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Lim, P.; Han, I.; Seow, K.; Chen, K. Hyperthermic Intraperitoneal Chemotherapy in Epithelial Ovarian Cancers. Encyclopedia. Available online: https://encyclopedia.pub/entry/49271 (accessed on 04 August 2024).
Lim P, Han I, Seow K, Chen K. Hyperthermic Intraperitoneal Chemotherapy in Epithelial Ovarian Cancers. Encyclopedia. Available at: https://encyclopedia.pub/entry/49271. Accessed August 04, 2024.
Lim, Pei-Qi, I-Hung Han, Kok-Min Seow, Kuo-Hu Chen. "Hyperthermic Intraperitoneal Chemotherapy in Epithelial Ovarian Cancers" Encyclopedia, https://encyclopedia.pub/entry/49271 (accessed August 04, 2024).
Lim, P., Han, I., Seow, K., & Chen, K. (2023, September 16). Hyperthermic Intraperitoneal Chemotherapy in Epithelial Ovarian Cancers. In Encyclopedia. https://encyclopedia.pub/entry/49271
Lim, Pei-Qi, et al. "Hyperthermic Intraperitoneal Chemotherapy in Epithelial Ovarian Cancers." Encyclopedia. Web. 16 September, 2023.
Hyperthermic Intraperitoneal Chemotherapy in Epithelial Ovarian Cancers
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This entry is adapted from the peer-reviewed paper 10.3390/ijms231710078

Most patients with epithelial ovarian cancers (EOCs) are at advanced stages (stage III–IV), for which the recurrence rate is high and the 5-year survival rate is low. The most effective treatment for advanced diseases involves a debulking surgery followed by adjuvant intravenous chemotherapy with carboplatin and paclitaxel. Nevertheless, systemic treatment with intravenous chemotherapeutic agents for peritoneal metastasis appears to be less effective due to the poor blood supply to the peritoneal surface with low drug penetration into tumor nodules. Based on this reason, hyperthermic intraperitoneal chemotherapy (HIPEC) emerges as a new therapeutic alternative. By convection and diffusion, the hyperthermic chemotherapeutic agents can directly contact intraperitoneal tumors and produce cytotoxicity. In a two-compartment model, the peritoneal–plasma barrier blocks the leakage of chemotherapeutic agents from peritoneal cavity and tumor tissues to local vessels, thus maintaining a higher concentration of chemotherapeutic agents within the tumor tissues to facilitate tumor apoptosis and a lower concentration of chemotherapeutic agents within the local vessels to decrease systemic toxicity. 

hyperthermic intraperitoneal chemotherapy HIPEC ovarian cancer survival

1. Introduction

Ovarian cancer is the second most common gynecologic malignancy in developed countries and the third most common gynecologic malignancy in developing countries [1]. Approximately 75% of affected women have stage III (disease that has spread throughout the peritoneal cavity or that involves lymph nodes) or stage IV (disease that has spread to more distant sites) disease at diagnosis. The 10-year survival rate of women with advanced disease is only 10% to 15%, and it has been the same for the past 20 years [2]. The most effective treatment for advanced diseases involves a cytoreductive debulking surgery to reduce the tumor burden followed by six cycles of adjuvant intravenous chemotherapy with carboplatin and paclitaxel. Alternatively, an interval cytoreductive surgery is performed after three cycles of neoadjuvant chemotherapy [3].
Peritoneal carcinomatosis of ovarian, fallopian tube or primary peritoneal cancers is deemed a technical obstacle to complete resection [4]. However, systemic treatment with intravenous chemotherapeutic agents for peritoneal metastasis appears to be less effective as compared to its use for lung or liver metastases. This realistic finding is due to the poor blood supply to the peritoneal surface with low drug penetration into tumor nodules, thereby preventing eradication of tumor growth. Based on this reason, locoregional drug delivery has emerged, and this route allows chemotherapeutic agents to be administered in a higher dose by instillation in the peritoneum (intraperitoneal) [5][6]. Intraperitoneal administration of chemotherapeutic agents specifically targets remaining microscopic diseases after complete cytoreduction. By way of delivering chemotherapy directly within the peritoneal cavity, poorly vascularized tumors could be more exposed to the local high concentration of chemotherapy. On the other hand, the blood–peritoneal barrier also limits the passage of this high concentration of chemotherapy back to the blood vessels, thus minimizing systemic toxicity while maximizing local effects. Currently, many randomized trials, meta-analyses and real-world data reveal that the administration of adjuvant intraperitoneal chemotherapy after cytoreduction improves overall survival (OS) and progression-free survival (PFS) in patients with advanced ovarian cancers [2].
Hyperthermic intraperitoneal chemotherapy (HIPEC) was first used clinically in 1980 by Spratt et al., who performed hyperthermic chemoperfusion with thiotepa in a patient with pseudomyxoma peritonei. Theoretically, hyperthermia has direct cytotoxic effects on tumor cells and induces the production of heat shock proteins that serve as receptors for natural killer (NK) cells; these actions lead to apoptosis of tumor cells and inhibition of angiogenesis. Practically, heat is directly cytotoxic, improves chemotherapy penetration into the tumor tissues and is synergistic with commonly used chemotherapeutic agents including cisplatin, paclitaxel, oxaliplatin and mitomycin c [2][7]. The optimal temperatures for administration of chemotherapeutic agents fall between 42 and 43 °C. The synergy between heat and drug cytotoxicity starts at 39 °C and falls off at 43 °C. Temperatures above 44 °C can cause apoptosis in normal cells [6].

