Bitter Melon Cancer Cell Studies

Bitter melon's appearance in the cancer literature is real and the in vitro data are genuinely interesting — the cucurbitacin triterpenoids, the momordicin compounds, and especially the MAP30 ribosome-inactivating protein have all shown documented antiproliferative activity against multiple human cancer cell lines, and Traditional Chinese Medicine has used bitter melon for “tumors” and “swellings” in classical formularies for centuries. But it is essential to be honest about the evidence quality: the great majority of bitter melon cancer research is in vitro (cells in a dish) or animal-model work; the human clinical trial literature is limited to small phase-I safety and pilot pharmacokinetic studies, with no completed phase-III randomized controlled trials demonstrating clinical benefit in any cancer. Bitter melon is NOT a cancer treatment. It cannot replace surgery, chemotherapy, radiation, targeted therapy, or immunotherapy. The reasonable framing is that bitter melon may have value as one component of an integrative supportive protocol under oncologist supervision — helping with quality-of-life issues like glucose regulation in patients on glucocorticoids or with cancer-associated metabolic dysregulation — but it does not have the evidence base to be used as an anticancer therapy in its own right. This page exists to summarize the actual research so patients and their families can make informed decisions, not to promote bitter melon as a cancer remedy.

Table of Contents

1. The Honest Framing: What This Evidence Is and Is Not
2. Cucurbitacin Antiproliferative Activity
3. MAP30: The Ribosome-Inactivating Protein
4. Momordicins, Momordicosides, and Triterpenoid Saponins
5. In Vitro Cell-Line Antiproliferative Data
6. Animal-Model Tumor Studies
7. Traditional Chinese Use for “Tumors” and “Swellings”
8. The Limited Human Clinical Trial Evidence
9. Why Cell-Culture Data Often Does Not Translate
10. A Reasonable Integrative Role
11. Cautions: What Patients With Cancer Should Know
12. Key Research Papers
13. Connections

The Honest Framing: What This Evidence Is and Is Not

The bitter melon and cancer literature comprises roughly several hundred peer-reviewed papers as of the mid-2020s, distributed approximately as follows:

• In vitro (cell culture) studies — the large majority. These studies expose cancer cell lines (such as HepG2 liver cancer, MCF-7 and MDA-MB-231 breast cancer, A549 lung cancer, HCT-116 colon cancer, PC-3 prostate cancer) to bitter melon extracts, fractions, or purified compounds and measure proliferation, apoptosis, cell-cycle arrest, and gene expression changes. Many show antiproliferative effects at micromolar to millimolar concentrations.
• Animal-model studies — a smaller but substantial body of work, mostly in mice with xenografted human tumors or chemically induced tumors. Many show tumor growth inhibition, particularly with the MAP30 protein administered by injection.
• Mechanistic and biochemical studies — characterization of the molecular targets and pathways (apoptosis induction, cell-cycle checkpoint activation, mTOR inhibition, anti-angiogenesis).
• Human pharmacokinetic and phase-I safety studies — a small handful, mostly for the MAP30 protein and primarily examining tolerability rather than efficacy.
• Phase-II and phase-III randomized controlled trials demonstrating clinical anticancer benefit — essentially none. There is no high-quality human clinical evidence that bitter melon, in any form or dose, treats or cures any cancer.

This distribution is typical of botanical anticancer literature in general. Cell-culture and animal data are abundant; high-quality human clinical data are sparse. The translation gap is one of the central problems in cancer pharmacology, and bitter melon is no exception. The honest position is that the in vitro and animal evidence is interesting enough to justify continued investigation but is nowhere near sufficient to recommend bitter melon as a cancer treatment.

This page is written to help patients with cancer, their families, and their physicians have an accurate conversation about what bitter melon is and is not. It is not written to promote bitter melon as an alternative to evidence-based oncology care, and patients who are considering substituting bitter melon for conventional cancer therapy should not do so — the human consequences of that decision are well documented and uniformly bad.

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Cucurbitacin Antiproliferative Activity

The cucurbitacins are a family of bitter triterpenoid compounds found across the cucurbit family (squash, pumpkin, cucumber, bitter melon, gourds), responsible for much of the bitter flavor and for some of the toxic potential of certain wild cucurbits (cucurbitacin poisoning from improperly bred zucchini and yellow squash is a documented entity, producing severe gastrointestinal distress). Cucurbitacins B, D, E, and I are the most studied for antiproliferative activity.

