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Plot per-gene mutation distributions on a protein-domain map (lollipop / needle plots) showing mutation position, recurrence count, and variant classification with maftools, g3-lollipop, trackViewer, and ProteinPaint. Use when visualizing recurrent mutation hotspots on a single gene's protein, marking domain boundaries from UniProt/Pfam, comparing missense vs truncating distributions, or contrasting two cohorts on the same lollipop.

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Build OncoPrint and co-mutation matrix plots from somatic-variant cohorts using ComplexHeatmap, maftools, and comut.py with alteration-type stacking, sample ordering by mutational burden, mutual-exclusivity overlays, and clinical annotation tracks. Use when visualizing per-sample mutation patterns across recurrent driver genes, comparing alteration classes, or identifying mutually-exclusive / co-occurring driver pairs.

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Reconcile gene trees against a species tree under probabilistic models of duplication, transfer, and loss (DTL) using ALE (Szöllősi 2013 amalgamated likelihood), GeneRax (Morel 2020 ML reconciliation), AleRax (Morel 2024 co-estimation), Whale.jl (Bayesian DL+WGD), RANGER-DTL 2 parsimony, NOTUNG, ecceTERA, and Treerecs. Use when inferring ancestral gene-family content, distinguishing duplication from horizontal transfer from differential loss, rooting deep species trees from gene-content signals (STRIDE / Williams 2017 ALE-rooting), counting DTL events per branch, refining noisy gene trees against a species tree, modeling WGD events jointly with DTL, or producing publication-grade gene-family histories for phylogenomic / comparative analyses.

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Map N6-methyladenosine (m6A) RNA modifications at single-nucleotide resolution using miCLIP (Linder 2015), miCLIP2 + m6Aboost machine learning (Kortel 2021), GLORI (Liu 2023, antibody-free chemical conversion), DART-seq (Meyer 2019, APOBEC1-YTH fusion), m6Anet (nanopore direct RNA), or MeRIP-seq with calibration. Use when distinguishing antibody-based from antibody-free m6A detection methods, applying the DRACH motif constraint, reconciling cross-method disagreements (DART 44% in DRACH vs GLORI), or detecting m6Am at the cap.

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Detect single-nucleotide crosslink (CL) sites in CLIP-seq data using truncation patterns (iCLIP/eCLIP CITS), crosslink-induced mutations (HITS-CLIP CIMS deletions, PAR-CLIP T-to-C), or HMM/kernel-density methods (PureCLIP, PARalyzer, CTK). Use when single-nucleotide resolution is required for motif registration (mCross), allele-specific binding (BEAPR), variant-effect prediction, or comparing crosslink chemistry across CLIP variants.

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Corrects the gene-independent copy-number artifact in CRISPR-Cas9 screens (Aguirre 2016 / Munoz 2016 Cancer Discov) where amplified loci appear essential from DNA-damage burden of simultaneous cuts. Covers the gene-independent DNA-damage / G2-arrest mechanism, CRISPRcleanR (Iorio 2018) unsupervised pre-hoc correction, CERES (Meyers 2017) joint CN + gene-effect model, Chronos (Dempster 2021) DepMap-standard population-dynamics + CN model with lowest residual bias, the decision tree by data availability, the Spearman LFC-vs-CN diagnostic, focal-amplification examples (ERBB2 in HER2+, MYC in colorectal, FGFR1 in head and neck), and CRISPRi/a alternatives that bypass the artifact. Use when screening cancer cell lines, diagnosing essentiality at amplified loci, choosing CRISPRcleanR / CERES / Chronos, deciding whether CN correction is needed before MAGeCK / BAGEL2 / drugZ, or switching from Cas9 to CRISPRi.

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Designs and analyzes combinatorial CRISPR screens covering paired-Cas9 (Big Papi, Najm 2018), enhanced AsCas12a multiplex (enCas12a, DeWeirdt 2021), in4mer 4-guide-array Cas12a (Esmaeili Anvar N et al 2024 Nat Commun 15:3577) and the Inzolia paralog-pair library, paralog-buffering detection (Dede 2020 Genome Biol; Thompson 2021 Nat Commun 12:1302), genetic-interaction (GI) scoring as observed_double_LFC minus expected_additive_double_LFC, synthetic-lethal and synthetic-rescue interaction interpretation, the half-of-essentiality buffered by paralogs phenomenon, multiplex screen statistical analysis with MAGeCK MLE interaction terms, and the relationship to single-cell combinatorial Perturb-seq. Use when designing a paralog or pathway-pair screen, choosing between paired-Cas9 (Big Papi) and Cas12a multiplex (Inzolia), interpreting genetic interaction scores, identifying synthetic-lethal targets for drug development, or scaling beyond single-gene CRISPR screens.

