> For the complete documentation index, see [llms.txt](https://www.brexatlas.org/llms.txt). Markdown versions of documentation pages are available by appending `.md` to page URLs; this page is available as [Markdown](https://www.brexatlas.org/bre-001/bre-004.md).

# BRE 004

## Electric Fields and Pancreatic Cancer

**Clinical Cancer Name:** Pancreatic Adenocarcinoma

**Common Cancer Name:** Pancreatic Cancer

## Source

Giladi, M., Schneiderman, R. S., Porat, Y., Munster, M., Itzhaki, A., Mordechovich, D., Cahal, S., Kirson, E. D., Weinberg, U., & Palti, Y. (2014).

*Mitotic disruption and reduced clonogenicity of pancreatic cancer cells in vitro and in vivo by tumor treating fields.*

*Pancreatology, 14*(1), 54–63.

<https://doi.org/10.1016/j.pan.2013.11.009>

***

## BRE-004 Scoring Section

### BRS Score

**BRS**: 8.3 / 10

**STEMD:** S8 / T8 / E9 / M8 / D8

**External Evidence Level**: Moderate–High (strong in-vitro + in-vivo pancreatic cancer models)

### Score Interpretation

BRE-004 receives a **strong score** because it successfully extends Tumor Treating Fields (TTFields) evidence from glioma into pancreatic cancer — a completely different tissue type.

It demonstrates both **in-vitro** and **in-vivo** relevance, showing reduced clonogenicity and clear mitotic disruption. This significantly strengthens questions around **cross-tissue transferability** of bioelectric anti-cancer effects.

**Key Strengths Highlighted by Scoring**:

* First major expansion beyond brain cancer
* Frequency optimization data (150 kHz)
* Combination therapy potential
* Reproducible mitotic disruption mechanisms

## Entry Summary

BRE-004 asks one of the most important questions in the early history of bioelectric oncology:

Are Tumor Treating Fields only useful for brain cancer, or can they work in other cancers too?

The first entries in this encyclopedia focused on glioma and glioblastoma.

BRE-004 moves into a completely different tissue type: pancreatic cancer.

This study is important because it helps answer whether the biological principles observed in brain cancer might extend to cancers elsewhere in the body.

BREXAtlas identifies BRE-004 as one of the earliest studies supporting the possibility that bioelectric cancer response is not limited to a single tissue.

## Question This BRE Helps Answer

<details>

<summary>Can electric fields affect cancers outside the brain?</summary>

**What BREXAtlas found:**

Yes.

This study demonstrated that pancreatic cancer cells responded to Tumor Treating Fields.

Researchers observed:

* Reduced cancer-cell proliferation
* Reduced clonogenicity
* Increased mitotic abnormalities
* Reduced tumor growth
* Enhanced response to chemotherapy

These findings suggest that TTFields may have broader anti-cancer effects than originally recognized.

</details>

<details>

<summary>What is clonogenicity and why does it matter?</summary>

Most people have never heard the word.

Clonogenicity refers to a cancer cell's ability to survive, reproduce, and form future colonies of cancer cells.

A cancer treatment may damage cells temporarily.

A stronger treatment prevents those cells from successfully reproducing.

**What BREXAtlas found:**

TTFields reduced clonogenicity in pancreatic cancer cells.

In simple language:

The cancer cells became less capable of producing future generations of cancer cells.

</details>

<details>

<summary>Did pancreatic cancer require a different frequency?</summary>

**What BREXAtlas found:**

Yes.

The optimal frequency reported in this study was:

150 kHz

This is important because previous entries identified:

| Cancer Type           | Frequency |
| --------------------- | --------- |
| Glioma / Brain Cancer | 200 kHz   |
| Ovarian Cancer        | 200 kHz   |
| Pancreatic Cancer     | 150 kHz   |

This strengthens the emerging BREXAtlas observation that different cancers may respond best to different frequencies.

</details>

## Cell Lines Cataloged in This Entry

### Human Pancreatic Cancer

* AsPC-1
* BxPC-3

### Animal Model

* PC-1.0

## Treatment Parameters

| Parameter                 | Value                           |
| ------------------------- | ------------------------------- |
| Treatment Type            | Tumor Treating Fields           |
| Frequency                 | 150 kHz                         |
| In Vitro Intensity        | 2.9 ± 0.2 V/cm RMS              |
| In Vivo Intensity         | 1.6 ± 0.1 V/cm RMS              |
| Cell Study Duration       | 72 hours                        |
| Animal Treatment Duration | Continuous treatment for 7 days |

## What BREXAtlas Found

BRE-004 provides evidence for three major observations.

### Finding 1: Pancreatic Cancer Responds to TTFields

The anti-cancer effects observed in brain cancer studies were also observed in pancreatic cancer models.

This suggests TTFields may not be tissue-exclusive.