The mechanism of action involves disruption of the actin cytoskeleton through binding to actin filaments, inhibition of the JAK/STAT signaling pathway (particularly STAT3, which is constitutively activated in many cancers and drives proliferation, survival, and angiogenesis), and induction of mitochondrial-pathway apoptosis. Cucurbitacin B has shown low-micromolar IC50 values (the concentration that inhibits 50% of cell growth) against multiple human cancer cell lines.

The translational problem with cucurbitacins is the same one that plagues many natural-product anticancer compounds: the effective concentration in cell culture is often higher than what can be achieved safely in human plasma. Cucurbitacins are also gastrotoxic at oral doses approaching the antiproliferative threshold, so simply scaling up bitter melon intake to attempt to reach therapeutic cucurbitacin levels would produce intolerable gastrointestinal toxicity well before any anticancer effect could be measured.

Some research groups have explored purified, formulated cucurbitacin preparations as potential anticancer leads, but these have not advanced to widely available clinical therapy.

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MAP30: The Ribosome-Inactivating Protein

MAP30 (Momordica Anti-HIV Protein of 30 kDa) is a single-chain ribosome-inactivating protein (RIP) isolated from bitter melon seeds by Lee-Huang and colleagues at NYU in the early 1990s. Type I RIPs catalytically depurinate adenine residues in ribosomal RNA, irreversibly inactivating the affected ribosome and shutting down protein synthesis. The most famous Type II RIPs are ricin (from castor beans) and abrin (from rosary peas), which are extremely toxic; Type I RIPs like MAP30 are considerably less toxic because they lack the lectin chain that enables cellular uptake, so they typically must be administered by injection and have limited systemic toxicity.

MAP30 has been studied for two main indications:

• Anti-HIV activity — the original Lee-Huang work showed that MAP30 inhibits HIV reverse transcriptase, HIV integrase, and viral replication in cell culture. This was the basis for the original NIH interest in bitter melon as an HIV adjunct in the late 1980s and 1990s. Clinical translation never materialized at scale because effective antiretroviral therapy became available in the mid-1990s.
• Antitumor activity — MAP30 inhibits proliferation and induces apoptosis in multiple cancer cell lines, particularly hepatocellular carcinoma, breast cancer, and prostate cancer cell lines. Tumor growth inhibition has been demonstrated in mouse xenograft models, especially when MAP30 is coupled to a tumor-targeting antibody (an “immunotoxin” design that selectively delivers the RIP to cancer cells).

The translational potential of MAP30 has been somewhat overshadowed by the development of more potent and more easily formulated anticancer agents. As of the mid-2020s, MAP30 has not advanced to FDA-approved clinical use, though research continues, particularly in the immunotoxin space where targeting specificity can be engineered.

The implication for whole-plant bitter melon consumption: MAP30 is a protein, so it is largely degraded by gastric protease when bitter melon is taken orally. Oral bitter melon intake provides essentially no systemic MAP30 exposure. The MAP30 research is interesting science but is not the basis for any putative anticancer effect of dietary or supplement-form bitter melon.

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Momordicins, Momordicosides, and Triterpenoid Saponins

Beyond cucurbitacins and MAP30, the bitter melon triterpenoid chemistry includes a complex family of cucurbitane-type triterpenoids called momordicins and their glycosylated derivatives, the momordicosides. Several have been identified as antiproliferative against cancer cell lines, with mechanisms involving apoptosis induction (via caspase-3 and caspase-9 activation), cell-cycle arrest (typically at G1/S or G2/M checkpoints), and modulation of NF-kappa-B signaling.

Momordicin I and momordicin II, isolated from the leaves of bitter melon, have shown cytotoxic activity against leukemia cell lines. The MeOH extract of bitter melon fruit has shown activity against MCF-7 breast cancer cells through induction of mitochondrial-pathway apoptosis. The combination of multiple triterpenoid compounds present in a typical bitter melon preparation produces a complex pharmacological profile that is difficult to attribute to any single constituent.

The Ray et al. 2010 work on bitter melon extract in breast cancer cell lines, and the Pitchakarn et al. 2010 work on prostate cancer cells, are representative of this body of literature. Both showed dose-dependent antiproliferative effects in cell culture at concentrations achievable with standardized extracts, with apoptosis induction as the dominant mechanism.

