}{v_{r - 1}}...{v_{r - i + 1}}.

    Step 3. Let {t_i} = {F^{ - 1}}({u_i}; {\eta _{real}}, {\lambda _{real}}), where F(\cdot) is the CDF (1.2) of IWD, i = 1, 2, ..., r.

    Then, {t_1} < {t_2} < ... < {t_r} are progressive type-Ⅱ censored data from {\text{IW(}}\eta {\text{, }}\lambda {\text{)}} with a censoring scheme Q. Calculation results can be found in Tables 13.

    MSE(\hat \theta ) = \frac{1}{N}\sum\limits_{i = 1}^N {{{({{\hat \theta }_i} - {\theta _{real}})}^2}} . (5.1)

    From Table 1 to Table 3, we have the following conclusions:

    (i) Obviously, considering the same n and r, the censoring scheme Q has a great influence on MSE.

    (ii) Considering the same n, r and Q, the BE of \eta under SE loss function is the better than the MLE and IME.

    (iii) Considering the same n, r and Q, the BE \lambda under SE loss function is better than others. However, the BE of \lambda under SSE loss function is close to the BE under LINEX loss function.

    (iv) Considering the same n, r and Q, for the reliability R(t), MSEs of MLEs and BEs under SE and SSE loss functions are relatively close, while, MSEs of BEs under LINEX loss function are larger than others.

    From Table 4, We know that CP values for \eta and \lambda are all close to 95%.

    There is a set of real data from Dumonceaux and Antle [22], which represents the maximum flood level (in millions of cubic feet per second) of the Susquehanna River at Harrisburg, Pennsylvania over 20 four-year periods (1890–1969) as:

    0.265, 0.269, 0.297, 0.315, 0.324, 0.338, 0.379, 0.379, 0.392, 0.402, 0.412, 0.416, 0.418, 0.423, 0.449, 0.484, 0.494, 0.613, 0.654, 0.740.

    According to the data, we can plot the empirical CDF and the CDF of the IWD, as shown in Figure1. In the IWD, we using the BEs under SE loss function as the value of parameter, i.e. \eta = 0.0336, \lambda = 2.0431. According to Figure 1, we can see that the IWD can well model the data. Therefore, we can conclude that this distribution is valid.

    Figure 1.  The empirical CDF and the CDF of IWD.

    Now, the real data with censoring scheme ({Q_1}, {Q_2}, ..., {Q_{10}}) = (1, 1, ..., 1) are as follows:

    0.265, 0.297, 0.324, 0.379, 0.392, 0.412, 0.418, 0.449, 0.494, 0.654.

    Before proceeding with the estimation, it is necessary to establish the existence and uniqueness of the maximum likelihood estimate. However, proving this can be a complicated process due to the nonlinearity of the system of Eq (2.5). For this reason, we visualize it through Figure 2, where L1 represents \frac{{\partial L(\eta, \lambda; t)}}{{\partial \eta }} in Eq (2.3) and L2 represents \frac{{\partial L(\eta, \lambda; t)}}{{\partial \lambda }} in Eq (2.4).

    Figure 2.  The Partial derivatives of log-likelihood function.

    From Figure 2, we know that the two curves intersect at only one point, indicating the presence of a unique MLE.

    The estimates and generalized confidence intervals that obtained by using these proposed methods are shown in Table 5.

    Table 5.  The results of real data analysis ({t_0} = 0.412).
    MLEs BEs IMEs GCIs
    SE SSE LINEX
    \eta 0.0582 0.0336 0.0196 0.0514 0.0238 (0.0101, 0.0732)
    \lambda 3.2009 2.0431 2.5710 2.9821 3.6513 (1.7307, 9.2871)
    R({t_0}) 0.6301 0.3859 0.3743 0.5330 0.4546

     | Show Table
    DownLoad: CSV

    In this paper, we have investigated the point estimation and interval estimation of parameters based on progressive type-Ⅱ censored sample for IWD. First, the Newton-Raphson iteration method is used to solve the likelihood equations of parameters and obtain their MLEs. Then, the BEs are derived based on SE and SSE loss functions, respectively. Finally, the IMEs are derived by generalized pivotal quantity. Additionally, the GCIs are also constructed by generalized pivotal quantity. Monte Carlo simulation is used to present the effect of the above estimators. The simulation results revealed that the estimators derived using Bayesian approach perform better than other methods in terms of MSE. Moreover, a real set of data is analyzed and the results coincide with simulation. Monte Carlo simulation results indicate that Bayesian estimation under the SE loss function works best among all the methods mentioned in this paper.

