A

Disease A

Slug:Chronic_Pancreatitis
B

Disease B

Slug:Pancreatic_Ductal_Adenocarcinoma
G

Causal Mechanism Graphs

Chronic Pancreatitis

graph LR
    Exocrine_Insufficiency["Exocrine Insufficiency"]
    Recurrent_Acinar_Cell_Injury["Recurrent Acinar Cell Injury"]
    Smoking["Smoking"]
    Alcohol_Consumption["Alcohol Consumption"]
    Endocrine_Insufficiency["Endocrine Insufficiency"]
    Weight_Loss["Weight Loss"]
    Diabetes_Mellitus["Diabetes Mellitus"]
    Steatorrhea["Steatorrhea"]

    Exocrine_Insufficiency --> Steatorrhea
    Exocrine_Insufficiency --> Weight_Loss
    Endocrine_Insufficiency --> Diabetes_Mellitus
    Alcohol_Consumption --> Recurrent_Acinar_Cell_Injury
    Smoking --> Recurrent_Acinar_Cell_Injury

    style Exocrine_Insufficiency fill:#dbeafe
    style Recurrent_Acinar_Cell_Injury fill:#dbeafe
    style Smoking fill:#dcfce7
    style Alcohol_Consumption fill:#dcfce7
    style Endocrine_Insufficiency fill:#dbeafe
    style Weight_Loss fill:#fef3c7
    style Diabetes_Mellitus fill:#fef3c7
    style Steatorrhea fill:#fef3c7

Pancreatic Ductal Adenocarcinoma

graph LR
    USP20_Cholesterol_Metabolism_CD8_Exhaustion_Checkpoint["USP20 Cholesterol-Metabolism CD8 Exhaustion Checkpoint"]
    Tumor_Suppressor_Inactivation["Tumor Suppressor Inactivation"]
    Myeloid_Suppression_Relief_and_CD8_Effector_Infiltration["Myeloid Suppression Relief and CD8 Effector Infiltration"]
    Adaptive_mTOR_and_JUN_AP1_Transcriptional_Program["Adaptive mTOR and JUN-AP1 Transcriptional Program"]
    Regulatory_T_Cell_Relief["Regulatory T-Cell Relief"]
    Tumor_Cell_FAS_Induction_and_CD8_Mediated_Killing["Tumor-Cell FAS Induction and CD8-Mediated Killing"]
    Early_Dissemination_and_EMT["Early Dissemination and EMT"]
    Desmoplastic_Stroma["Desmoplastic Stroma"]
    Chronic_Pancreatic_Inflammation["Chronic Pancreatic Inflammation"]
    Perineural_Invasion["Perineural Invasion"]
    Mitochondrial_Remodeling_and_Ferroptosis_Vulnerability["Mitochondrial Remodeling and Ferroptosis Vulnerability"]
    Acquired_RASON_Inhibitor_Resistance["Acquired RAS(ON) Inhibitor Resistance"]
    PDAC_Immunotherapy_PhysiCell_Model["PDAC Immunotherapy PhysiCell Model"]
    RTK_and_Feedback_Pathway_Reactivation["RTK and Feedback Pathway Reactivation"]
    CDK8_CXCL2_Adaptive_Immune_Reversal["CDK8-CXCL2 Adaptive Immune Reversal"]
    Acinar_to_Ductal_Metaplasia["Acinar-to-Ductal Metaplasia"]
    Mutant_KRAS_Vaccine_Immunologic_Interception["Mutant KRAS Vaccine (Immunologic Interception)"]
    CAF_Mediated_T_Cell_Exclusion["CAF-Mediated T Cell Exclusion"]
    Daraxonrasib_RASON_Multiselective_Inhibitor["Daraxonrasib (RAS(ON) Multiselective Inhibitor)"]
    Obesity_and_Diet["Obesity and Diet"]
    Immunosuppressive_TME_Reversibility_under_RASON_Inhibition["Immunosuppressive TME Reversibility under RAS(ON) Inhibition"]
    Cyclophilin_A_Loss_and_Reduced_Tri_Complex_Engagement["Cyclophilin A Loss and Reduced Tri-Complex Engagement"]
    Immune_Evasion["Immune Evasion"]
    Antigen_Presentation_Restoration["Antigen Presentation Restoration"]
    Chronic_Pancreatitis["Chronic Pancreatitis"]
    MYC_Amplification_Driven_RAS_Independent_Proliferation["MYC Amplification-Driven RAS-Independent Proliferation"]
    PDAC_CAF_Mediated_Invasion_PhysiCell_Model["PDAC CAF-Mediated Invasion PhysiCell Model"]
    KRAS_Oncogene_Activation["KRAS Oncogene Activation"]
    Tobacco_Smoking["Tobacco Smoking"]
    On_Target_RAS_Reactivation_and_KRAS_Amplification["On-Target RAS Reactivation and KRAS Amplification"]
    RAS_Independent_Cell_Cycle_Uncoupling["RAS-Independent Cell-Cycle Uncoupling"]
    Extracellular_Vesicle_Mediated_Immune_Escape["Extracellular Vesicle-Mediated Immune Escape"]