2. Molecular and Cellular Mechanisms of Actions: HIPEC and Chemotherapeutic Agents

2.1. HIPEC

The first study for HIPEC, which started with an animal model, was conducted by Euler in 1974. Because traditional treatment of surgical resection or systemic intravenous chemotherapy may be less effective, the goal of hyperthermia is to enhance the antitumor effect of chemotherapeutic agents. It is very important to understand the pharmacokinetic behavior and drug–tissue transport after intraperitoneal chemotherapy. However, both standardization of the HIPEC techniques and the results from clinical trials are still equivocal. Therefore, it is still controversial with regard to the efficacy and safety of HIPEC for clinical malignancies including ovarian, colorectal, appendix and peritoneal cancers. The clinicians in favor of HIPEC use RCTs of ovarian cancers to support the benefit of HIPEC, while those who oppose the application of HIPEC use negative RCT results of colorectal cancers [5].
During HIPEC, relevant drug properties of chemotherapeutic agents include molecular weight, hydrodynamic size, charge and configuration; relevant physical parameters, treatment variables and carrier properties include hydrostatic pressure, temperature and viscosity. An overview of the drug properties, physical parameters, treatment variables, carrier properties and tumor microenvironment (TME) properties is summarized in Table 1.
Table 1. An overview of relevant factors that affect tissue transport during intraperitoneal drug delivery (IPDD).

Physical parameter, treatment, variable, carrier properties

Hydrostatic pressure

Osmolarity

Temperature

pH

Viscosity

Exposure time

Drug properties

Concentration

Molecular weight

Hydrodynamic diameter

Configuration

Water solubility

Protein binding

Charge ionization

TME properties

Interstitial fluid pressure

Retardation coefficient

Solid pressure

Cellular composition

Hydraulic conductivity

Stromal and vascular density

Viscoelasticity, stiffness

Geometrical arrangement
The relevant molecular and cellular mechanisms of HIPEC actions are described below. Two critical factors that affect tissue transport after intraperitoneal drug delivery (IPDD) are convection (pressure gradient) and diffusion (concentration gradient) [5].
Figure 1 shows the pharmacokinetic model of HIPEC which is delivered based on (Cp/Cb)IP/(Cp/Cb)IV, where Cp represents the concentration of the drug in the peritoneum and Cb represents the concentration of the drug in blood. In terms of chemotherapeutic agents used during HIPEC, area under the curve (AUC) represents drug concentration and exposure time to the tumor in the peritoneum [8][9]. The mechanisms of HIPEC involve a two-compartment model to describe the pharmacokinetics of IPDD [5][8][9][10]; intraperitoneal chemotherapy drugs are delivered via convection and diffusion gradients. Figure 1 illustrates the bidirectional models for intravenous (IV) and intraperitoneal (IP) therapy. The outer layer of the tumor can achieve a high concentration of drug levels by direct exposure (IP), while the drug can reach the inner core layer of the tumor by microcirculation through systemic circulation (IV). Between the two compartments is the peritoneal–plasma barrier (PPB), which plays a key role in the compartmental model and can decrease the drug clearance rate from the peritoneal cavity to systemic circulation. During IP therapy, the PPB blocks the leakage of chemotherapeutic agents from the peritoneal cavity and tumor tissues to local vessels, thus maintaining a higher concentration of chemotherapeutic agents within the tumor tissues to facilitate tumor apoptosis, and a lower concentration of chemotherapeutic agents within the local vessels to decrease systemic toxicity.
Figure 1. Bidirectional models for intravenous and intraperitoneal therapy. The outer layer of the tumor can achieve a high concentration of drug levels by direct exposure, while the drug can reach the inner core layer of the tumor by microcirculation through systemic circulation. Between the two compartments is the peritoneal–plasma barrier, which can decrease drug clearance rate from peritoneal cavity to systemic circulation.
The molecular and cellular actions of HIPEC are mainly via convection, diffusion and hyperthermia.