    The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.

    This research was funded by National Natural Science Foundation of China (No. 71661012).

    The authors declare there is no conflict of interest.



    [1] H. Zhu, T. Li, Y. Du, M. Li, Pancreatic cancer: challenges and opportunities, BMC Med., 16 (2018), 214. doi: 10.1186/s12916-018-1215-3
    [2] R. L. Siegel, K.D. Miller, A. Jemal, Cancer statistics, 2019, CA Cancer J. Clin., 69 (2019), 7-34. doi: 10.3322/caac.21551
    [3] J. Kleeff, M. Korc, M. Apte, C. La Vecchia, C. D. Johnson, A. V. Biankin, et al., Pancreatic cancer, Nat. Rev. Dis. Primers, 2 (2016), 16022. doi: 10.1038/nrdp.2016.22
    [4] A. Martín-Blázquez, C. Jiménez-Luna, C. Díaz, J. Martínez-Galán, J. Prados, F. Vicente, et al., Discovery of Pancreatic Adenocarcinoma Biomarkers by Untargeted Metabolomics, Cancers, 12 (2020), 1002. doi: 10.3390/cancers12041002
    [5] W. Lu, N. Li, F. Liao, Identification of key genes and pathways in pancreatic cancer gene expression profile by integrative analysis, Genes, 10 (2019), 612. doi: 10.3390/genes10080612
    [6] C. von Mering, M. Huynen, D. Jaeggi, S. Schmidt, P. Bork, B. Snel, STRING: a database of predicted functional associations between proteins, Nucleic Acids Res., 31 (2003), 258-261. doi: 10.1093/nar/gkg034
    [7] P. Shannon, A. Markiel, O. Ozier, N. S. Baliga, J. T. Wang, D. Ramage, et al., Cytoscape: a software environment for integrated models of biomolecular interaction networks, Genome Res., 13 (2003), 2498-2504. doi: 10.1101/gr.1239303
    [8] D. W. Huang, B. T. Sherman, Q. Tan, J. Kir, D. Liu, D. Bryant, et al., DAVID Bioinformatics Resources: expanded annotation database and novel algorithms to better extract biology from large gene lists, Nucleic Acids Res., 35 (2007), W169-W175. doi: 10.1093/nar/gkm415
    [9] Gene Ontology Consortium, The Gene Ontology Resource: 20 years and still GOing strong, Nucleic Acids Res., 47 (2019), D330-D338. doi: 10.1093/nar/gky1055
    [10] M. Kanehisa, Y. Sato, M. Kawashima, M. Furumichi, M. Tanabe, KEGG as a reference resource for gene and protein annotation, Nucleic Acids Res., 44 (2016), D457-D462. doi: 10.1093/nar/gkv1070
    [11] Z. Tang, C. Li, B. Kang, G. Gao, C. Li, Z. Zhang, GEPIA: a web server for cancer and normal gene expression profiling and interactive analyses, Nucleic Acids Res., 45 (2017), W98-W102. doi: 10.1093/nar/gkx247
    [12] T. Li, J. Fan, B. Wang, N. Traugh, Q. Chen, J.S. Liu, et al., TIMER: A Web Server for Comprehensive Analysis of Tumor-Infiltrating Immune Cells, Cancer Res., 77 (2017), e108-e110. doi: 10.1158/0008-5472.CAN-17-0307
    [13] B. Ru, C. N. Wong, Y. Tong, J. Y. Zhong, S. S. W. Zhong, W. C. Wu, et al., TISIDB: an integrated repository portal for tumor-immune system interactions, Bioinformatics, 35 (2019), 4200-4202. doi: 10.1093/bioinformatics/btz210
    [14] M. Franz, H. Rodriguez, C. Lopes, K. Zuberi, J. Montojo, G. D. Bader, et al., GeneMANIA update 2018, Nucleic Acids Res., 46 (2018), W60-W64. doi: 10.1093/nar/gky311
    [15] Y. Zhou, B. Zhou, L. Pache, M. Chang, A. H. Khodabakhshi, O. Tanaseichuk, et al., Metascape provides a biologist-oriented resource for the analysis of systems-level datasets, Nat. Commun., 10 (2019), 1523. doi: 10.1038/s41467-019-09234-6
    [16] A. Subramanian, H. Kuehn, J. Gould, P. Tamayo, J.P. Mesirov, GSEA-P: a desktop application for Gene Set Enrichment Analysis, Bioinformatics, 23 (2007), 3251-3253. doi: 10.1093/bioinformatics/btm369