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In Vitro Cell-Line Antiproliferative Data

The in vitro bitter melon anticancer literature spans most of the common human cancer cell lines used in pharmacology screening:

• Breast cancer — MCF-7 (estrogen receptor positive), MDA-MB-231 (triple negative), T-47D. Studies show antiproliferative activity in the micromolar to milligrams-per-milliliter range
• Prostate cancer — PC-3, LNCaP, DU-145. Pitchakarn 2010, Ru 2011, and others have characterized androgen-receptor-independent antiproliferative effects
• Colorectal cancer — HCT-116, SW480, HT-29. Antiproliferative effects with apoptosis induction
• Liver cancer — HepG2, Hep3B, HuH-7. Multiple studies, including with MAP30 protein
• Lung cancer — A549 (adenocarcinoma), NCI-H460. Modest activity in cell culture
• Leukemia — U937, K-562, HL-60. Cytotoxic effects with caspase-pathway apoptosis
• Pancreatic cancer — MIA PaCa-2, BxPC-3. Antiproliferative effects in cell culture and some growth inhibition in xenograft models (Kaur 2013)
• Head and neck cancer — Cal27, JHU-022. Antiproliferative effects characterized by Bhattacharya and colleagues
• Glioma — U87. Some apoptosis-inducing activity

The pattern across these cell-line studies is broadly consistent: bitter melon extracts and fractions show antiproliferative activity against most human cancer cell lines tested, at concentrations in the micromolar to low-millimolar range, with apoptosis as the dominant mechanism. The breadth of activity is interesting but also raises a concern that the underlying mechanism may not be cancer-selective — many of the same effects can be demonstrated against normal cells at similar concentrations, which is the typical pattern for general cytotoxic agents and is the reason such cell-culture findings often do not translate to clinical benefit.

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Animal-Model Tumor Studies

Animal-model studies of bitter melon in tumor systems are more clinically relevant than cell-culture work because they incorporate pharmacokinetics, distribution, and the tumor microenvironment. The main paradigms used are:

• Chemically induced tumors — e.g., DMBA (dimethylbenz[a]anthracene) skin papillomas in mice, or AOM (azoxymethane)-induced colon carcinogenesis. Bitter melon supplementation has reduced tumor incidence and burden in several such models (Singh et al. 1998, others).
• Xenograft models — human cancer cell lines implanted into immunodeficient mice; bitter melon administered orally, by intraperitoneal injection, or (for MAP30) intravenously. Multiple studies have shown reduced tumor volume and weight at endpoint.
• Spontaneous tumor models — less common because they are slower and more expensive, but a few studies have used p53-deficient mice or other tumor-prone genetic backgrounds.

The animal-model data are stronger than the cell-culture data alone because they address some of the pharmacokinetic and microenvironment questions. They are still not human clinical trials. The standard caveat is that the great majority of agents that show promising activity in mouse cancer models fail to show clinical benefit in subsequent human trials — the attrition rate from positive mouse data to positive human phase-III trial is somewhere between 90% and 99% across the broader anticancer pharmacology literature.

For the broader context of cancer and integrative approaches, see our Cancer overview page.

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Traditional Chinese Use for “Tumors” and “Swellings”

Traditional Chinese Medicine's classical materia medica texts (the Bencao Gangmu of Li Shizhen, completed in 1578, is the most comprehensive) include bitter melon (kŭgua) among the agents indicated for what was called zīng liū (lumps and tumors) and zhōng zhāng (swellings). The classical TCM concept of zīng liū is broader than what we now call cancer and includes various benign tumors, lymphadenopathies, cysts, and inflammatory swellings, so it is not strictly equivalent to oncological cancer.

The TCM theoretical framing involved bitter melon's cooling and detoxifying nature being appropriate for what was conceived as “heat-toxin” or “stagnation” underlying tumor formation. Bitter melon was rarely used alone in classical TCM cancer formularies; it was more commonly combined with other “clearing” agents like banzhilian (Scutellaria barbata), baihua-shecao (Hedyotis diffusa), and xiakucao (Prunella vulgaris) in complex multi-herb formulas.

Modern integrative oncology in mainland China and Taiwan continues to use bitter melon in some traditional formulas for cancer patients, typically as adjuncts to standard Western oncologic care rather than as substitutes. The Chinese-language clinical literature includes some small studies of these traditional formulas for chemotherapy-induced quality-of-life improvement, fatigue reduction, and symptom management, with bitter melon as one constituent of complex herbal mixtures. The methodological quality is highly variable and the formulations are not standardized, so the data are difficult to integrate into Western evidence frameworks.