    Chronic_Pancreatic_Inflammation --> Acinar_to_Ductal_Metaplasia
    Acinar_to_Ductal_Metaplasia --> Tumor_Suppressor_Inactivation
    KRAS_Oncogene_Activation --> Immunosuppressive_TME_Reversibility_under_RASON_Inhibition
    KRAS_Oncogene_Activation --> Acquired_RASON_Inhibitor_Resistance
    KRAS_Oncogene_Activation --> Early_Dissemination_and_EMT
    KRAS_Oncogene_Activation --> Acinar_to_Ductal_Metaplasia
    KRAS_Oncogene_Activation --> Tumor_Suppressor_Inactivation
    Tumor_Suppressor_Inactivation --> Desmoplastic_Stroma
    Tumor_Suppressor_Inactivation --> Extracellular_Vesicle_Mediated_Immune_Escape
    Desmoplastic_Stroma --> CAF_Mediated_T_Cell_Exclusion
    CAF_Mediated_T_Cell_Exclusion --> Immune_Evasion
    Extracellular_Vesicle_Mediated_Immune_Escape --> Immune_Evasion
    Early_Dissemination_and_EMT --> Perineural_Invasion
    Cyclophilin_A_Loss_and_Reduced_Tri_Complex_Engagement --> Acquired_RASON_Inhibitor_Resistance
    RAS_Independent_Cell_Cycle_Uncoupling --> Acquired_RASON_Inhibitor_Resistance
    On_Target_RAS_Reactivation_and_KRAS_Amplification --> Acquired_RASON_Inhibitor_Resistance
    RTK_and_Feedback_Pathway_Reactivation --> Acquired_RASON_Inhibitor_Resistance
    Adaptive_mTOR_and_JUN_AP1_Transcriptional_Program --> Acquired_RASON_Inhibitor_Resistance
    Mitochondrial_Remodeling_and_Ferroptosis_Vulnerability --> Acquired_RASON_Inhibitor_Resistance
    MYC_Amplification_Driven_RAS_Independent_Proliferation --> Acquired_RASON_Inhibitor_Resistance
    Myeloid_Suppression_Relief_and_CD8_Effector_Infiltration --> Immunosuppressive_TME_Reversibility_under_RASON_Inhibition
    Tumor_Cell_FAS_Induction_and_CD8_Mediated_Killing --> Immunosuppressive_TME_Reversibility_under_RASON_Inhibition
    Antigen_Presentation_Restoration --> Immunosuppressive_TME_Reversibility_under_RASON_Inhibition
    Regulatory_T_Cell_Relief --> Immunosuppressive_TME_Reversibility_under_RASON_Inhibition
    USP20_Cholesterol_Metabolism_CD8_Exhaustion_Checkpoint --> Immunosuppressive_TME_Reversibility_under_RASON_Inhibition
    CDK8_CXCL2_Adaptive_Immune_Reversal --> Acquired_RASON_Inhibitor_Resistance
    Tobacco_Smoking --> KRAS_Oncogene_Activation
    Tobacco_Smoking --> Chronic_Pancreatic_Inflammation
    Chronic_Pancreatitis --> Chronic_Pancreatic_Inflammation
    Obesity_and_Diet --> Chronic_Pancreatic_Inflammation
    Daraxonrasib_RASON_Multiselective_Inhibitor --> KRAS_Oncogene_Activation
    Mutant_KRAS_Vaccine_Immunologic_Interception --> KRAS_Oncogene_Activation
    PDAC_CAF_Mediated_Invasion_PhysiCell_Model --> Desmoplastic_Stroma
    PDAC_Immunotherapy_PhysiCell_Model --> Immune_Evasion