    [17] H. Läubli, L. Borsig, Altered cell adhesion and glycosylation promote cancer immune suppression and metastasis, Front. Immunol., 10 (2019), 2120. doi: 10.3389/fimmu.2019.02120
    [18] M. Janiszewska, M.C. Primi, T. Izard, Cell adhesion in cancer: Beyond the migration of single cells, J. Biol. Chem., 295 (2020), 2495-2505. doi: 10.1074/jbc.REV119.007759
    [19] C. Walker, E. Mojares, A. Del Río Hernández, Role of Extracellular Matrix in Development and Cancer Progression, Int. J. Mol. Sci., 19 (2018), 3028. doi: 10.3390/ijms19103028
    [20] M. Wyganowska-Świątkowska, M. Tarnowski, D. Murtagh, E. Skrzypczak-Jankun, J. Jankun, Proteolysis is the most fundamental property of malignancy and its inhibition may be used therapeutically (Review), Int. J. Mol. Med., 43 (2019), 15-25.
    [21] S. Perumal, O. Antipova, J. P. Orgel, Collagen fibril architecture, domain organization, and triple-helical conformation govern its proteolysis, Proc. Natl. Acad. Sci., 105 (2008), 2824-2829. doi: 10.1073/pnas.0710588105
    [22] S. Xu, H. Xu, W. Wang, S. Li, H. Li, T. Li, et al., The role of collagen in cancer: from bench to bedside, J. Transl. Med., 17 (2019), 309. doi: 10.1186/s12967-019-2058-1
    [23] A. Bastidas-Ponce, K. Scheibner, H. Lickert, M. Bakhti, Cellular and molecular mechanisms coordinating pancreas development, Development, 144 (2017), 2873-2888. doi: 10.1242/dev.140756
    [24] M. Singh, N. Yelle, C. Venugopal, S. K. Singh, EMT: Mechanisms and therapeutic implications, Pharmacol. Ther., 182 (2018), 80-94. doi: 10.1016/j.pharmthera.2017.08.009
    [25] S. P. Turunen, O. Tatti-Bugaeva, K. Lehti, Membrane-type matrix metalloproteases as diverse effectors of cancer progression, Biochim. Biophys. Acta Mol. Cell Res., 1864 (2017), 1974-1988. doi: 10.1016/j.bbamcr.2017.04.002
    [26] J. F. Wang, Y. Q. Gong, Y. H. He, W. W. Ying, X. S. Li, X. F. Zhou, et al., High expression of MMP14 is associated with progression and poor short-term prognosis in muscle-invasive bladder cancer, Eur. Rev. Med. Pharmacol. Sci., 24 (2020), 6605-6615.
    [27] A. Kasurinen, S. Gramolelli, J. Hagström, A. Laitinen, A. Kokkola, Y. Miki, et al., High tissue MMP14 expression predicts worse survival in gastric cancer, particularly with a low PROX1, Cancer Med., 8 (2019), 6995-7005. doi: 10.1002/cam4.2576
    [28] Y. Jin, Z. Y. Liang, W. X. Zhou, L. Zhou, High MMP14 expression is predictive of poor prognosis in resectable hepatocellular carcinoma, Pathology, 52 (2020), 359-365.
    [29] F. Duan, Z. Peng, J. Yin, Z. Yang, J. Shang, Expression of MMP-14 and prognosis in digestive system carcinoma: a meta-analysis and databases validation, J. Cancer, 11 (2020), 1141-1150. doi: 10.7150/jca.36469
    [30] O. R. Grafinger, G. Gorshtein, T. Stirling, M. I. Brasher, M. G. Coppolino, β1 integrinmediated signaling regulates MT1-MMP phosphorylation to promote tumor cell invasion, J. Cell Sci., 133 (2020), jcs239152.
    [31] W. Jiang, Y. Zhang, K. T. Kane, M. A. Collins, D. M. Simeone, M. P. di Magliano, et al., CD44 regulates pancreatic cancer invasion through MT1-MMP, Mol. Cancer Res., 13 (2015), 9-15. doi: 10.1158/1541-7786.MCR-14-0076
    [32] D. R. Gerecke, P. F. Olson, M. Koch, J. H. Knoll, R. Taylor, D. L. Hudson, et al., Complete primary structure of two splice variants of collagen XⅡ, and assignment of alpha 1(XⅡ) collagen (COL12A1), alpha 1(IX) collagen (COL9A1), and alpha 1(XIX) collagen (COL19A1) to human chromosome 6q12-q13, Genomics, 41 (1997), 236-242. doi: 10.1006/geno.1997.4638