The honest interpretation: traditional use does establish a long history of bitter melon being tried for tumor-like conditions, but it does not establish efficacy by modern evidence standards. The traditional use is part of the reason for continued scientific investigation, not a substitute for clinical evidence.

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The Limited Human Clinical Trial Evidence

Human clinical trials of bitter melon specifically for cancer treatment are sparse. The published evidence consists primarily of:

• Phase-I safety and pharmacokinetic studies — small studies (typically 10-30 patients) assessing tolerability and serum compound levels in cancer patients given standardized bitter melon extracts. These have generally shown bitter melon to be well tolerated at typical doses, with the expected mild gastrointestinal adverse effects.
• Small pilot studies in specific cancers — for example, a small study of bitter melon extract in patients with advanced pancreatic cancer (Kaur et al. and colleagues) that was primarily designed to assess safety and to look for preliminary signals of pharmacokinetic exposure.
• Adjunctive integrative oncology pilot studies — mostly conducted in Asia, often without strict randomization or placebo control, examining bitter melon as part of multi-herb formulas in patients undergoing standard chemotherapy or after surgical resection.
• Quality-of-life and supportive care studies — a handful of trials assessing whether bitter melon improves cancer-related fatigue, glucose dysregulation in patients on glucocorticoids, or other symptomatic endpoints rather than tumor outcomes.

Notably absent from the literature: well-designed, adequately powered, placebo-controlled randomized trials of bitter melon as a primary or adjunctive anticancer treatment, with tumor response rate, progression-free survival, or overall survival as endpoints. The Memorial Sloan Kettering Cancer Center About Herbs database (a widely consulted oncology integrative-medicine resource) summarizes the bitter melon evidence as “preliminary” for anticancer indications and specifically does not recommend bitter melon as a cancer therapy.

The closest the evidence base has come to a positive clinical signal is in the diabetes-and-cancer intersection: bitter melon's established blood-sugar-lowering effect may be of supportive value to cancer patients with hyperglycemia (whether pre-existing type 2 diabetes or glucocorticoid-induced steroid hyperglycemia from cancer treatment regimens), and there is emerging interest in the metabolic-syndrome-cancer connection where AMPK activation may have indirect anticancer effects in tumors that exploit Warburg-effect glycolytic metabolism. But these are hypotheses, not established clinical benefits.

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Why Cell-Culture Data Often Does Not Translate

Patients and family members reading the bitter melon cancer literature often reasonably ask: if cell-culture studies show antiproliferative activity against multiple human cancer cell lines, why is there not clinical evidence of efficacy? The disconnect between in vitro and human clinical results has several well-recognized causes, and understanding them is helpful for interpreting any natural-product cancer claim, not just bitter melon's:

1. Concentration mismatch — the concentration of bitter melon compounds that inhibits cancer cell proliferation in a dish is often higher than the concentration that can be achieved safely in human plasma. A compound that kills MCF-7 cells at 100 micromolar in vitro may be impossible to dose to 100 micromolar in vivo without unacceptable systemic toxicity.
2. Pharmacokinetic limitations — oral bioavailability of many bitter melon constituents is low. Polypeptide-p and MAP30 are proteins largely destroyed by gastric protease. Many of the triterpenoids have limited intestinal absorption and undergo extensive first-pass hepatic metabolism. The compound that worked at 50 micromolar in cell culture may achieve only 0.5 micromolar in plasma after a typical oral dose.
3. Tumor microenvironment — cancer cells in a Petri dish are not embedded in stroma, are not perfused by leaky tumor vasculature, do not have hypoxic cores, do not have surrounding immune cells, and are not subject to the immunosuppressive cytokine milieu of an actual human tumor. Many compounds that work beautifully in cell culture fail in real tumors because they cannot reach the relevant cells at relevant concentrations or because the tumor microenvironment renders the cancer cells resistant.
4. Selection bias in cell-line work — cancer cell lines used in screening are typically highly proliferative, genetically simplified, and often heavily passaged. They may not represent the heterogeneity, drug resistance, or evolutionary capacity of actual human tumors.
5. Off-target toxicity — many compounds that kill cancer cells in vitro also damage normal cells at similar concentrations. The clinical question is not just “does it kill cancer cells” but “does it kill cancer cells preferentially enough that it can be dosed to clinical benefit without unacceptable toxicity.”
6. Publication bias — in vitro studies showing positive antiproliferative effects are more likely to be published than studies showing no effect. The body of published in vitro data therefore systematically overestimates the likelihood of clinical translation.