2.2. Paclitaxel

There is compelling evidence proving that paclitaxel (PTX) can kill cancer cells through induction of apoptosis. This is predominantly based on paclitaxel’s combination with microtubules to affect microtubule stabilization. As a result, consequent arrest of the cell cycle at the mitotic phase can be determined as paclitaxel-induced cytotoxicity [11].
There are also studies suggestive of different sensitivities of paclitaxel to microtubules of different statuses, and the concentration of paclitaxel is viewed as the main factor of the apoptogenic mechanism [11][12]. The detailed mechanisms of paclitaxel’s actions can be described as three types of pathways (Figure 2). First, paclitaxel inhibits the microtubules to disassemble to form tubulin dimers, thus blocking the growth of the tumors at the G2/M phase to induce subsequent cell death. Second, apoptosis of tumor cells is also facilitated by paclitaxel via the p53 and reactive oxygen species (ROS) pathway. Finally, paclitaxel can induce immune PXT pathway activation to inhibit the growth of the tumor cells. In comparison to other chemotherapeutic agents, paclitaxel is a water-insoluble and high-molecular-weight compound, so intraperitoneally (IP) administered paclitaxel is gradually drained from the peritoneum through lymphatic stomata. The characteristic of prolonged retention for IP paclitaxel allows it to directly and progressively penetrate peritoneal disseminated tumors.
Figure 2. Different types of PTX pathways for inducing death of tumor cells.
An improved understanding of the cell cycle and apoptosis is helpful in depicting paclitaxel-induced apoptosis. Based on the aforementioned pathways, novel paclitaxel-based regimens can emerge for next-generation cancer therapy.

2.3. Cisplatin

Platinum-based anticancer drugs are widely used in chemotherapy to treat neoplasms by affecting DNA and subsequent RNA transcription and translation. Cisplatin is one of the most widely used platinum-based chemotherapy agents used to attack different cancers and sarcomas. The main mechanism of cisplatin is that it cross-links with the purine bases on DNA, leading to impairment in DNA repair and subsequent cell death [13]. Furthermore, cisplatin can also attack mitochondria and trigger the production of ROS. These actions can destroy lysosomes, causing a release of lysosomal protease, and impair the endoplasmic reticulum to affect calcium storage [14]. The main obstacle in using this type of drug is the development of drug resistance and toxicity. It is important to understand the mechanisms of action of drug transportation and metabolic pathways. Much evidence has indicated that the therapeutic and toxic effects of platinum drugs on cells are not only due to covalent adduct formation between platinum complexes and DNA, but also RNA and many proteins. Some studies have suggested that drug resistance of platinum-based chemotherapeutic agents is mainly induced by increasing expression of various transporters and increasing repair of platinum–DNA adducts. In terms of precision medicine, functional genomics is important to predict the platinum–drug response of patients, and genetic polymorphism constitutes the basis of individualized cancer therapy [14].

3. Therapeutic Effects of HIPEC in Epithelial Ovarian Cancers

The therapeutic effects of HIPEC on women with ovarian cancers have been explored. Table 2 and Table 3 are summaries of clinical studies that focused on HIPEC treatment for primary advanced ovarian cancers and recurrent ovarian cancers, respectively.
Table 2. A summary of clinical studies investigating HIPEC treatment for primary advanced ovarian cancers.

Authors

Study Design

Patients

Treatment

Results

Lim MC (2017)

Prospective, randomized multicenter trial

1. Patients with stage III/IV primary advanced epithelial ovarian cancer who have optimal cytoreductive surgery;

2. Total: 184 patients.

Groups:

1. Intraoperative HIPEC with cisplatin (75 mg/m2, 90 min);

2. Control arm (no HIPEC)

1. HIPEC:

  2-year PFS: 43.2%;

  5-year PFS: 20.9%;

  5-year OS: 51.0%.