    [33] J. Sapudom, T. Pompe, Biomimetic tumor microenvironments based on collagen matrices, Biomater. Sci., 6 (2018), 2009-2024. doi: 10.1039/C8BM00303C
    [34] Y. H. Xu, J. L. Deng, L. P. Wang, H. B. Zhang, L. Tang, Y. Huang, et al., Identification of Candidate Genes Associated with Breast Cancer Prognosis, DNA Cell Biol., 39 (2020), 1205-1227. doi: 10.1089/dna.2020.5482
    [35] Y. Chen, W. Chen, X. Dai, C. Zhang, Q. Zhang, J. Lu, Identification of the collagen family as prognostic biomarkers and immune-associated targets in gastric cancer, Int. Immunopharmacol., 87 (2020), 106798. doi: 10.1016/j.intimp.2020.106798
    [36] Y. Wu, Y. Xu, Integrated bioinformatics analysis of expression and gene regulation network of COL12A1 in colorectal cancer, Cancer Med., 9 (2020), 4743-4755. doi: 10.1002/cam4.2899
    [37] Z. Xiang, J. Li, S. Song, J. Wang, W. Cai, W. Hu, et al., A positive feedback between IDO1 metabolite and COL12A1 via MAPK pathway to promote gastric cancer metastasis, J. Exp. Clin. Cancer Res., 38 (2019), 314. doi: 10.1186/s13046-019-1318-5
    [38] R. Januchowski, M. Świerczewska, K. Sterzyńska, K. Wojtowicz, M. Nowicki, M. Zabel, Increased Expression of Several Collagen Genes is Associated with Drug Resistance in Ovarian Cancer Cell Lines, J. Cancer, 7 (2016), 1295-1310. doi: 10.7150/jca.15371
    [39] D. Öhlund, O. Franklin, E. Lundberg, C. Lundin, M. Sund, Type Ⅳ collagen stimulates pancreatic cancer cell proliferation, migration, and inhibits apoptosis through an autocrine loop, BMC Cancer, 13 (2013), 154. doi: 10.1186/1471-2407-13-154
    [40] M. A. Shields, S. Dangi-Garimella, S. B. Krantz, D. J. Bentrem, H. G. Munshi, Pancreatic cancer cells respond to type I collagen by inducing snail expression to promote membrane type 1 matrix metalloproteinase-dependent collagen invasion, J. Biol. Chem., 286 (2011), 10495-10504. doi: 10.1074/jbc.M110.195628
    [41] A. Habtezion, M. Edderkaoui, S.J. Pandol, Macrophages and pancreatic ductal adenocarcinoma, Cancer Lett., 381 (2016), 211-216. doi: 10.1016/j.canlet.2015.11.049
    [42] M. Yu, R. Guan, W. Hong, Y. Zhou, Y. Lin, H. Jin, et al., Prognostic value of tumorassociated macrophages in pancreatic cancer: a meta-analysis, Cancer Manag. Res., 11 (2019), 4041-4058. doi: 10.2147/CMAR.S196951
    [43] A. Ocana, C. Nieto-Jiménez, A. Pandiella, A. J. Templeton, Neutrophils in cancer: prognostic role and therapeutic strategies, Mol. Cancer, 16 (2017), 137. doi: 10.1186/s12943-017-0707-7
    [44] A. Deicher, R. Andersson, B. Tingstedt, G. Lindell, M. Bauden, D. Ansari, Targeting dendritic cells in pancreatic ductal adenocarcinoma, Cancer Cell Int., 18 (2018), 85. doi: 10.1186/s12935-018-0585-0
    [45] C. Yang, H. Cheng, Y. Zhang, K. Fan, G. Luo, Z. Fan, et al., Anergic natural killer cells educated by tumor cells are associated with a poor prognosis in patients with advanced pancreatic ductal adenocarcinoma, Cancer Immunol. Immunother., 67 (2018), 1815-1823. doi: 10.1007/s00262-018-2235-8
    [46] S. Quintero-Fabián, R. Arreola, E. Becerril-Villanueva, J.C. Torres-Romero, V. AranaArgáez, J. Lara-Riegos, et al., Role of Matrix Metalloproteinases in Angiogenesis and Cancer, Front. Oncol., 9 (2019), 1370. doi: 10.3389/fonc.2019.01370