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Resolve subclonal copy number, whole-genome doubling, and copy-number tumor evolution from bulk sequencing with Battenberg, TITAN, and MEDICC2. Covers clonal versus subclonal copy-number states, haplotype phasing for subclonal resolution, cancer cell fraction, whole-genome-doubling detection and timing relative to mutations, mirrored subclonal allelic imbalance, and copy-number phylogenies. Use when a tumor is heterogeneous and bulk data shows non-integer copy number, when calling subclonal CNAs, detecting or timing whole-genome doubling, reconstructing copy-number evolution, or deciding between Battenberg and TITAN.

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Builds QSAR / QSPR models using chemprop D-MPNN, MolFormer, Uni-Mol, ChemBERTa, random forest baselines, and Gaussian processes with explicit handling of OECD 5 principles, applicability domain (kNN, leverage, conformal prediction, Mahalanobis), scaffold-balanced splits, ensemble uncertainty, calibration (Platt, isotonic), feature importance (SHAP, atomic attribution), and prospective validation. Use when building target-specific predictive models from in-house bioassay data, ADMET endpoints, or selectivity profiles.

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Implements multiplicity control for confirmatory clinical trials using graphical procedures (Bretz-Maurer-Hommel), gatekeeping (parallel, serial, mixed), Hochberg/Hommel/Holm with PRDS, and the closed-testing principle (Marcus-Peritz-Gabriel; Goeman 2021 admissibility). Covers FDA Multiple Endpoints Final Guidance (October 2022), graphical procedures via R gMCP, primary + key-secondary + subgroup hierarchies, and FWER vs FDR distinction. Use when designing the multiplicity strategy for confirmatory trials with multiple primary or key secondary endpoints.

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Implements missing-data sensitivity analyses for confirmatory clinical trials including MMRM under MAR (with Kenward-Roger correction), reference-based multiple imputation (J2R, CR, CIR, LMCF per Carpenter-Roger 2013), Permutt delta-adjustment / tipping-point analysis, pattern-mixture identifying restrictions (CCMV, NCMV, ACMV), and the Cro vs Bartlett variance debate. Use when handling missing primary or secondary endpoint data in regulatory submissions following NRC 2010 and ICH E9(R1).

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Performs logistic regression for clinical trial outcomes (binary, ordinal, multinomial) with marginal-vs-conditional estimand reporting per FDA 2023 covariate adjustment guidance, g-computation/standardisation for marginal effects, modified Poisson for RR, Brant test for proportional odds, Firth penalty for separation, and Hauck-Donner detection. Use when modeling binary or ordinal endpoints in confirmatory or exploratory clinical trials.

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Standardizes molecular structures using the ChEMBL structure pipeline for normalization and parent selection plus RDKit rdMolStandardize for explicit custom steps such as tautomer canonicalization, salt/solvent stripping, charge handling, stereochemistry handling, mixture selection, and isotope normalization. Explicitly compares ChEMBL, canSARchem, RDKit, and PubChem standardization choices. Use when preparing libraries for QSAR training, joining datasets across sources, deduplicating compound collections, or building canonical compound registries.

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Computes and interprets treatment effect measures (OR, RR, RD, HR, NNT) with calibrated confidence intervals (Wilson, Newcombe, Miettinen-Nurminen, MOVER, profile likelihood, Bender NNT) and reports marginal vs conditional estimands per FDA 2023 covariate adjustment guidance. Use when reporting treatment effects in confirmatory trials, comparing effect sizes across studies, or constructing forest plots.

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Reads, validates, and prepares CDISC SDTM and ADaM clinical trial data for analysis. Covers SDTM domain joins (DM, AE, EX, VS, LB, DS), ADaM architecture (ADSL, BDS, OCCDS, ADTTE) with traceability, treatment-emergent AE conventions, baseline derivation, SUPPQUAL/NSV handling, Define-XML 2.1, and Pinnacle 21 / CORE validation. Use when working with clinical trial datasets in CDISC SDTM/ADaM format, preparing analysis-ready data, or validating for regulatory submission.

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Performs alchemical free-energy calculations including relative binding free energy (RBFE / FEP+) and absolute binding free energy (ABFE) via OpenFE, FEP+, GROMACS, AMBER pmemd, and OpenMM with explicit lambda scheduling, soft-core potentials, MBAR/BAR analysis, cycle-closure validation, and protocol-appropriate enhanced sampling. Compares ML alternatives (Boltz-2 affinity, DeepDock). Use when ranking analogs by binding affinity beyond docking accuracy, performing prospective lead optimization, or validating SAR predictions.