    style USP20_Cholesterol_Metabolism_CD8_Exhaustion_Checkpoint fill:#dbeafe
    style Tumor_Suppressor_Inactivation fill:#dbeafe
    style Myeloid_Suppression_Relief_and_CD8_Effector_Infiltration fill:#dbeafe
    style Adaptive_mTOR_and_JUN_AP1_Transcriptional_Program fill:#dbeafe
    style Regulatory_T_Cell_Relief fill:#dbeafe
    style Tumor_Cell_FAS_Induction_and_CD8_Mediated_Killing fill:#dbeafe
    style Early_Dissemination_and_EMT fill:#dbeafe
    style Desmoplastic_Stroma fill:#dbeafe
    style Chronic_Pancreatic_Inflammation fill:#dbeafe
    style Perineural_Invasion fill:#dbeafe
    style Mitochondrial_Remodeling_and_Ferroptosis_Vulnerability fill:#dbeafe
    style Acquired_RASON_Inhibitor_Resistance fill:#dbeafe
    style PDAC_Immunotherapy_PhysiCell_Model fill:#ecfccb
    style RTK_and_Feedback_Pathway_Reactivation fill:#dbeafe
    style CDK8_CXCL2_Adaptive_Immune_Reversal fill:#dbeafe
    style Acinar_to_Ductal_Metaplasia fill:#dbeafe
    style Mutant_KRAS_Vaccine_Immunologic_Interception fill:#fce7f3
    style CAF_Mediated_T_Cell_Exclusion fill:#dbeafe
    style Daraxonrasib_RASON_Multiselective_Inhibitor fill:#fce7f3
    style Obesity_and_Diet fill:#dcfce7
    style Immunosuppressive_TME_Reversibility_under_RASON_Inhibition fill:#dbeafe
    style Cyclophilin_A_Loss_and_Reduced_Tri_Complex_Engagement fill:#dbeafe
    style Immune_Evasion fill:#dbeafe
    style Antigen_Presentation_Restoration fill:#dbeafe
    style Chronic_Pancreatitis fill:#dcfce7
    style MYC_Amplification_Driven_RAS_Independent_Proliferation fill:#dbeafe
    style PDAC_CAF_Mediated_Invasion_PhysiCell_Model fill:#ecfccb
    style KRAS_Oncogene_Activation fill:#dbeafe
    style Tobacco_Smoking fill:#dcfce7
    style On_Target_RAS_Reactivation_and_KRAS_Amplification fill:#dbeafe
    style RAS_Independent_Cell_Cycle_Uncoupling fill:#dbeafe
    style Extracellular_Vesicle_Mediated_Immune_Escape fill:#dbeafe
S

Association Signals

Signal 1
LITERATURE LITERATURE_ASSOCIATION A_BEFORE_B
Population:International Pancreatitis Study Group multicentre historical cohort, 2015 subjects with chronic pancreatitis recruited across six countries, mean follow-up 7.4 years, with observed pancreatic cancers compared against country-specific incidence adjusted for age and sex.
Temporal: A before B: , B before A: , Same time:
OTHER: 16.5
CI: -
p:
FDR:
Standardized incidence ratio of pancreatic cancer among subjects with at least two years of follow-up, and 14.4 at five years. The unrestricted ratio of 26.3 is deliberately not used: excluding early follow-up removes cancers that were already present when pancreatitis was diagnosed. Metric type is OTHER because the enum has no standardized incidence ratio value.
PMID:8479461 (SUPPORT)
Source: HUMAN_CLINICAL
"For subjects with a minimum of two or five years of follow-up, the respective standardized incidence ratios were 16.5 (95 percent confidence interval, 11.1 to 23.7) and 14.4 (95 percent confidence interval, 8.5 to 22.8)."
Measures incident pancreatic cancer forward from a defined chronic pancreatitis cohort against expected population rates, which is what a directed A_BEFORE_B risk signal requires, and reports the lag-adjusted ratios that exclude reverse causation.
H

Hypotheses

Sustained pancreatic inflammation and the fibrotic, regenerative response to it provide the context from which pancreatic ductal adenocarcinoma arises, in the same way cirrhosis does for hepatocellular carcinoma.
PMID:38408777 (SUPPORT)
Source: HUMAN_CLINICAL
"The disease is manifested by abdominal pain, deterioration in quality of life, food maldigestion and malabsorption, diabetes, and an increased risk for pancreatic adenocarcinoma."
Names increased pancreatic adenocarcinoma risk among the established consequences of chronic pancreatitis, in a clinical management review.
PMID:35142721 (SUPPORT)
Source: HUMAN_CLINICAL
"There is an increased risk of PDAC in patients with CP, and incidence rates increase with CP disease duration."
The cancer-specific anchor for this pair, and the strongest of the two: a systematic review and meta-analysis reporting not just elevated risk but a dose-response in disease duration, which is the pattern expected if the inflammation is causal rather than merely co-occurring.
Y

Raw YAML

Show YAML
name: com_Chronic_Pancreatitis__Pancreatic_Ductal_Adenocarcinoma
creation_date: "2026-08-27T00:00:00Z"
curation_status: CANDIDATE
notes: >-
  Split out of the former `kb/disorders/Metastatic_Pancreatic_Adenocarcinoma.yaml`'s
  (since folded into `Pancreatic_Ductal_Adenocarcinoma`, design decisions §3a)
  `environmental:` block (dismech#8296, dismech#8551). That entry listed
  `Chronic pancreatitis` as an exposure, but chronic pancreatitis is a
  first-class `Disease` entry in its own right
  (`kb/disorders/Chronic_Pancreatitis.yaml`) rather than something external to
  the organism acting on it.