### Finding 2: Frequency May Be Tissue-Specific

Pancreatic cancer demonstrated optimal response near 150 kHz rather than the 200 kHz frequently observed in earlier glioma studies.

This supports continued investigation into tissue-specific frequency optimization.

### Finding 3: Electric Fields May Improve Existing Treatments

Researchers observed enhanced chemotherapy response when TTFields were added.

This introduces a new question:

Can electric fields become treatment amplifiers rather than standalone treatments?

## Observed Responses

Researchers reported:

* Reduced proliferation
* Increased cell volume
* Reduced clonogenicity
* Increased abnormal mitotic figures
* Reduced G2/M population
* Increased sub-G1 population
* Reduced tumor volume
* Enhanced chemotherapy response

Taken together, these findings suggest substantial disruption of normal cancer-cell division.

## Mechanisms

### MEC-001: Mitotic Disruption

BRE-004 reinforces one of the earliest recurring mechanisms in the encyclopedia.

Cancer cells attempting to divide appeared vulnerable to electric-field exposure.

### MEC-007: Mitotic Spindle Disruption

The study supports interference with structures required for proper chromosome separation.

### MEC-008: Chromosome Missegregation

Cancer cells exposed to TTFields demonstrated abnormal division patterns consistent with chromosome segregation errors.

### MEC-009: Cytokinesis Disruption

The process of splitting one cell into two daughter cells appeared impaired.

### MEC-010: Microtubule Interference

The study supports disruption of microtubule-dependent structures involved in mitosis.

## Public Source Validation

Public TTFields literature recognizes this study as one of the foundational investigations extending TTFields beyond glioblastoma.

The paper is frequently cited because it demonstrated:

* Pancreatic cancer responsiveness
* Frequency optimization
* Mitotic disruption
* Combination-treatment potential

BREXAtlas interpretation aligns with the published findings while organizing them into a broader cross-cancer framework.

## Connections to Other BRE Entries

### Connected to BRE-001

**Connection:**

BRE-001 established TTFields as a treatment capable of disrupting cancer-cell division in glioma.

**How BRE-004 expands it:**

BRE-004 demonstrates similar mitotic disruption in pancreatic cancer.

This supports the possibility that mitotic vulnerability may be shared across multiple cancers.

**Recommended Reading:** BRE-001

### Connected to BRE-002

**Connection:**

BRE-002 focused on frequency optimization.

**How BRE-004 expands it:**

BRE-004 provides another frequency datapoint.

Pancreatic cancer responded optimally at 150 kHz instead of the 200 kHz observed in several glioma and ovarian models.

This strengthens the emerging Frequency Specificity Framework.

**Recommended Reading:** BRE-002

### Connected to BRE-003

**Connection:**

BRE-003 expanded TTFields mechanisms beyond mitosis into DNA-repair interference.

**How BRE-004 contributes:**

BRE-004 reinforces the original anti-mitotic foundation upon which later mechanism discoveries are built.

Together, BRE-003 and BRE-004 suggest TTFields may affect multiple biological systems simultaneously.

### Connected to Future Pancreatic Cancer Entries

BRE-004 becomes the foundational pancreatic cancer reference entry within BREXAtlas.

Future pancreatic studies should be compared against:

* AsPC-1
* BxPC-3
* PC-1.0

to determine whether the observed 150 kHz pattern remains consistent.

## Research Gaps Identified

### RG-016: Pancreatic Frequency Gap

Do all pancreatic cancer cell lines respond best at approximately 150 kHz?

### RG-017: Cross-Tissue Frequency Gap

Why do some cancers appear to respond best at 150 kHz while others respond near 200 kHz?

### RG-018: Combination Therapy Gap

Can TTFields consistently enhance chemotherapy effectiveness?

### RG-019: Universality Gap

How many cancer types share anti-mitotic electric-field vulnerabilities?

### RG-020: Translation Gap

Can pancreatic cancer laboratory findings translate into meaningful patient outcomes?

## Why This Entry Matters

For researchers, BRE-004 is one of the first strong indicators that TTFields may not be limited to brain tumors.

For patients and families, the significance is straightforward:

This study suggests pancreatic cancer cells may possess the same type of electrical vulnerability observed in other cancers.

That possibility opens the door to exploring bioelectric treatments across many cancer types rather than treating TTFields as a brain-cancer-only technology.

## Entry Conclusion

BRE-004 is the first major cross-cancer expansion study in the BREXAtlas Encyclopedia.

BRE-001 showed that electric fields could disrupt brain cancer cells.

BRE-002 showed that frequency matters.

BRE-003 suggested electric fields may influence DNA repair and radiation response.

BRE-004 demonstrates that similar anti-cancer effects can occur in pancreatic cancer.

The central question emerging from this study is:

If pancreatic cancer responds to bioelectric intervention, how many other cancers might respond as well?

For BREXAtlas, BRE-004 marks the beginning of the transition from a glioma-focused framework toward a true multi-cancer bioelectric response encyclopedia.


---

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