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Designs Bayesian clinical trials including Phase I dose-finding (BOIN, CRM, EWOC, mTPI-2), meta-analytic-predictive (MAP) priors with robust mixtures for external data borrowing, EXNEX for basket trials, hierarchical models for safety AE (Berry-Berry), Bayesian platform trials (I-SPY 2, GBM AGILE, REMAP-CAP), and posterior probability stopping rules. Covers FDA Bayesian Devices Guidance (2010), FDA Bayesian Methodology in Drugs Draft (January 2026), BOIN Fit-for-Purpose qualification (December 2021), and Project Optimus dose-optimisation. Use when designing dose-finding studies, platform trials, or sensitivity analyses with informative priors.

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Designs adaptive clinical trials including group-sequential (O'Brien-Fleming, Pocock, Lan-DeMets spending), sample-size re-estimation (blinded Friede-Kieser, unblinded Cui-Hung-Wang, Mehta-Pocock promising zone), seamless Phase 2/3 with treatment-arm selection, population enrichment, and response-adaptive randomisation. Covers FDA 2019 Final Adaptive Designs Guidance, FDA 2022 Master Protocols, and ICH E20 Step 2b/3 draft (June 2025, NOT final). Use when planning interim analyses, sample-size re-estimation, or master/platform-trial designs.

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Calls ChIP-seq peaks with MACS3, MACS2, HOMER, or SPP across narrow (TF) and broad (histone) modes. Handles input control matching, fragment-size modeling vs --nomodel, effective genome size, ENCODE-style IDR vs naive overlap, hyper-ChIPable artifacts, and aligner-specific shifts. Use when calling peaks from ChIP-seq alignments, choosing between narrow vs broad mode for a histone mark, deciding model vs nomodel for low-depth data, applying ENCODE pseudoreplicate IDR, or reconciling MACS vs HOMER vs SPP results.

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Identifies differentially bound ChIP-seq regions between conditions using DiffBind, csaw (sliding windows), DESeq2/edgeR/PyDESeq2 on count matrices, NormR (control-aware), or MAnorm2. Distinguishes three distinct normalization problems (composition bias, trended bias, global shifts) and matches each to its appropriate fix including spike-in scaling. Use when comparing ChIP-seq binding between experimental conditions, choosing normalization for global vs local changes, integrating spike-in data, or reconciling DiffBind/DESeq2 disagreement.

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Analyzes CUT&RUN (Skene Henikoff 2017) and CUT&Tag (Kaya-Okur 2019) chromatin profiling data. Handles SEACR vs MACS2 peak calling (with the btaf375 2025 benchmark guidance), pA-MNase vs pA-Tn5 vs pAG-Tn5 chimera differences, E. coli spike-in carryover normalization, IgG-only control logic (no input), characteristic fragment-size signatures (25-75 bp for CUT&Tag), and lower depth requirements (5M reads typical vs 25M for ChIP). Use when calling peaks from CUT&RUN/CUT&Tag, scaling by E. coli spike-in carryover, choosing SEACR norm mode, or comparing CUT&RUN/Tag results to traditional ChIP.

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Normalizes ChIP-seq data using exogenous spike-in (ChIP-Rx with Drosophila chromatin per Orlando 2014 / Egan 2016; E. coli carryover for CUT&RUN/CUT&Tag). Distinguishes RRPM from Rx-Input scaling, integrates with DiffBind / DESeq2 / edgeR / csaw via sizeFactors and DiffBind library-size vectors, applies the Patel et al 2024 *Nat Biotechnol* failure-mode framework, and validates that normalization is applied at the read level (not peak counts). Use when global signal shifts are expected (HDACi, BETi, EZH2i, dosage, target knockdown), when ChIPseqSpikeInFree detects post-hoc shifts, or when validating internal-control regions before publication.

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Prepares statistical reports for clinical trials following CONSORT 2025, SPIRIT 2025, ICH E9(R1) estimands, and FDA 2023 covariate adjustment guidance. Covers Table 1 generation, analysis populations (ITT/FAS/PP/Safety), the 5 ICH E9(R1) intercurrent-event strategies, MMRM under MAR (mmrm), reference-based MI (rbmi J2R/CR/CIR), Permutt tipping-point sensitivity, and Rubin's-rules vs frequentist variance debate. Use when preparing regulatory submissions, defining estimands, or implementing missing-data sensitivity analyses.

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Performs time-to-event analysis for clinical trials including Cox proportional hazards regression with PH diagnostics, restricted mean survival time (RMST) under non-PH, competing risks via Fine-Gray vs cause-specific Cox, weighted log-rank and MaxCombo for non-proportional hazards, recurrent events (Andersen-Gill, PWP, WLW), and interval-censored data. Use when analyzing time-to-event endpoints (OS, PFS, DOR, TTR, TTNT) in oncology or other clinical trials.

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