    [47] R. Shimizu-Hirota, W. Xiong, B. T. Baxter, S. L. Kunkel, I. Maillard, X.W. Chen, et al., MT1-MMP regulates the PI3Kδ·Mi-2/NuRD-dependent control of macrophage immune function, Genes Dev., 26 (2012), 395-413. doi: 10.1101/gad.178749.111
    [48] A. M. H. Larsen, D. E. Kuczek, A. Kalvisa, M. S. Siersbæk, M. L. Thorseth, A. Z. Johansen, et al., Collagen Density Modulates the Immunosuppressive Functions of Macrophages, J. Immunol., 205 (2020), 1461-1472. doi: 10.4049/jimmunol.1900789
    [49] D. E. Kuczek, A. M. H. Larsen, M. L. Thorseth, M. Carretta, A. Kalvisa, M. S. Siersbæk, et al., Collagen density regulates the activity of tumor-infiltrating T cells, J. Immunother. Cancer, 7 (2019), 68. doi: 10.1186/s40425-019-0556-6
    [50] E. L. Hopewell, C. Cox, S. Pilon-Thomas, L. L. Kelley, Tumor-infiltrating lymphocytes: Streamlining a complex manufacturing process, Cytotherapy, 21 (2019), 307-314. doi: 10.1016/j.jcyt.2018.11.004
    [51] H. Du, K. Hirabayashi, S. Ahn, N. P. Kren, S. A. Montgomery, X. Wang, et al., Antitumor Responses in the Absence of Toxicity in Solid Tumors by Targeting B7-H3 via Chimeric Antigen Receptor T Cells, Cancer Cell, 35 (2019), 221-237. doi: 10.1016/j.ccell.2019.01.002
    [52] J. Jacobs, V. Deschoolmeester, K. Zwaenepoel, C. Rolfo, K. Silence, S. Rottey, et al., CD70: An emerging target in cancer immunotherapy, Pharmacol. Ther., 155 (2015), 1-10. doi: 10.1016/j.pharmthera.2015.07.007
    [53] P. Yin, L. Gui, C. Wang, J. Yan, M. Liu, L. Ji, et al., Targeted delivery of CXCL9 and OX40L by mesenchymal stem cells elicits potent antitumor immunity, Mol. Ther., 28 (2020), 2553-2563. doi: 10.1016/j.ymthe.2020.08.005
    [54] J. Wu, Y. Wang, Z. Jiang, Immune induction identified by TMT proteomics analysis in autoinducer-2 treated macrophages, Expert Rev. Proteomics, 17 (2020), 175-185. doi: 10.1080/14789450.2020.1738223
    [55] C. Liang, J. Xu, Q. Meng, B. Zhang, J. Liu, J. Hua, et al., TGFB1-induced autophagy affects the pattern of pancreatic cancer progression in distinct ways depending on SMAD4 status, Autophagy, 16 (2020), 486-500. doi: 10.1080/15548627.2019.1628540
    [56] K. C. Ohaegbulam, A. Assal, E. Lazar-Molnar, Y. Yao, X. Zang, Human cancer immunotherapy with antibodies to the PD-1 and PD-L1 pathway, Trends Mol. Med., 21 (2015), 24-33. doi: 10.1016/j.molmed.2014.10.009
    [57] S. S. Potter, Single-cell RNA sequencing for the study of development, physiology and disease, Nat. Rev. Nephrol., 14 (2018), 479-492. doi: 10.1038/s41581-018-0021-7
    [58] J. Cheng, J. Zhang, Z. Wu, X. Sun, Inferring microenvironmental regulation of gene expression from single-cell RNA sequencing data using scMLnet with an application to COVID-19, Brief. Bioinform., 22 (2021), 988-1005. doi: 10.1093/bib/bbaa327
    [59] J. Zhang, M. Guan, Q. Wang, J. Zhang, T. Zhou, X. Sun, Single-cell transcriptome-based multilayer network biomarker for predicting prognosis and therapeutic response of gliomas, Brief. Bioinform., 21 (2020), 1080-1097. doi: 10.1093/bib/bbz040
    [60] J. Han, R. A. DePinho, A. Maitra, Single-cell RNA sequencing in pancreatic cancer, Nat. Rev. Gastroenterol. Hepatol., 18 (2021), 451-452. doi: 10.1038/s41575-021-00471-z
    [61] Q. Luo, Q. Fu, X. Zhang, H. Zhang, T. Qin, Application of Single-Cell RNA Sequencing in Pancreatic Cancer and the Endocrine Pancreas, Adv. Exp. Med. Biol., 1255 (2020), 143-152. doi: 10.1007/978-981-15-4494-1_12
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