  `disease_b` is `Pancreatic_Ductal_Adenocarcinoma`, not the
  `Metastatic_Pancreatic_Adenocarcinoma` entry this row came from. The cohort
  evidence measures incident pancreatic cancer in a chronic pancreatitis
  population without reference to stage at presentation, and nothing cited here
  addresses the metastatic entity specifically. Attaching a directed risk edge
  to the metastatic entry would assert more than the sources support -- the same
  correction the review of dismech#8195 applied to
  `com_Liver_Cirrhosis__Hepatocellular_Carcinoma`.

  The signal below uses the standardized incidence ratio computed after
  excluding the first two years of follow-up, 16.5 rather than the headline
  26.3. The unrestricted figure is inflated by cancers already present when
  pancreatitis was diagnosed, which is reverse causation rather than risk.
  PMID:35142721 is the more recent and more cancer-specific source and is cited
  in the hypothesis below, but the signal metric stays the 1993 cohort's SIR
  because a standardized incidence ratio measured forward from a defined
  pancreatitis cohort against expected population rates is a directed A_BEFORE_B
  quantity, which is what this slot holds; the meta-analysis reports incidence
  rising with disease duration rather than a single ratio.

  `kb/disorders/Pancreatic_Ductal_Adenocarcinoma.yaml` keeps its own
  `Chronic Pancreatitis` entry under `environmental:` rather than folding it in
  here, and the two divide the labour deliberately: that row carries the
  mechanistic route into the pathograph, which a comorbidity entry cannot
  express, and this entry carries the disease-disease epidemiology. Its `notes:`
  cross-references this file.

disease_a:
  slug: Chronic_Pancreatitis
  preferred_term: chronic pancreatitis
  term:
    id: MONDO:0005003
    label: chronic pancreatitis

disease_b:
  slug: Pancreatic_Ductal_Adenocarcinoma
  preferred_term: pancreatic ductal adenocarcinoma
  term:
    id: MONDO:0005184
    label: pancreatic ductal adenocarcinoma

directionality: A_BEFORE_B
effect_direction: RISK

hypotheses:
- description: >-
    Sustained pancreatic inflammation and the fibrotic, regenerative response to
    it provide the context from which pancreatic ductal adenocarcinoma arises,
    in the same way cirrhosis does for hepatocellular carcinoma.
  evidence:
  - reference: PMID:38408777
    reference_title: Management of chronic pancreatitis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The disease is manifested by abdominal pain, deterioration in quality of life, food maldigestion and malabsorption, diabetes, and an increased risk for pancreatic adenocarcinoma."
    explanation: >-
      Names increased pancreatic adenocarcinoma risk among the established
      consequences of chronic pancreatitis, in a clinical management review.
  - reference: PMID:35142721
    reference_title: "Chronic Pancreatitis Is a Risk Factor for Pancreatic Cancer, and Incidence Increases With Duration of Disease: A Systematic Review and Meta-analysis."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "There is an increased risk of PDAC in patients with CP, and incidence rates increase with CP disease duration."
    explanation: >-
      The cancer-specific anchor for this pair, and the strongest of the two:
      a systematic review and meta-analysis reporting not just elevated risk but
      a dose-response in disease duration, which is the pattern expected if the
      inflammation is causal rather than merely co-occurring.

association_signals:
- source: LITERATURE
  method: LITERATURE_ASSOCIATION
  population: >-
    International Pancreatitis Study Group multicentre historical cohort, 2015
    subjects with chronic pancreatitis recruited across six countries, mean
    follow-up 7.4 years, with observed pancreatic cancers compared against
    country-specific incidence adjusted for age and sex.
  directionality: A_BEFORE_B
  effect_direction: RISK
  statistics:
    metrics:
    - metric_type: OTHER
      metric_value: 16.5
      notes: >-
        Standardized incidence ratio of pancreatic cancer among subjects with at
        least two years of follow-up, and 14.4 at five years. The unrestricted
        ratio of 26.3 is deliberately not used: excluding early follow-up
        removes cancers that were already present when pancreatitis was
        diagnosed. Metric type is OTHER because the enum has no standardized
        incidence ratio value.
    evidence:
    - reference: PMID:8479461
      reference_title: Pancreatitis and the risk of pancreatic cancer. International Pancreatitis Study Group.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "For subjects with a minimum of two or five years of follow-up, the respective standardized incidence ratios were 16.5 (95 percent confidence interval, 11.1 to 23.7) and 14.4 (95 percent confidence interval, 8.5 to 22.8)."
      explanation: >-
        Measures incident pancreatic cancer forward from a defined chronic
        pancreatitis cohort against expected population rates, which is what a
        directed A_BEFORE_B risk signal requires, and reports the lag-adjusted
        ratios that exclude reverse causation.
Source:GitHub