2. Control group:

  2-year PFS: 43.5%

  5-year PFS: 16.0% (p = 0.569)

  5-year OS: 49.4% (p = 0.574)

W.J. van Driel (2018)

Multicenter, prospective, randomized phase III trial

1. Newly diagnosed stage III epithelial ovarian, fallopian tube, or peritoneal cancers;

2. Not eligible for primary cytoreductive surgery;

3. 245 patients.

Three cycles of carboplatin (AUC of 5 to 6 mg/mL/min) and paclitaxel (175 mg per square meter of body-surface area) after interval cytoreductive surgery for all patient.

Groups:

1. HIPEC with cisplatin (100 mg per square meter), with intra-abdominal temperature of 40 °C (104 °F), open technique;

2. Without HIPEC.

1. Median follow up: 4.7 years

2. Disease recurrence or death:

  • Without HIPEC: 110 out of 123 patients (89%);

  • With HIPEC: 99 of the 122 patients (81%);

  • (HR: 0.66; 95% CI: 0.50–0.87; p = 0.003).

3. Median recurrence-free survival (RFS):

  • Without HIPEC: 10.7 months;

  • With HIPEC: 14.2 months.

4. Median OS:

  • Without HIPEC: 33.9 months;

  • With HIPEC: 45.7 months.

Zhang G (2019)

Meta-analysis including randomized controlled trials and case–control trials

1. Patients with primary stage III/IV ovarian cancers;

2. 13 comparative studies.

Groups:

1. Interval CRS plus HIPEC;

2. Primary CRS plus HIPEC;

3. Without HIPEC.

1. Better outcomes of surgery and HIPEC in patients with primary advanced ovarian cancer (pooled HR for OS: 0.54; 95% CI: 0.45–0.66; pooled HR for PFS: 0.45; 95% CI: 0.32–0.62);

2. Favorable clinical outcome for stage III/IV ovarian cancer with initial diagnosis (HR: 0.64,95% CI: 0.50–0.82, HR: 0.36,95% CI: 0.20–0.65).

Lei Z (2020)

Multicenter retrospective cohort study

1. Patients with stage III primary epithelial ovarian cancers;

2. 584 patients.

1. Closed technique;

2. Circulating heated saline with cisplatin at a dose of 50 mg/m2

3. 43 °C, 60 min.

Median survival time:

1. HIPEC: 49.8 months;

2. Non-HIPEC 34.0 months

  • (HR: 0.63, 95%CI, 0.49–0.82, p < 0.001).

3-year overall survival rate:

1. Surgery + HIPEC: 60.3%

  (95% CI: 55.3–65.0%).

2. Surgery alone: 49.5% (95% CI: 41.0–57.4%) (weighted HR: 0.64; 95% CI: 0.50–0.82; p < 0.001).
Table 3. A summary of clinical studies investigating HIPEC treatment for recurrent ovarian cancers.

Authors

Study Design

Patients

Treatment

Results

Cascales-Campos (2011)

Descriptive study of outcomes in both primary and recurrent epithelial ovarian cancer

1. Patients previously diagnosed with primary stage IIIc (35 patients) or recurrent ovarian cancer (11 patients) treated using peritonectomy procedures and HIPEC;

2. Total: 46 patients.

A total of 37 patients (80.4%) received systemic chemotherapy (3–18 cycles per patient) before HIPEC and surgery.

Regimen dose of HIPEC:

1. Paclitaxel (60 mg/m2);

2. Cisplatin (75 mg/m2) in taxol-allergic patients

3. 60 min, 42 °C.

1. Median operation time: 380 min (200–540 min);

2. CC-0 (no macroscopic tumor residue at the end of cytoreduction) achieved in 38 patients (82.6%).

Spiliotis (2015)

Prospective randomized phase III study

1. Patients with advanced ovarian cancer (FIGO) IIIc and IV) who experienced disease recurrence after initial treatment with conservative or debulking surgery and systemic chemotherapy;

2. 120 patients.

Groups:

HIPEC (group A):

1. CRS was followed by the administration of HIPEC and subsequent systemic chemotherapy;

2. Platinum-sensitive disease (n = 34): cisplatin 100 mg/m2 + paclitaxel 175 mg/m2, 60 min at 42.5 °C;

3. Platinum-resistant disease (n = 26): doxorubicin 35 mg/m2 + (paclitaxel 175 mg/m2 or mitomycin 15 mg/m2), 60 min at 42.5 °C.