For these reasons, the established norm in clinical pharmacology is that promising in vitro data justify further investigation through animal models, then phase-I human safety studies, then phase-II efficacy studies, then phase-III randomized controlled trials. Each step typically eliminates a large fraction of candidates. Bitter melon has not advanced past the early stages of this pipeline for any cancer indication.

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A Reasonable Integrative Role

If bitter melon is not a cancer treatment, is there any legitimate role for it in the care of a cancer patient? The answer is qualified yes, in specific contexts and under oncologist supervision:

• Glycemic control in cancer patients with co-existing diabetes or prediabetes — bitter melon's established blood-sugar-lowering effect (per the Blood Sugar deep-dive) makes it a reasonable adjunct for cancer patients who also have type 2 diabetes, particularly those whose glucose control is destabilized by glucocorticoid-containing chemotherapy regimens (such as CHOP for lymphoma, R-CHOP for diffuse large B-cell lymphoma, or steroid-tapered protocols for many tumor types). The hyperglycemia of glucocorticoid use is a real clinical problem with documented effects on infection risk and possibly on cancer outcomes.
• Metabolic-syndrome management in cancer survivors — many cancer survivors develop metabolic syndrome after treatment due to weight gain, reduced activity, and chronic glucocorticoid or hormonal exposure. Bitter melon as part of a comprehensive metabolic recovery plan is reasonable.
• Dietary inclusion as a vegetable — eating bitter melon as a food (in stir-fries, curries, soups) provides a nutrient-dense, low-glycemic, bitter-rich vegetable that fits into most cancer-supportive dietary frameworks. The dose from food is well below any plausible anticancer threshold but is also far below any toxicity threshold.
• Use in patients with established TCM or Ayurvedic care — for patients already engaged with traditional medicine systems, bitter melon as part of culturally appropriate care, in coordination with conventional oncology, can be reasonable. The key is coordination and communication so that the conventional oncologist knows what the patient is taking.

What is not reasonable: substituting bitter melon for evidence-based cancer treatment, declining or delaying conventional therapy in favor of bitter melon, taking bitter melon at extreme doses in the hope of larger anticancer effect, or believing marketing claims that bitter melon “treats” or “cures” cancer.

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Cautions: What Patients With Cancer Should Know

• Bitter melon is NOT a cancer treatment. No randomized controlled trial demonstrates that bitter melon prevents, treats, or cures any cancer. Marketing claims that suggest otherwise are not supported by evidence.
• Tell your oncologist what you are taking. Any supplement, including bitter melon, may interact with chemotherapy, targeted therapy, or hormonal therapy. The interaction profile of bitter melon with specific chemotherapy agents is not well characterized, so disclosure is essential.
• Drug-herb interactions of concern — bitter melon can potentiate hypoglycemic drugs and could destabilize glucose control in patients on insulin or sulfonylureas during cancer treatment. Bitter melon's effect on cytochrome P450 enzymes is modest but not zero, so theoretical interactions with chemotherapy substrates of CYP3A4 should be considered.
• G6PD deficiency — absolute contraindication for seeds; this is particularly important for cancer patients of high-prevalence ancestry who may also be exposed to other oxidant drugs (dapsone, primaquine, methylene blue, rasburicase) as part of cancer or supportive care.
• Pregnancy — absolute contraindication; uterine-stimulating activity. This includes patients of reproductive age undergoing fertility-preserving cancer therapy.
• Cachexia and severe wasting — bitter melon may worsen weight loss in patients who already have cancer cachexia or severe nutritional compromise; the appetite-suppressing bitter-taste effect is potentially counterproductive in this population
• Hepatotoxicity risk in patients on hepatotoxic chemotherapy — some cancer drugs (methotrexate, irinotecan, regimens containing oxaliplatin) are hepatotoxic; adding a botanical with unclear hepatic interaction profile is not advisable without oncologist concurrence
• Bleeding risk — some bitter melon constituents may have mild antiplatelet effects; relevant if a patient is on anticoagulants, thrombocytopenic from chemotherapy, or approaching surgery
• Quality and standardization of supplements — supplement-form bitter melon products vary wildly in active compound content; cancer patients should choose products with third-party verification (USP, NSF, ConsumerLab) if using supplements at all