Non-HIPEC (group B): CRS followed by systemic chemotherapy.

Overall mean survival:

HIPEC: 26.7 months;

Non-HIPEC: 13.4 months

(p < 0.006).

3-year survival:

HIPEC: 75%;

Non-HIPEC: 18%

(p < 0.01).

Zhang G (2019)

Meta-analysis including randomized controlled trials and case–control trials

Patients with recurrent ovarian cancers.

Groups:

1. HIPEC;

2. Without HIPEC.

1. OS: improved for HIPEC group;

(HR: 0.45, 95% CI: 0.24–0.83)

2. PFS: no correlation between HIPEC and non-HIPEC group

(HR: 0.55, 95% CI: 0.27–1.11).

4. The Safety, Adverse Effects and Quality of Life in Patients Who Undergo HIPEC

Based on a review of the literature from 2008 to 2014, the morbidity and mortality from HIPEC was thought to be higher than that from CRS alone [15]. However, adverse events from grade 3 to 5 in the OVHIPEC trial were reported in 30 patients (25%) in the interval CRS group and in 32 patients (27%) in the interval CRS and HIPEC group (p = 0.76). The incidence of adverse events was not statistically different between these two arms. In terms of side effects of HIPEC, the most common grade 3 to 4 events were abdominal pain, infections, ileus, thromboembolic events and pulmonary events [2][3]. Another prospective, randomized multicenter trial reported in 2017 also showed no differences between the postoperative outcomes, including extent of surgery, estimated blood loss, residual tumor and hospitalization day between both groups, except operation time (487 min. vs. 404 min., p < 0.001) due to the HIPEC procedure. The most common adverse event was anemia: 67.4% in the HIPEC group and 50% in the control group (p = 0.025). The other common toxicity in the HIPEC group was the elevation of creatinine (15.2% vs. 4.3%, p = 0.026). There were no differences between groups in the incidence of transfusion (35.9% vs. 29.3%, p = 0.432), neutropenia (19.6% vs. 10.9%, p = 0.151) and thrombocytopenia (9.8% vs. 3.3%, p = 0.136) [16].
Acute renal failure is one of the most common toxicities of cisplatin. Cisplatin-related renal toxicity appears to be preventable by administration of sodium thiosulfate to protect renal function [17]. A retrospective study showed that the widespread use of RIFLE criteria for acute renal dysfunction would have major benefits in terms of accurately diagnosing patients undergoing HIPEC procedures [18]. Volume status optimization, early nutritional support, sufficient anticoagulation and point-of-care coagulation management are also encouraged postoperatively after the CRS and HIPEC procedures [19].
The effect of HIPEC on the patient’s health-related quality of life (HRQoL) was evaluated in the OVHIPEC trial. The researchers concluded that the addition of HIPEC to interval CRS does not negatively impact HRQoL in patients with stage III ovarian cancers [20]. Currently, there is still no conclusion nor consensus regarding the usage regimen and temperature setting of HIPEC yet. Because the effectiveness and adverse events are greatly affected by the time of administration, more clinical trials for the optimization and establishment of HIPEC are required in the future [21].
The main risk factors for prolonged length of stay after CRS/HIPEC were advanced age, hypoalbuminemia and multivisceral resection [22]. A retrospective single-center review in April 2021 presented a comparative analysis of the outcomes of CRS and HIPEC between patients under 65 and those ≥65 years. A total of 245 patients underwent CRS and HIPEC during the study period, with 76/245 (31%) ≥ 65 years at the time of intervention. The median length of hospital stay in the ≥65-year-old group was 14.5 days vs. 13 days in the <65-year-old group (p = 0.01). Likewise, significant morbidity (Clavien–Dindo ≥ Grade IIIa) was higher in the ≥65-year-old group than in the <65-year-old group (18.4% vs. 11.2%). This study demonstrated a higher perioperative major morbidity in the ≥65-year-old group, but a lower mortality in the patients undergoing CRS/HIPEC for disseminated intraperitoneal malignancy [23].
However, the effects and adverse effects of HIPEC remain to be investigated due to the relatively small sample size of the existent studies.

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Subjects: Obstetrics & Gynaecology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Pei-Qi Lim
,
I-Hung Han
,
Kok-Min Seow
,
Kuo-Hu Chen
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Update Date: 18 Sep 2023
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