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Key Research Papers

1. Lee-Huang S, Huang PL, Nara PL, Chen HC, Kung HF, Huang P, Huang HI, Huang PL (1990). MAP 30: a new inhibitor of HIV-1 infection and replication. FEBS Letters 272(1-2):12-18. — PubMed: Lee-Huang MAP30 1990
2. Lee-Huang S, Huang PL, Sun Y, Chen HC, Kung HF, Huang PL, Murphy WJ (2000). Inhibition of MDA-MB-231 human breast tumor xenografts and HER2 expression by anti-tumor agents GAP31 and MAP30. Anticancer Research 20(2A):653-659. — PubMed: Lee-Huang MAP30 breast cancer xenograft
3. Ray RB, Raychoudhuri A, Steele R, Nerurkar P (2010). Bitter melon (Momordica charantia) extract inhibits breast cancer cell proliferation by modulating cell cycle regulatory genes and promotes apoptosis. Cancer Research 70(5):1925-1931. — PubMed: Ray 2010 breast cancer
4. Pitchakarn P, Ogawa K, Suzuki S, Takahashi S, Asamoto M, Chewonarin T, Limtrakul P, Shirai T (2010). Momordica charantia leaf extract suppresses rat prostate cancer progression in vitro and in vivo. Cancer Science 101(10):2234-2240. — PubMed: Pitchakarn 2010 prostate
5. Kaur M, Deep G, Jain AK, Raina K, Agarwal C, Wempe MF, Agarwal R (2013). Bitter melon juice activates cellular energy sensor AMP-activated protein kinase causing apoptotic death of human pancreatic carcinoma cells. Carcinogenesis 34(7):1585-1592. — PubMed: Kaur 2013 pancreatic
6. Singh A, Singh SP, Bamezai R (1998). Momordica charantia (Bitter gourd) peel, pulp, seed and whole fruit extract inhibits mouse skin papillomagenesis. Toxicology Letters 94(1):37-46. — PubMed: Singh 1998 skin papilloma
7. Grossmann ME, Mizuno NK, Dammen ML, Schuster T, Ray A, Cleary MP (2009). Eleostearic acid inhibits breast cancer proliferation by means of an oxidation-dependent mechanism. Cancer Prevention Research 2(10):879-886. — PubMed: Grossmann 2009 eleostearic acid
8. Yasui Y, Hosokawa M, Sahara T, Suzuki R, Ohgiya S, Kohno H, Tanaka T, Miyashita K (2005). Bitter gourd seed fatty acid rich in 9c, 11t, 13t-conjugated linolenic acid induces apoptosis and up-regulates the GADD45, p53 and PPARgamma in human colon cancer Caco-2 cells. Prostaglandins, Leukotrienes and Essential Fatty Acids 73(2):113-119. — PubMed: Yasui 2005 colon cancer CLA
9. Manoharan G, Jaiswal SR, Singh J (2014). Effect of alpha, beta-momorcharin on viability, caspase activity, cytochrome c release and on cytosolic calcium levels in different cancer cell lines. Molecular and Cellular Biochemistry 388(1-2):233-240. — PubMed: Manoharan 2014 momorcharin
10. Nagasawa H, Watanabe K, Inatomi H (2002). Effects of bitter melon (Momordica charantia L.) or ginger rhizome (Zingiber offifinale Rosc) on spontaneous mammary tumorigenesis in SHN mice. American Journal of Chinese Medicine 30(2-3):195-205. — PubMed: Nagasawa 2002 mammary tumor
11. Ru P, Steele R, Nerurkar PV, Phillips N, Ray RB (2011). Bitter melon extract impairs prostate cancer cell-cycle progression and delays prostatic intraepithelial neoplasia in TRAMP model. Cancer Prevention Research 4(12):2122-2130. — PubMed: Ru 2011 prostate TRAMP
12. Memorial Sloan Kettering Cancer Center, About Herbs Database — Bitter Melon entry, regularly updated — MSKCC Integrative Medicine: Bitter Melon

PubMed Topic Searches

• PubMed: Bitter melon cancer cell apoptosis
• PubMed: MAP30 cancer
• PubMed: Cucurbitacin anticancer activity
• PubMed: Bitter melon pancreatic cancer
• PubMed: Bitter melon integrative oncology
• PubMed: Momordicin/momordicoside anticancer

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Connections

• Bitter Melon (Main Page)
• Bitter Melon Benefits Hub
• Bitter Melon for Blood Sugar
• Bitter Melon for Diabetes Complications
• Bitter Melon for Weight Loss
• Cancer (Overview)
• Leukemia
• Lymphoma
• Metastatic Cancers
• Diabetes
• Metabolic Syndrome
• Insulin Resistance
• Berberine
• Gymnema
• Cinnamon
• All Herbs

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